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Arginine  Technical Reports

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Record 1 from database: MEDLINE
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Title

Diagnostic studies with intravenous and intranasal growth hormone-releasing peptide-2 in children of short stature.

Author

Pihoker C; Middleton R; Reynolds GA; Bowers CY; Badger TM

Address

Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, USA.

Source

J Clin Endocrinol Metab, 1995 Oct, 80:10, 2987-92

Abstract

GH secretion is primarily regulated by the hypothalamic-releasing hormones GHRH and somatostatin. Additionally, several neurotransmitters act at the hypothalamus and pituitary to modulate GH release. The agents commonly used in clinical practice to diagnose GH deficiency, such as arginine, insulin and L-dopa, act through the neural GH network. Many children with a poor GH response to conventional agents have a significant serum GH response to iv GHRH. GH-releasing peptides (GHRPs) are synthetic peptides that like GHRH act directly on pituitary somatotrophs to stimulate GH release. GHRP-2, an investigational drug, is one of the most potent members of the GHRP family. It has been shown to be effective in adults via the oral and intranasal as well as the iv route of administration. In this study, GH responses to GHRP-2 were compared with GH responses to other provocative agents in children of short stature. GHRP-2 was administered iv or intranasally to children with short stature. In the same subjects, GHRP-2 was administered iv in combination with GHRH. Twenty-four children undergoing evaluation for GH deficiency received at least one conventional agent (arginine, L-dopa/exercise, insulin) in addition to iv GHRH and GHRP-2. The GH responses to GHRH or GHRP-2 were similar in each child, and both were equally reliable predictors of pituitary reserve. The conventional agents used in GH testing were less likely to predict the capacity of the pituitary to release GH than were either GHRH or GHRP-2. There was no correlation between maximal GH response to standard tests with GH responses to GHRH or GHRP-2. A subset of the group of 21 children who had a robust response to iv GHRP-2 were later administered GHRH+GHRP-2 simultaneously. The GH response to GHRH+GHRP-2 was synergistic in this group of 12 children, similar to previously reported observations in adults of normal stature. Fifteen of the 21 children who had a robust response to the iv GH-releasing factors also received intranasal GHRP-2. All 15 of these children had a significant GH response to intranasal GHRP-2 over a dose range of 5-20 micrograms/kg per dose. The mean peak GH response to 15 micrograms/kg was 31.3 micrograms/L. The intranasal preparation was well tolerated.(ABSTRACT TRUNCATED AT 400 WORDS)

Language of Publication

English

Unique Identifier

96001292

MeSH Heading (Major)

Growth Disorders|*DI/*ET; Hormones, Synthetic|AD/*DU; Oligopeptides|AD/*DU; Somatotropin|BL/*DF/*SE; Somatotropin-Releasing Hormone|AD/*DU

MeSH Heading

Administration, Intranasal; Adolescence; Adult; Arginine|DU; Child; Child, Preschool; Comparative Study; Exercise; Female; Human; Injections, Intravenous; Insulin|DU; Levodopa|DU; Male; Support, Non-U.S. Gov't

Publication Type

CLINICAL TRIAL; CONTROLLED CLINICAL TRIAL; JOURNAL ARTICLE

ISSN

0021-972X

Country of Publication

UNITED STATES

Record 2 from database: MEDLINE
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Title

Maturation of the regulation of growth hormone secretion in young males with hypogonadotropic hypogonadism pharmacologically exposed to progressive increments in serum testosterone.

Author

Giustina A; Scalvini T; Tassi C; Desenzani P; Poiesi C; Wehrenberg WB; Rogol AD; Veldhuis JD

Address

Department of Internal Medicine, University of Brescia, Italy. Giustina@master.cci.unibs.it

Source

J Clin Endocrinol Metab, 1997 Apr, 82:4, 1210-9

Abstract

To study the onset of the action of gonadal sex steroids on the GH axis in spontaneous puberty, which is prolonged and sparingly predictable, we present a clinical investigative paradigm in which six previously untreated boys with isolated hypogonadotropic hypogonadism were exposed to progressively higher testosterone levels designed to mimic the androgen environment recognized during the early stages of puberty. We administered three incremental doses of testosterone (25-, 50-, and 100-mg im injections), each over a period of 4 weeks. Studies of overnight pulsatile GH secretion and GH responses to GHRH alone or combined with L-arginine (a functional somatostatin antagonist) were performed before testosterone administration and after each dose of testosterone. Serum testosterone, but not estrogen, levels increased progressively in all subjects during therapy. Deconvolution analysis of GH release profiles disclosed that GH secretory burst mass was stimulated significantly even by 25 mg testosterone. This parameter was not altered further by higher doses of testosterone. Spontaneous GH secretory burst number and amplitude increased significantly only after the 50- and 100-mg testosterone treatments, after which the serum GH response to GHRH and arginine also rose significantly. In contrast, the GH response to GHRH alone was not significantly affected by any dose of testosterone. Serum testosterone levels correlated significantly with the primary parameters of nocturnal GH secretion. In summary, our experimental model suggests that in males even very small increases in circulating testosterone occurring during the earliest stages of puberty are able to amplify pulsatile GH secretion. Our concomitant secretagogue data further suggest that testosterone exerts its action at different sites in the hypothalamo-somatotropic axis, i.e. directly at the pituitary level, and also at hypothalamic loci, possibly increasing both GHRH and somatostatin release.

Language of Publication

English

Unique Identifier

97255251

MeSH Heading (Major)

Arginine|*TU; Hypogonadism|DT/*ME; Somatotropin-Releasing Hormone|*TU; Somatropin|BL/*SE/UR; Testosterone|*BL

MeSH Heading

Adolescence; Circadian Rhythm; Drug Combinations; Entropy; Human; Insulin-Like Growth Factor Binding Protein 3|BL; Insulin-Like Growth Factor I|ME; Longitudinal Studies; Male; Pulsatile Flow; Sex Hormones|BL; Support, Non-U.S. Gov't

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE

ISSN

0021-972X

Country of Publication

UNITED STATES

Record 3 from database: MEDLINE
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Title

Combined pituitary deficiencies of growth hormone, thyroid stimulating hormone and prolactin due to Pit-1 gene mutation: a case report.

Author

Holl RW; Pfäffle R; Kim C; Sorgo W; Teller WM; Heimann G

Address

Department of Paediatrics I, University Children's Hospital, Ulm/Donau, Germany.

Source

Eur J Pediatr, 1997 Nov, 156:11, 835-7

Abstract

A child exhibited postnatal obstipation and icterus together with severe growth failure during the 1st year of life, a small facial skull and a prominent forehead. Endocrine work-up established the diagnosis of combined pituitary deficiencies of growth hormone, TSH and prolactin. Subsequently, the Pit-1 gene was analysed in the patient and both parents. A single point mutation was detected in exon 6 of the child: a C to G transversion on one allele, causing arginine in position 271 to be substituted by tryptophan (R271 W). This position is known as a "hot spot" for mutations. The inheritance is autosomal-dominant, as the mutated gene product interferes with DNA-binding of the wild-type protein. In contrast, other mutations in the PIT-1 gene are inherited in an autosomal-recessive mode. Conclusion: Diagnosing Pit-1 gene mutations as a rare cause of combined pituitary deficiency is important both for genetic counselling as well as for predicting the future course in the patient (spontaneous puberty, no glucocorticoid substitution necessary during stress periods).

Language of Publication

English

Unique Identifier

98052286

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MeSH Heading (Major)

DNA-Binding Proteins|*GE; Growth Disorders|*GE/ME; Homeodomain Proteins|*GE; Pituitary Hormones|*DF/ME; Point Mutation|*; Transcription Factors|*GE

MeSH Heading

Arginine; Case Report; DNA Mutational Analysis; Human; Infant; Male; Prolactin|DF/ME; Somatotropin|DF/ME; Thyrotropin|DF/ME; Tryptophan

Publication Type

JOURNAL ARTICLE

ISSN

0340-6199

Country of Publication

GERMANY

Record 4 from database: MEDLINE
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Title

Pituitary dwarfism in the R271W Pit-1 gene mutation.

Author

Aarskog D; Eiken HG; Bjerknes R; Myking OL

Address

Barneklinikken, Bergen, Norway.

Source

Eur J Pediatr, 1997 Nov, 156:11, 829-34

Abstract

The Pit-1 gene encodes the POU-domain transcription factor Pit-1 which is important for the differentiation of the anterior pituitary and regulation of the PRL, GH and TSH genes. As a member of the POU domain transcription factors, Pit-1 contains a DNA-binding region, consisting of a POU-specific domain and a POU homeodomain. Mutation of the Pit-1 gene causes hypoplasia of the pituitary gland and deficiencies of GH, PRL and TSH. In a DNA sample from a 3-month-old girl with severe growth deficiency from birth, single stranded conformational polymorphism analysis of the Pit-1 gene identified a gel shift in exon 6. DNA-sequencing disclosed a single base mutation in codon 271 (CGG to TGG) that changes arginine to tryptophan (R271W) in the POU homeodomain. The patient presented distinct facial features with prominent forehead, marked mid-facial hypoplasia with depressed nasal bridge, deep-set eyes and a short nose with anteverted nostrils. MRI examination showed a hypoplastic pituitary gland. Low serum GH did not respond to insulin-arginine provocation or GHRH tests. PRL levels below the detection limit did not increase in response to a TRH test. T4 and free T4 was below detection limit (< 20 nmol/l and < 4 pmol/l). TSH was 2.0 mU/l and showed a blunt response to 6.0 mU/l following TRH test. TBG was normal. In spite of inappropriately low TSH and very low T4, T3 was in the low normal range (1.4-1.6 nmol/l) and she was clinically euthyroid. The thyroid function tests are consistent with increased monodeiodination activity and increased conversion of T4 to T3, possibly related to the Pit-1 gene mutation. GH and T4 treatment resulted in catch-up growth continued during 5 years of therapy. Conclusion: Reports of nine other cases of R271W mutations of different populations as well as the present Norwegian patient suggest codon 271 of exon 6 to be a "hot spot" for Pit-1 mutations. To enable rapid and simple detection of this type of de novo mutation we have designed a specific amplification-created-restriction-site assay to check for the R271W mutation in patients suspected to have this rare form of genetic defect in growth hormone production.

Language of Publication

English

Unique Identifier

98052285

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MeSH Heading (Major)

Dwarfism|*GE/ME; DNA-Binding Proteins|*GE/ME; Homeodomain Proteins|*GE/ME; Mutation|*; Transcription Factors|*GE/ME

MeSH Heading

Arginine; Case Report; DNA Mutational Analysis; Female; Human; Infant; Pituitary Gland|ME; Pituitary Hormones|ME; Polymorphism, Single-Stranded Conformational; Thyroid Hormones|ME; Tryptophan

Publication Type

JOURNAL ARTICLE

ISSN

0340-6199

Country of Publication

GERMANY

Record 5 from database: MEDLINE
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Title

Metabolic and hormonal studies of type 1 (insulin-dependent) diabetic patients after successful pancreas and kidney transplantation.

Author

Landgraf R; Nusser J; Riepl RL; Fiedler F; Illner WD; Abendroth D; Land W

Address

Department of Internal Medicine, Klinikum Innenstadt, FRG.

Source

Diabetologia, 1991 Aug, 34 Suppl 1:, S61-7

Abstract

Long-term normalization of glucose metabolism is necessary to prevent or ameliorate diabetic complications. Although pancreatic grafting is able to restore normal blood glucose and glycated haemoglobin, the degree of normalization of the deranged diabetic metabolism after pancreas transplantation is still questionable. Consequently glucose, insulin, C-peptide, glucagon, and pancreatic polypeptide responses to oral glucose and i.v. arginine were measured in 36 Type 1 (insulin-dependent) diabetic recipients of pancreas and kidney allografts and compared to ten healthy control subjects. Despite normal HbA1 (7.2 +/- 0.2%; normal less than 8%) glucose disposal was normal only in 44% and impaired in 56% of the graft recipients. Normalization of glucose tolerance was achieved at the expense of hyperinsulinaemia in 52% of the subjects. C-peptide and glucagon were normal, while pancreatic polypeptide was significantly higher in the graft recipients. Intravenous glucose tolerance (n = 21) was normal in 67% and borderline in 23%. Biphasic insulin release was seen in patients with normal glucose tolerance. Glucose tolerance did not deteriorate up to 7 years post-transplant. In addition, stress hormone release (cortisol, growth hormone, prolactin, glucagon, catecholamines) to insulin-induced hypoglycaemia was examined in 20 graft recipients and compared to eight healthy subjects. Reduced blood glucose decline indicates insulin resistance, but glucose recovery was normal, despite markedly reduced catecholamine and glucagon release. These data demonstrate the effectiveness of pancreatic grafting in normalizing glucose metabolism, although hyperinsulinaemia and deranged counterregulatory hormone response are observed frequently.

Language of Publication

English

Unique Identifier

92038615

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MeSH Heading (Major)

Blood Glucose|*ME; Diabetes Mellitus, Insulin-Dependent|BL/*SU; Hormones|*BL; Insulin|*BL; Kidney Transplantation|MT/*PH; Pancreas Transplantation|MT/*PH

MeSH Heading

Adult; Arginine|DU; Comparative Study; Epinephrine|BL; Female; Glucagon|BL; Glucose Tolerance Test; Human; Male; Norepinephrine|BL; Prolactin|BL; Prospective Studies; Reference Values; Somatotropin|BL; Support, Non-U.S. Gov't

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE

ISSN

0012-186X

Country of Publication

GERMANY

CAS Registry/EC Number

0 (Blood Glucose); 0 (Hormones); 11061-68-0 (Insulin); 51-41-2 (Norepinephrine); 51-43-4 (Epinephrine); 7004-12-8 (Arginine); 9002-62-4 (Prolactin); 9002-72-6 (Somatotropin); 9007-92-5 (Glucagon)

Record 6 from database: MEDLINE
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Title

Replacement therapy: arginine vasopressin (AVP), growth hormone (GH), cortisol, thyroxine, testosterone and estrogen.

Author

Mitchell DH; Owens B

Address

Division of Medical Oncology, University of Colorado Health Sciences Center, Denver 80262, USA.

Source

J Neurosci Nurs, 1996 Jun, 28:3, 140-52; quiz 152-4

Abstract

Replacement therapy is routinely used to treat hormone deficiencies of patients who have had surgery or radiation therapy that damages the hypothalamus or pituitary gland. Hormones commonly replaced include: arginine vasopressin (AVP), growth hormone (GH), cortisol, thyroxine (T4), testosterone and estrogen. AVP, synthesized in the hypothalamus, is stored in and released by the posterior lobe of the pituitary gland. GH is synthesized and released by the anterior pituitary gland. The other hormones are produced and released by target glands each of which is stimulated by a specific anterior pituitary hormone, which in turn is controlled by release of a specific hypothalamic hormone. Feedback control by a high circulating concentration of the target gland's hormone regulates hypothalamic hormone release. Deficiency of AVP, important for water balance in the body, is restored with the synthetic analogue, 1-desamino-8-D-arginine vasopressin (DDAVP); it is given as a nasal spray or by injection. GH is required for normal growth in the developing child; recombinant GH, produced in bacteria, is injected subcutaneously. Adrenocorticotropic hormone (ACTH) controls release of cortisol which is produced by the adrenal cortex and enables the body to cope with stress; cortisol is replaced with prednisolone given orally. Thyroid stimulating hormone (TSH) controls release of the thyroid hormones, T4 and triiodothyronine (T3), which promote growth and development, and regulate energy metabolism; for replacement of T4, oral synthetic L-thyroxine is given. Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) control release of testosterone, which promotes maturation of sperm and development of male sexual characteristics; replacement testosterone is administered intramuscularly. In females, FSH and LH control release of estrogens and progesterone which prepare the reproductive tract for release of the ovum, fertilization, implantation and development of the embryo, replacement by estrogen and progesterone preparations which are orally effective is given in a cyclic manner. A transdermal delivery system is available. Nursing implications include cautions and contraindications, potential problems of over-replacement, drug interactions as well as patient teaching points.

Language of Publication

English

Unique Identifier

96416073

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MeSH Heading (Major)

Pituitary Hormones|*DF/SE/*TU

MeSH Heading

Argipressin|TU; Drug Monitoring; Estrogens|TU; Female; Homeostasis; Human; Hydrocortisone|TU; Male; Patient Education; Self Care; Somatotropin|TU; Testosterone|TU; Thyroxine|TU

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0888-0395

Country of Publication

UNITED STATES

Record 7 from database: MEDLINE
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Title

Treatment effects of intranasal growth hormone releasing peptide-2 in children with short stature.

Author

Pihoker C; Badger TM; Reynolds GA; Bowers CY

Address

Department of Pediatrics, University of Washington, Seattle 98105, USA.

Source

J Endocrinol, 1997 Oct, 155:1, 79-86

Abstract

Growth hormone-releasing peptide (GHRP)-2 is a synthetic six amino acid peptide that is a potent GH secretagogue. Although it shares no structural homology with GH-releasing hormone, in clinical studies its actions on the pituitary release of GH are similar. It is effective when administered orally and intranasally. For children with GH deficiency, such noninvasive treatments are most desirable and in need of development. Fifteen children with short stature participated in this study. All of the children had a height < 2 S.D. below mean for age, poor height velocity, delayed bone age, and low serum concentrations of IGF-1. These children had been tested with standard GH secretagogues, e.g. arginine, insulin, and L-dopa. Fifty percent of the children were GH deficient, the remainder had idiopathic short stature. The children received testing with GHRH and GHRP-2 as an acute i.v. bolus of 1 microgram/kg; all children in this study demonstrated a GH response > 20 micrograms/l. Each child in this study also demonstrated a GH response > 10 micrograms/l in response to intranasal GHRP-2, in the dose range of 5-20 micrograms/kg. The children were administered intranasal GHRP-2, 5-15 micrograms/kg, twice a day for 3 months, then three times a day. Fifteen children participated in the study for 6 months; six of the children have participated for 18-24 months. Height velocity, serum IGF-1, IGF-binding protein 3 (IGFBP-3) and GH-binding protein (GHBP) concentrations, and GH responses to GHRP-2 by i.v. bolus and intranasal spray were examined during treatment. Height velocity increased from 3.7 +/- 0.2 cm/year to 6.1 +/- 0.3 cm/year at 6 months, 6.0 +/- 0.4 cm/year at 18-24 months. There were no significant changes in IGF-1 or IGF-PB3 concentrations, or in acute GH responses to i.v. or intranasal GHRP-2. GHBP concentrations rose significantly, from 439 +/- 63 pmol/l to 688 +/- 48 pmol/l. In this study, intranasal GHRP-2 administration was well tolerated, and produced a modest but significant increase in growth velocity.

Language of Publication

English

Unique Identifier

98051448

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MeSH Heading (Major)

Growth Disorders|BL/*DT/PP; Hormones, Synthetic|*AD/TU; Oligopeptides|*AD/DU/TU; Somatotropin|*SE; Somatotropin-Releasing Hormone|*DU

MeSH Heading

Administration, Intranasal; Analysis of Variance; Carrier Proteins|BL; Child; Child, Preschool; Drug Administration Schedule; Female; Human; Injections, Intravenous; Insulin-Like Growth Factor Binding Protein 3|BL; Insulin-Like Growth Factor I|AN; Male; Statistics, Nonparametric; Support, Non-U.S. Gov't

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE

ISSN

0022-0795

Country of Publication

ENGLAND

Record 8 from database: MEDLINE
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Title

Serum testosterone and growth hormone/insulin-like growth factor-I in adults with spinal cord injury.

Author

Tsitouras PD; Zhong YG; Spungen AM; Bauman WA

Address

Spinal Cord Damage Research Center, Mount Sinai Medical Center, New York, USA.

Source

Horm Metab Res, 1995 Jun, 27:6, 287-92

Abstract

Aging is associated with relative growth hormone and/or testosterone (T) hormone deficiency, and those with SCI may have a premature deficiency of these two hormones. The effects of SCI, duration of injury (DOI), and advancing age with that of human growth hormone (hGH) and insulin-like growth factor I (IGF-I), as well as potential associations between them, were studied. Data were obtained from 20 male subjects with SCI and 16 gender- and age-matched controls. Serum total and free T were lower in subjects with SCI compared with controls (mean +/- SEM, 3.12 +/- 0.29 versus 4.68 +/- 0.28 ng/ml, p < 0.001 and 1.89 +/- 0.18 versus 2.46 +/- 0.22 ng/ml, p < 0.05, respectively). Nine of the 20 subjects with SCI, but none of the controls, had abnormally low serum total T. Arginine-stimulated values for hGH were lower in the group with SCI compared with controls (198 +/- 18 versus 267 +/- 27 ng/ml, p < 0.05). Serum luteinizing hormone and follicular stimulating hormone, as well as body mass index, were not significantly different between the groups. Serum total and free T were correlated with advancing age in controls (r = 0.62, p < 0.01 and r = 0.51, < 0.05, respectively) but not in SCI (r = 0.19, p > 0.43 and r = 0.39, p = 0.09). However, serum total and free T declined with increasing DOI in SCI (r = 0.56, p < 0.01 and r = 0.44, p = 0.05, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Language of Publication

English

Unique Identifier

96031768

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MeSH Heading (Major)

Insulin-Like Growth Factor I|*ME; Somatotropin|*BL; Spinal Cord Injuries|*BL; Testosterone|*BL

MeSH Heading

Adult; Aging|BL; Hormones|BL; Human; Male; Middle Age

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE

ISSN

0018-5043

Country of Publication

GERMANY

Record 9 from database: MEDLINE
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Title

Auxological and endocrinological evaluation of children with hydrocephalus and/or meningomyelocele.

Author

Hochhaus F; Butenandt O; Schwarz HP; Ring Mrozik E

Address

Department of Paediatrics, Dr. von Haunersches Kinderspital, Ludwig-Maximilians-University of Munich, Germany.

Source

Eur J Pediatr, 1997 Aug, 156:8, 597-601

Abstract

Short stature and precocious puberty are frequently found in children with hydrocephalus and/or meningomyelocele (MMC). However, aetiology and pathophysiology have not been well characterized. In this study, 108 patients aged between 3 and 17.8 years were evaluated. Growth was documented on the basis of arm span measurements. Short arm span was found in 47 (43.5%) children with hydrocephalus and/or MMC. Mean arm span was -2.0 standard deviation score (SDS) (-6.4 to +0.8) in 43 girls and -14 SDS (-5.6 to +1.3) in 65 boys. When growth deficiency (more than -2.0 SDS) was diagnosed by arm span measurement (24 F, 23 M) or when early sexual maturation was found (6 F, 9 M), endocrine evaluation followed. Levels of serum insulin-like growth factor and insulin-like growth factor binding protein-3 were low in 22 of 62 (33.8%) patients. In 9 of 62 (14.5%) patients, insulin-like growth factor-1 and insulin-like growth factor binding protein-3 levels were found to be increased. Growth hormone (GH) deficiency was diagnosed by means of two different stimulation tests (clonidine and arginine) in 7 of 62 (11.3%) patients. In another 3 of 62 (4.8%) children, 12 h night time GH sampling showed low maximum peak levels and decreased area under the curve values, suggesting neurosecretory GH dysfunction. Precocious puberty or early onset of puberty associated with elevated luteinising hormone and follicle stimulating hormone concentrations after stimulation with luteinising hormone releasing hormone was found in 13 of 108 (12.0%) patients (age 7-9 years). Free thyroxine was abnormally low in 2 of 62 (3.2%) patients. Cortisol was within the normal range in all 62 (100%) tested patients. CONCLUSIONS: Short arm span in children with hydrocephalus and/or MMC is frequently accompanied by GH deficiency or neurosecretory GH dysfunction. Early onset of puberty is another frequent finding. Both hormonal disorders may be the consequence of damage to the hypothalamus or the pituitary gland caused by increased intracerebral pressure or increased mass of cerebrospinal fluid.

Language of Publication

English

Unique Identifier

97411195

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MeSH Heading (Major)

Arm|*AH; Growth Disorders|*ET; Hydrocephalus|*CO; Meningomyelocele|*CO; Puberty, Precocious|*ET; Somatropin|*DF

MeSH Heading

Adolescence; Body Height; Child; Child, Preschool; Cross-Sectional Studies; Enzyme-Linked Immunosorbent Assay; Female; Hormones|AN; Human; Intracranial Pressure; Male; Radioimmunoassay

Publication Type

JOURNAL ARTICLE

ISSN

0340-6199

Country of Publication

GERMANY

Record 10 from database: MEDLINE
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Title

Differences between somatostatin-28 and somatostatin-14 with respect to their biological effects in healthy humans and acromegalics.

Author

Hadjidakis DJ; Raptis SA; Souvatzoglou A; Karaiskos C; Diamantopoulos EJ; Moulopoulos SD

Address

 

Source

Clin Physiol Biochem, 1986, 4:6, 372-83

Abstract

In order to compare the effects of somatostatin-28 (SS-28) with those of somatostatin-14 (SS-14) in humans, we administered both compounds randomly in 5 healthy persons and 3 patients with active acromegaly. Blood glucose, growth hormone, insulin, glucagon, TSH, FSH, LH and prolactin were estimated after arginine, TRH and LHRH stimulation in the normals and without stimulation in the acromegalics. Both substances were administered in doses of 25, 50, 200 and 250 micrograms. Our results indicate that SS-28 is at least 5 times more potent in man than SS-14 as far as inhibition of growth hormone, insulin, glucagon and prolactin secretion is concerned. On the other hand SS-28 is at least 2 times more potent than SS-14 in the inhibition of TSH, FSH and LH. If this difference in potency is calculated on the basis of equimolarity, the action of SS-28 becomes even much greater. According to these findings, SS-28 appears to be either the main hormone and SS-14 a fragment of it with a lesser degree of biologic activity, or the prohormone with special properties.

Language of Publication

English

Unique Identifier

87132032

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MeSH Heading (Major)

Acromegaly|BL/*DT; Somatostatin|*PD

MeSH Heading

Adult; Blood Glucose|ME; Comparative Study; Glucagon|BL; Hormones|BL; Human; Insulin|BL; Middle Age; Random Allocation; Somatotropin|BL; Support, Non-U.S. Gov't

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL

ISSN

0252-1164

Country of Publication

SWITZERLAND

CAS Registry/EC Number

0 (Blood Glucose); 0 (Hormones); 11061-68-0 (Insulin); 51110-01-1 (Somatostatin); 75037-27-3 (somatostatin 28); 9002-72-6 (Somatotropin); 9007-92-5 (Glucagon)

Record 11 from database: MEDLINE
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Title

Surgical and genetic aspects of persistent müllerian duct syndrome.

Author

Loeff DS; Imbeaud S; Reyes HM; Meller JL; Rosenthal IM

Address

Department of Surgery, Cook County Hospital, Chicago, IL 60612.

Source

J Pediatr Surg, 1994 Jan, 29:1, 61-5

Abstract

Persistent müllerian duct syndrome (PMDS) is characterized by the presence of a uterus, cervix, and fallopian tubes in an otherwise normally differentiated 46.XY male. During embryogenesis, regression of müllerian structures in normal males is mediated by antimüllerian hormone (AMH), also called müllerian inhibiting substance (MIS), produced by fetal Sertoli's cells. PMDS has been attributed to deficient AMH activity or to abnormalities in the AMH receptor. The authors report on two patients with PMDS in whom the abnormalities were discovered during surgery for inguinal hernia and cryptorchidism. During the initial operations in each case, testicular biopsies were obtained, and the gonads and müllerian elements were replaced in the pelvis. A second operative procedure, performed several months later, included proximal salpingectomies with dissection of the vasa deferentia on pedicles of myometrium. This permitted excision of the vestigial uterine corpus, leaving a tiny remnant of cervix with the vasa deferentia. The testes were further mobilized so that bilateral orchidopexies could be completed. In the first case, a molecular abnormality was present at position 377 of the first exon of the AMH gene. Thymine replaced cytosine, which altered a CGG arginine codon to a TGG tryptophan codon, rendering the AMH molecule unstable. The molecular abnormality in the first case differs from the first abnormality in AMH reported by Knebelmann et al, thus indicating heterogeneity in this condition. The molecular basis for deficient AMH activity in the second patient has not yet been defined. No molecular abnormalities were found in the exons of this patient's AMH gene.

Language of Publication

English

Unique Identifier

94165935

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MeSH Heading (Major)

Growth Inhibitors|*GE; Mullerian Ducts|*; Pseudohermaphroditism|DI/*GE/*SU; Testicular Hormones|*GE

MeSH Heading

Case Report; Codon; Cryptorchidism|SU; Hernia, Inguinal|SU; Human; Infant; Male; Methods

Publication Type

JOURNAL ARTICLE

ISSN

0022-3468

Country of Publication

UNITED STATES

Record 12 from database: MEDLINE
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Title

Growth retardation in childhood leukemia and lymphoma. Special reference to patients with CNS relapse.

Author

Yamada S; Ishii E; Okabe Y; Kai T; Kuroiwa T; Hasuo K; Akazawa K; Tasaka H; Ueda K

Address

Department of Pediatrics, Faculty of Medicine, Kyushu University, Fukuoka, Japan.

Source

Am J Pediatr Hematol Oncol, 1992 Aug, 14:3, 236-40

Abstract

We studied the growth of 89 patients who were long-term survivors of childhood leukemia and lymphoma. Eight patients with CNS relapse had a greater decrease in height standard deviation score (SDS) after the relapse than 81 patients without CNS relapse (p less than 0.0001). Two patients who received cranial irradiation when they were younger than 2 years of age demonstrated a marked decrease in height SDS more than 3.0 SD. Five patients appeared to have a decline in height SDS before their CNS relapse. There were no apparent changes in the weight of patients with or without CNS relapse. In endocrine studies, all eight patients with CNS relapse failed to show the normal growth hormone (GH) response to arginine, GH-releasing factor, and glucagon-propranolol tests, while spontaneous GH secretion during sleep was normal. Magnetic resonance imaging (MRI) revealed small pituitary glands in seven patients with CNS relapse. These findings suggest that in leukemia and lymphoma patients with CNS relapse, GH secretion is impaired at the hypothalamic level, resulting in a secondary atrophy of the pituitary gland. The MRI together with selected endocrinologic tests may help to clarify the mechanism of growth impairment in such patients. A decline in height SDS in each patient may be a useful marker for predicting a CNS relapse in a child with leukemia or lymphoma.

Language of Publication

English

Unique Identifier

92377933

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MeSH Heading (Major)

Central Nervous System Diseases|BL/*ET; Growth Disorders|BL/*ET/PA; Leukemia, Lymphocytic, Acute, L1|BL/*CO/PA; Leukemia, Nonlymphocytic, Acute|BL/*CO/PA; Lymphoma, Non-Hodgkin's|BL/*CO/PA

MeSH Heading

Adolescence; Body Height|PH; Child; Child, Preschool; Female; Hormones|BL; Human; Infant; Magnetic Resonance Imaging; Male; Pituitary Gland, Anterior|PA; Somatotropin|BL; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE

ISSN

0192-8562

Country of Publication

UNITED STATES

CAS Registry/EC Number

0 (Hormones); 9002-72-6 (Somatotropin)

Record 13 from database: MEDLINE
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Title

Hormonal and metabolic responses to exercise across time of day and menstrual cycle phase.

Author

Galliven EA; Singh A; Michelson D; Bina S; Gold PW; Deuster PA

Address

Department of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA.

Source

J Appl Physiol, 1997 Dec, 83:6, 1822-31

Abstract

Two studies, each utilizing short-term treadmill exercise of a different intensity, assessed the metabolic and hormonal responses of women to exercise in the morning (AM) and late afternoon (PM). In study 1, plasma concentrations of growth hormone, arginine vasopressin, catecholamines, adrenocorticotropic hormone, cortisol, lactate, and glucose were measured before, during, and after high-intensity exercise (90% maximal O2 uptake) in the AM and PM. In study 2, plasma concentrations of adrenocorticotropic hormone, cortisol, lactate, and glucose were measured before, during, and after moderate-intensity exercise (70% maximal O2 uptake) in the AM and PM in the follicular (days 3-9), midcycle (days 10-16), and luteal (days 18-26) phases of the menstrual cycle. The results of studies 1 and 2 revealed no significant diurnal differences in the magnitude of responses for any measured variable. In addition, study 2 revealed a significant time-by-phase interaction for glucose (P = 0. 014). However, net integrated responses were similar across cycle phases. These data suggest that metabolic and hormonal responses to short-term, high-intensity exercise can be assessed with equal reliability in the AM and PM and that there are subtle differences in blood glucose responses to moderate-intensity exercise across menstrual cycle phase.

Language of Publication

English

Unique Identifier

98067112

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MeSH Heading (Major)

Exercise|*PH; Hormones|*PH; Menstrual Cycle|ME/*PH

MeSH Heading

Adult; Blood Glucose|ME; Circadian Rhythm|PH; Female; Glucocorticoids|BL; Heart Rate|PH; Human; Hydrocortisone|BL; Hypothalamo-Hypophyseal System|PH; Lactic Acid|BL; Oxygen Consumption|PH; Pituitary-Adrenal System|PH; Time Factors

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE

ISSN

8750-7587

Country of Publication

UNITED STATES

Record 14 from database: MEDLINE
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Title

Hormonal and metabolic abnormalities in the malnourished cancer patient: effects on host-tumor interaction.

Author

Heber D; Byerley LO; Tchekmedyian NS

Address

Department of Medicine, University of California, Los Angeles School of Medicine 90024-1742.

Source

JPEN J Parenter Enteral Nutr, 1992 Nov-Dec, 16:6 Suppl, 60S-64S

Abstract

Many common metastatic cancers are associated with marked weight loss at the time of diagnosis. Anorexia clearly plays a major role in weight loss in the cancer patient, but cannot explain all of the weight loss noted. Malnourished patients with localized cancers under metabolic ward conditions fail to gain weight when given apparently adequate calories for anabolism, thus suggesting that these patients are hypermetabolic. Increased whole body protein breakdown, increased lipolysis, and increased gluconeogenesis have been repeatedly demonstrated in malnourished cancer patients. Protein and glucose metabolism are closely linked, and both are regulated by a number of the same hormones and metabolites. For example, when increased glucose production in malnourished cancer patients is inhibited pharmacologically, protein catabolism is proportionally decreased. Studies of glucose, growth hormone, cortisol, and insulin secretion following an oral glucose load in well-nourished cancer patients are consistent with insulin resistance but no other hormonal abnormalities. Malnourished cancer patients have elevated levels of growth hormone that are further stimulated by arginine and insulin infusion. No abnormalities of thyroid function were noted in cancer patients. Current studies are underway to determine the mechanisms and effects of progestational steroids and cytokines on both food intake and intermediary lipid metabolism.

Language of Publication

English

Unique Identifier

93164386

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MeSH Heading (Major)

Hormones|*ME; Neoplasms|CO/*ME; Nutrition Disorders|ET/*ME

MeSH Heading

Cachexia|ET/ME; Human; Support, U.S. Gov't, P.H.S.; Weight Loss

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0148-6071

Country of Publication

UNITED STATES

CAS Registry/EC Number

0 (Hormones)

Record 15 from database: MEDLINE
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Title

Acute effects of a somatostatin analogue on kidney function in type 1 diabetic patients.

Author

Pedersen MM; Christensen SE; Christiansen JS; Pedersen EB; Mogensen CE; Orskov H

Address

Second University Clinic of Internal Medicine, Aarhus Kommunehospital, Denmark.

Source

Diabet Med, 1990 May, 7:4, 304-9

Abstract

Suppression of growth hormone by means of somatostatin has been suggested as a possible adjunct therapy in Type 1 diabetes. To assess the acute effect of the somatostatin analogue SMS 201-995 on kidney function in uncomplicated Type 1 diabetes, 13 normoalbuminuric, normotensive diabetic patients were investigated before and during IV infusion of SMS 201-995 (8 micrograms h-1). A control experiment with infusion of carrier only was also performed. The SMS infusion induced a reduction in the glomerular filtration rate (clearance of 125I-iothalamate) and renal plasma flow (131I-hippuran) from 140 +/- 15 (mean +/- SD) and 550 +/- 69 to 131 +/- 14 (2p less than 0.005) and 492 +/- 73 ml min-1 1.73-m-2 (2p less than 0.001), while filtration fraction and total renal resistance rose (both 2p less than 0.001). Urinary albumin excretion rate, blood pressure, and blood glucose concentration were unchanged. Plasma growth hormone and glucagon were significantly suppressed. The reduction in glomerular filtration rate and renal plasma flow correlated with the fall in glucagon concentration (r = 0.57, 2p = 0.04, and r = 0.63, 2p = 0.02). The urinary flow rate was markedly reduced, urine osmolality increased, and fractional excretion of sodium, calcium, and phosphate were reduced. Arginine vasopressin, atrial natriuretic peptide, angiotensin II, and aldosterone were unchanged by the SMS infusion. Thus SMS 201-995 acutely reduces glomerular filtration rate and renal plasma flow in uncomplicated Type 1 diabetes and has an antidiuretic effect. The effects may be related to suppression of glucagon secretion.

Language of Publication

English

Unique Identifier

90249201

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MeSH Heading (Major)

Diabetes Mellitus, Insulin-Dependent|BL/*PP/UR; Kidney|DE/*PP; Octreotide|*PD

MeSH Heading

Adult; Blood Glucose|ME; Electrolytes|UR; Glomerular Filtration Rate|DE; Hormones|BL; Human; Renal Circulation|DE; Support, Non-U.S. Gov't; Vascular Resistance|DE

Publication Type

JOURNAL ARTICLE

ISSN

0742-3071

Country of Publication

ENGLAND

CAS Registry/EC Number

0 (Blood Glucose); 0 (Electrolytes); 0 (Hormones); 83150-76-9 (Octreotide)

Record 16 from database: MEDLINE
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Title

The effect of bingeing and vomiting on hormonal secretion.

Author

Kaye WH; Gwirtsman HE; George DT

Address

University of Pittsburgh, School of Medicine, Department of Psychiatry, Western Psychiatric Institute and Clinic, PA 15212.

Source

Biol Psychiatry, 1989 Mar 15, 25:6, 768-80

Abstract

Women who are of normal weight and have bulimia nervosa have multiple neuroendocrine disturbances. The reasons for these neuroendocrine abnormalities are not known, but there are reasons to suspect that bingeing and vomiting behavior could be contributory. It is well known that food consumption in healthy volunteers increases plasma insulin, cortisol, and prolactin secretion and suppresses growth hormone secretion, whereas activation of the emetic reflex increases plasma arginine vasopressin (AVP) secretion. The purpose of this study was to investigate the effects of bingeing and vomiting on these hormones. In comparison with healthy control women consuming a large meal, bulimic patients, when bingeing and vomiting, had an exaggerated secretion of either the amount and/or the duration of insulin, cortisol, and prolactin. Vasopressin secretion was not increased during or after bingeing and vomiting, probably because bulimic subjects do not become nauseated. In addition, bulimic patients had significantly reduced baseline plasma prolactin and possibly elevated baseline cortisol compared with controls. In summary, this study supports the presence of neuroendocrine disturbances in bulimia and raises a question as to whether or not excessive and prolonged food consumption (and/or vomiting) are contributory.

Language of Publication

English

Unique Identifier

89166709

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MeSH Heading (Major)

Bulimia|*BL; Hormones|*BL

MeSH Heading

Adult; Argipressin|BL; Blood Glucose|ME; Feeding Behavior|PH; Female; Human; Hydrocortisone|BL; Insulin|BL; Prolactin|BL; Somatotropin|BL; Vomiting|BL

Publication Type

JOURNAL ARTICLE

ISSN

0006-3223

Country of Publication

UNITED STATES

CAS Registry/EC Number

0 (Blood Glucose); 0 (Hormones); 11061-68-0 (Insulin); 113-79-1 (Argipressin); 50-23-7 (Hydrocortisone); 9002-62-4 (Prolactin); 9002-72-6 (Somatotropin)

Record 17 from database: MEDLINE
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Title

Effect of two regimens of intravenous amino acid infusion on renal haemodynamics, renal tubular function and sodium and water homeostatic hormones in healthy humans.

Author

S‡rensen SS; Lauridsen IN; Thomsen K; Pedersen EB

Address

Department of Medicine C, Aarhus Kommunehospital, Denmark.

Source

Nephrol Dial Transplant, 1991, 6:6, 410-9

Abstract

The effect of two different regimens of intravenous infusion of amino acids on glomerular filtration rate (GFR), renal plasma flow (RPF), tubular sodium and water handling judged from the clearance of lithium (CLi), and plasma concentrations of angiotensin II (Ang II), aldosterone (Aldo), arginine vasopressin (AVP), atrial natriuretic peptide (ANP), growth hormone (GH), and glucagon was investigated in healthy humans. In the first protocol (n = 11) the infusion lasted 90 min; both GFR and RPF increased significantly (median increase 7.1% and 9.1% respectively, P less than 0.05 both). In the second protocol (n = 13) the infusion lasted 30 min; both GFR and RPF tended to increase (median increase 3.5% and 7.4%) but the change did not reach significance. The changes in tubular sodium and water handling were similar in the two protocols. Absolute reabsorption rates in the proximal tubules were unaltered, resulting in an increased output into the distal tubules that was totally compensated for by an increased distal reabsorption. Thus no changes in urinary excretion of sodium and water were observed. Ang II, Aldo, AVP, ANP and GH were unchanged by amino acid infusion, but glucagon increased. It is suggested that the alterations in renal haemodynamics and distal tubular reabsorption may be mediated by glucagon.

Language of Publication

English

Unique Identifier

91343159

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MeSH Heading (Major)

Amino Acids|*AD/BL/PD; Body Water|*ME; Hemodynamics|*DE; Kidney Tubules|*DE/ME; Renal Circulation|*DE; Sodium|*ME

MeSH Heading

Adult; Female; Glomerular Filtration Rate|DE; Hormones|BL; Human; Infusions, Intravenous; Male; Middle Age; Osmolar Concentration; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE

ISSN

0931-0509

Country of Publication

GERMANY

CAS Registry/EC Number

0 (Amino Acids); 0 (Hormones); 7440-23-5 (Sodium)

Record 18 from database: MEDLINE
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Title

Role of growth hormone in the amino acid-induced acute rise in renal function in man.

Author

Hirschberg R; Kopple JD

Address

Division of Nephrology and Hypertension, Harbor-UCLA Medical Center, Torrance.

Source

Kidney Int, 1987 Sep, 32:3, 382-7

Abstract

To examine whether plasma growth hormone is necessary for the amino acid-induced rise in effective renal plasma flow (ERPF, PAH clearance) and GFR (inulin clearance), arginine HCl, 500 mg/kg, was infused for 30 minutes into eight normal and six growth hormone-deficient individuals. During infusion, ERPF increased in the normal and growth hormone-deficient subjects by 28.9 +/- 11.4 SD-% (P less than 0.01) and 46.5 +/- 14.4% (P less than 0.001). GFR rose by 23.7 +/- 5.9% (P less than 0.05) and 42.7 +/- 29.1% (P less than 0.001) in the two groups. Plasma growth hormone rose only in the normal subjects, while glucagon increased in both groups. Infusion of arginine HCl, 200 mg/kg, into normals increased ERPF and GFR without increasing plasma osmolality. Lower arginine doses essentially did not affect ERPF, GFR, growth hormone, or glucagon. Infusion of D-glucose into normals raised plasma osmolality as high as with arginine HCl, 500 mg/kg, but increased ERPF only slightly and not GFR; D-glucose infusion caused a delayed rise in growth hormone that was unassociated with an increase in ERPF or GFR. An infusion of ammonium chloride with sodium chloride, which provided an amount of chloride similar to the 500 mg/kg arginine HCl dose, did not change ERPF and GFR; this suggests that the chloride load did not cause the altered renal hemodynamics stimulated by arginine HCl. These findings indicate that neither normal plasma growth hormone levels nor a rise in growth hormone mediates the arginine-induced acute increase in ERPF or GFR. This effect is also not due to the osmolar load but could be caused by the rise in plasma glucagon.

Language of Publication

English

Unique Identifier

88036834

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MeSH Heading (Major)

Arginine|BL/*PD; Glomerular Filtration Rate|*/DE; Renal Circulation|*/DE; Somatotropin|BL/DF/*PH

MeSH Heading

Adult; Female; Glucagon|BL; Glucose|PD; Human; Male; Osmolar Concentration; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE

ISSN

0085-2538

Country of Publication

UNITED STATES

CAS Registry/EC Number

50-99-7 (Glucose); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin); 9007-92-5 (Glucagon)

Record 19 from database: MEDLINE
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Title

Naloxone increases the response of growth hormone and prolactin to stimuli in obese humans.

Author

Plewe G; Schneider U; Krause U; Beyer J

Address

 

Source

J Endocrinol Invest, 1987 Apr, 10:2, 137-41

Abstract

Opiates stimulate the growth hormone and prolactin responses to stimuli in non-obese humans. Obese patients, however, show lowered growth hormone and prolactin responses and raised beta-endorphin levels. We therefore investigated the effect of the opiate antagonist naloxone on the stimulated growth hormone and prolactin secretions in a controlled double-blind study in obese patients. All patients received 200 micrograms TRH and 0.5 g/kg b.w. arginine together with 2 mg of naloxone or placebo i.v. in a randomized sequence. The TRH- and arginine-induced increases in prolactin and growth hormone were significantly greater after administration of naloxone (p less than 0.05). Naloxone also produced a significant increase in ACTH, cortisol and beta-endorphin when compared with placebo. TSH, triiodothyronine, thyroxine, insulin, glucagon and blood glucose showed no significant differences between both days of the trial. The effect of naloxone on growth hormone and prolactin secretions in obese humans can thus be regarded as a partial normalization. We therefore conclude that the hypothalamic regulatory disturbance of growth hormone and prolactin secretions in the obese could be caused by raised opiate levels.

Language of Publication

English

Unique Identifier

87223760

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MeSH Heading (Major)

Naloxone|*PD; Obesity|*BL; Prolactin|*BL; Somatotropin|*BL

MeSH Heading

Adult; Arginine|PD; Corticotropin|BL; Double-Blind Method; Endorphins|BL; Female; Human; Hydrocortisone|BL; Male; Middle Age; Protirelin|PD

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL

ISSN

0391-4097

Country of Publication

ITALY

CAS Registry/EC Number

0 (Endorphins); 24305-27-9 (Protirelin); 465-65-6 (Naloxone); 50-23-7 (Hydrocortisone); 60617-12-1 (beta-Endorphin); 7004-12-8 (Arginine); 9002-60-2 (Corticotropin); 9002-62-4 (Prolactin); 9002-72-6 (Somatotropin)

Record 20 from database: MEDLINE
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Title

Correlation between pituitary growth hormone reserve and degree of growth failure in children with short stature.

Author

Kajiwara S; Igarashi N; Imura E; Sato T

Address

Department of Pediatrics, School of Medicine, Kanazawa University, Japan.

Source

Eur J Pediatr, 1988 Aug, 147:6, 584-7

Abstract

The correlation between a releasable pituitary growth hormone (GH) pool and degree of growth failure was examined in 30 children with GH deficiency (group I) and 19 children with normal short stature (group II). Based on the responsiveness of GH to GH-releasing hormone (GHRH), group I, with low GH responses (below 7 ng/ml) to both insulin and arginine, was classified into three subgroups; Ia (peak value less than 10 ng/ml, n = 19), Ib (10-20 ng/ml, n = 5) and Ic (above 20 ng/ml, n = 6). Group II, with a GH response above 10 ng/ml to either insulin or arginine, was also divided into IIa (below 20 ng/ml, n = 5) and IIb (above 20 ng/ml, n = 14). Body length and growth velocity in Ia and Ib were significantly reduced vs Ic; bone age in Ia was retarded vs Ic; plasma somatomedin C (Sm-C) levels in Ia and Ib were decreased vs Ic, who had almost normal levels (0.90 +/- 0.55 U/ml). The incidence of other combined pituitary hormone deficiencies and previous perinatal distress was definitely high in Ia and Ib, but zero in Ic. In group II also, body length and growth velocity were significantly decreased in IIa vs IIb (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Language of Publication

English

Unique Identifier

89030812

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MeSH Heading (Major)

Growth Disorders|*BL; Somatotropin|*BL/DF

MeSH Heading

Adolescence; Adult; Age Determination by Skeleton; Arginine|DU; Body Height; Child; Child, Preschool; Female; Growth; Human; Insulin|DU; Male; Somatotropin-Releasing Hormone|DF/PD

Publication Type

JOURNAL ARTICLE

ISSN

0340-6199

Country of Publication

GERMANY, WEST

CAS Registry/EC Number

11061-68-0 (Insulin); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin); 9034-39-3 (Somatotropin-Releasing Hormone)

Record 21 from database: MEDLINE
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Title

Dissociation between circulating concentrations of immunoreactive growth hormone releasing factor and growth hormone in normal human subjects.

Author

Sopwith AM; Penny ES; Lytras N; Besser GM; Rees LH

Address

 

Source

Clin Sci, 1987 Feb, 72:2, 181-5

Abstract

Using a highly specific radioimmunoassay we have measured immunoreactive human growth hormone releasing factor (ir-hGRF) concentrations in the peripheral circulation of a total of 12 normal subjects. Neither insulin-induced hypoglycaemia, intravenous arginine nor oral carbohydrate caused any change in venous plasma ir-hGRF concentrations, despite the expected stimulation and suppression respectively of growth hormone secretion. Growth hormone secretion was not increased by oral fat or protein but each of these two foods stimulated ir-hGRF concentrations two- to four-fold. Spontaneous pulses of growth hormone secretion on control days were unaccompanied by any increase in plasma ir-hGRF. The dissociation between peripheral circulating ir-hGRF and growth hormone responses demonstrated under different circumstances suggests that an important source of human growth hormone releasing factor lies outside the hypothalamus and that secretion from this source is unconnected with the normal control of pituitary growth hormone secretion.

Language of Publication

English

Unique Identifier

87132142

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MeSH Heading (Major)

Somatotropin|*BL; Somatotropin-Releasing Hormone|*BL/IM

MeSH Heading

Adult; Arginine|PD; Diet; Human; Insulin|PD; Male; Radioimmunoassay; Support, Non-U.S. Gov't

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL

ISSN

0143-5221

Country of Publication

ENGLAND

CAS Registry/EC Number

11061-68-0 (Insulin); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin); 9034-39-3 (Somatotropin-Releasing Hormone)

Record 22 from database: MEDLINE
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Title

Growth hormone deficiency in the Rothmund-Thomson syndrome.

Author

Kaufmann S; Jones M; Culler FL; Jones KL

Address

 

Source

Am J Med Genet, 1986 Apr, 23:4, 861-8

Abstract

We describe the first proven occurrence of growth hormone deficiency in an individual with the Rothmund-Thomson syndrome. This was suspected because of the patient's severely retarded growth and bone age and her failure to respond normally to growth hormone stimulation testing with l-DOPA, arginine, and growth hormone releasing factor. In addition, we have briefly reviewed other genetic and malformation syndromes that have been found associated with growth hormone deficiency. We recommend that growth hormone deficiency be considered in these syndromes, especially when the growth failure is more marked than expected.

Language of Publication

English

Unique Identifier

86183910

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MeSH Heading (Major)

Poikiloderma Congenitale|GE/*ME; Skin Diseases|*ME; Somatotropin|*DF

MeSH Heading

Arginine|DU; Case Report; Child; Dwarfism|ET/GE; Female; Human; Insulin-Like Growth Factor I|BL; Levodopa|DU; Somatotropin-Releasing Hormone|DU; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE

ISSN

0148-7299

Country of Publication

UNITED STATES

CAS Registry/EC Number

0 (Levodopa); 67763-96-6 (Insulin-Like Growth Factor I); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin); 9034-39-3 (Somatotropin-Releasing Hormone)

Record 23 from database: MEDLINE
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Title

Evaluation of growth hormone secretion: provocative testing vs endogenous 24-hour growth hormone profile.

Author

Shulman DI; Bercu BB

Address

University of South Florida College of Medicine, All Children's Hospital, St Petersburg.

Source

Acta Paediatr Scand Suppl, 1987, 337:, 61-71

Abstract

A total of 55 children underwent hGH provocative testing with two or more provocative agents, and measurement of endogenous 24-hour hGH secretion. Patients were divided into groups according to their peak hGH secretory response to provocative testing and their mean 24-hour hGH concentration. Peak hGH response to provocative testing was significantly greater in control children and in children with hGH neurosecretory dysfunction (GHND) than in the classical hGH deficient group. Mean 24-hour hGH concentration was significantly greater in the control group than in either the classical hGH deficient or GHND groups. Responses to provocative stimuli were intermediate for the GHND group compared to the classical hGH deficient and the control groups. The mean peak hGH secretory response to insulin-induced hypoglycaemia in the GHND group was poor compared to controls and was greatest following clonidine. The mean peak hGH response to an intravenous bolus of growth hormone releasing hormone was intermediate for the GHND group compared to hGH deficient and control groups. Highest nocturnal peak, first hGH pulse after sleep, mean peak hGH pulse and total number of pulses were also intermediate for the GHND group compared to the other groups. The control group had significantly more pulses greater than 5 ng/ml than did the other groups. Night-time and daytime hGH pools were lower in the classical hGH deficient and GHND groups compared to controls; however, there was overlap between groups. Six of seven children in the GHND group have responded to exogenous hGH therapy with increased linear growth velocity. Measurements of endogenous 24-hour hGH secretion may identify a subgroup of hGH deficient children who are not detected by provocative testing yet who may respond to exogenous hGH therapy with improved linear growth.

Language of Publication

English

Unique Identifier

88129888

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MeSH Heading (Major)

Growth Disorders|*DI; Somatotropin|DF/*SE

MeSH Heading

Adolescence; Arginine|DU; Child; Clonidine|DU; Comparative Study; Female; Human; Insulin|DU; Levodopa|DU; Male; Pituitary Function Tests; Somatotropin-Releasing Hormone|DU; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.; Time Factors

Publication Type

JOURNAL ARTICLE

ISSN

0300-8843

Country of Publication

SWEDEN

CAS Registry/EC Number

0 (Levodopa); 11061-68-0 (Insulin); 4205-90-7 (Clonidine); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin); 9034-39-3 (Somatotropin-Releasing Hormone)

Record 24 from database: MEDLINE
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Title

Insulinhypoglycemia but not arginine infusion stimulates circulating plasma growth hormone-releasing hormone (GHRH) concentrations in children.

Author

Rosskamp R; Schmid G; Klumpp J; Tegeler A

Address

Universitäts-Kinderklinik und Poliklinik, Bonn, Germany.

Source

Horm Metab Res, 1987 Sep, 19:9, 434-6

Abstract

The effect of insulinhypoglycemia and arginine infusion on circulating concentrations of plasma growth hormone-releasing hormone (GHRH) and growth hormone (GH) has been studied in 24 children (4.4 to 14.3 years). Plasma GH and GHRH concentrations were determined by RIA. Basal plasma GHRH levels were detectable in the plasma of all patients ranging from 6.8 to 27.1 pg/ml. Injection of 0.1 U/kg body wt. insulin i.v. resulted in an increase of plasma GHRH levels (11.1 +/- 1.4 pg/ml vs. 18.8 +/- 2.6 pg/ml; P less than 0.01) preceding that of plasma GH (1.5 +/- 0.4 ng/ml vs. 13.6 +/- 1.3 ng/ml; P less than 0.01). Infusion of 0.5 gm/kg body wt. arginine hydrochloride did increase GH concentrations (2.0 +/- 0.6 ng/ml vs. 13.9 +/- 2.3 ng/ml; P less than 0.01) but did not change circulating plasma GHRH levels. Since the source of peripheral GHRH concentrations is not known the importance of these findings remains to be determined.

Language of Publication

English

Unique Identifier

88084983

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MeSH Heading (Major)

Arginine|*PD; Hypoglycemia|*PP; Insulin|*PD; Somatotropin|*BL; Somatotropin-Releasing Hormone|*BL

MeSH Heading

Adolescence; Child; Child, Preschool; Comparative Study; Female; Human; Male

Publication Type

JOURNAL ARTICLE

ISSN

0018-5043

Country of Publication

GERMANY, WEST

CAS Registry/EC Number

11061-68-0 (Insulin); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin); 9034-39-3 (Somatotropin-Releasing Hormone)

Record 25 from database: MEDLINE
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Title

Plasma GH responses to GHRH and other provocative stimuli in idiopathic GH deficiency with or without abnormal delivery.

Author

Hanew K; Goh M; Sato S; Shimizu Y; Sasaki A; Yoshinaga K

Address

 

Source

Tohoku J Exp Med, 1987 Jan, 151:1, 81-8

Abstract

Seventeen patients with idiopathic growth hormone deficiency (GHD) were divided into two groups: one has no perinatal abnormalities (group A, n = 7) and the other has perinatal abnormalities, i.e. breech delivery and asphyxia (group B, n = 10). To see whether there are any differences in hypothalamo-pituitary dysfunctions in the two groups, the pituitary growth hormone (GH) reserve was examined. After 100 micrograms of synthetic growth hormone releasing hormone (GHRH) injection, group A showed a much higher peak values compared to group B (mean +/- S.E.: 16.1 +/- 3.5 ng/ml vs. 3.6 +/- 0.7 ng/ml, p less than 0.01), although there were no differences in their baseline GH values. In addition, plasma GH responses to arginine and L-dopa, which were performed at the diagnosis of GHD, were also greater in group A than group B (mean peak value: arginine, 3.4 +/- 0.5 ng/ml vs 1.8 +/- 0.5 ng/ml, p less than 0.05; L-dopa, 3.2 +/- 0.7 ng/ml vs. 1.3 +/- 0.2 ng/ml, p less than 0.01). There were no significant differences in the bone ages in the two groups, but bone age to chronological age ratio and pubertal development were significantly lower in group B. High frequency of primipara was observed in group B (7/10) compared to group A (2/7). These results indicate that pituitary GH reserve is much impaired in GHD with abnormal delivery compared to that without abnormal delivery, probably depending on the irreversible hypothalamo-pituitary damages due to prolonged anoxic state during the delivery. Especially, such risks seems to be high when cases of breech presentation are delivered from primipara mothers.

Language of Publication

English

Unique Identifier

87206920

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MeSH Heading (Major)

Asphyxia Neonatorum|CO/*PP; Breech Presentation|*; Hypothalamo-Hypophyseal System|*PP; Somatotropin|*DF/SE; Somatotropin-Releasing Hormone|*DU

MeSH Heading

Adolescence; Adult; Arginine|DU; Child; Child, Preschool; Female; Human; Levodopa|DU; Male; Parity; Pregnancy; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE

ISSN

0040-8727

Country of Publication

JAPAN

CAS Registry/EC Number

0 (Levodopa); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin); 9034-39-3 (Somatotropin-Releasing Hormone)

Record 26 from database: MEDLINE
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Title

Preservation of dopaminergic and alpha-adrenergic function in children with growth hormone neurosecretory dysfunction.

Author

Bercu BB; Root AW; Shulman DI

Address

 

Source

J Clin Endocrinol Metab, 1986 Oct, 63:4, 968-73

Abstract

The integrity of dopaminergic and alpha-adrenergic neurotransmitter regulation of GH secretion was examined in children with decreased GH secretion. Children with GH neurosecretory dysfunction (GHND; n = 16) those with classical GH deficiency (n = 9), and short but otherwise normal children (n = 12) underwent 24 h GH studies (blood sampling every 20 min for 24 h) and provocative tests using arginine, insulin hypoglycemia, L-dopa (dopaminergic) and clonidine (alpha-adrenergic), and GH-releasing hormone (GHRH). GHND was defined as children with height in the first percentile or below, growth velocity of 4 cm/yr or less, low plasma somatomedin-C for age, delayed skeletal age by 2 or more yr, peak serum GH responses to any one (or more) provocative test of 10 ng/ml or more, and mean 24-h GH concentration below 3 ng/ml. GHND and GH-deficient children had reduced endogenous GH secretion, expressed as mean serum 24-h GH concentration [1.6 +/- 0.1 (+/- SEM) and 2.1 +/- 0.1 vs. 6.1 +/- 0.5 ng/ml (GH-deficient and GHND vs. normal, respectively); P less than 0.01]. the mean peak serum GH levels after arginine [8.2 +/- 2.0 vs. 20.8 +/- 6.6 ng/ml (GHND vs. normal); P less than 0.05] and insulin [9.3 +/- 1.0 vs. 16.2 +/- 1.7 ng/ml (GHND vs. normal); P less than 0.01) were lower in GHND children. The mean peak responses after L-dopa [13.4 +/- 3.4 vs. 14.6 +/- 4.7 ng/ml (GHND vs. normal); P = NS] and clonidine [19.0 +/- 2.2 vs. 23.3 +/- 3.8 ng/ml (GHND vs. normal); P = NS] were preserved in GHND children. In GH-deficient children, mean peak serum GH concentrations after all four provocative tests were low (arginine, 2.7 +/- 0.8; insulin, 2.6 +/- 0.8; L-dopa, 3.0 +/- 0.9; clonidine, 3.4 +/- 1.0 ng/ml; all P less than 0.01 vs. normal). The mean peak serum GH concentration after GHRH was blunted in GH-deficient children (9.1 +/- 1.7 ng/ml) compared to those in GHND (32.9 +/- 8.5 ng/ml) and normal (43.2 +/- 6.4 ng/ml) children (P less than 0.01). The area under the GH curve after GHRH stimulation was greater for normal than GHND children (P less than 0.05). These data demonstrate preservation of dopaminergic and alpha-adrenergic neurotransmitter pathways in GHND children. They further suggest a defect in the release of pituitary GH secondary to an abnormality in alternative neurotransmitter pathways resulting in decreased GHRH and/or increased somatostatin secretion.

Language of Publication

English

Unique Identifier

86304856

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MeSH Heading (Major)

Dopamine|*PH; Receptors, Adrenergic, alpha|*PH; Somatotropin|*SE

MeSH Heading

Adolescence; Arginine|DU; Child; Clonidine|DU; Female; Growth Disorders|BL; Human; Insulin|DU; Levodopa|DU; Male; Somatotropin-Releasing Hormone|DU; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE

ISSN

0021-972X

Country of Publication

UNITED STATES

CAS Registry/EC Number

0 (Levodopa); 0 (Receptors, Adrenergic, alpha); 11061-68-0 (Insulin); 4205-90-7 (Clonidine); 51-61-6 (Dopamine); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin); 9034-39-3 (Somatotropin-Releasing Hormone)

Record 27 from database: MEDLINE
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Title

Serum insulin-like growth factors I and II concentrations and growth hormone and insulin responses to arginine infusion in children with protein-energy malnutrition before and after nutritional rehabilitation.

Author

Soliman AT; Hassan AE; Aref MK; Hintz RL; Rosenfeld RG; Rogol AD

Address

 

Source

Pediatr Res, 1986 Nov, 20:11, 1122-30

Abstract

Serum insulin, growth hormone (GH), insulin-like growth factors (IGFs) I and II, cortisol, and albumin concentrations were measured in 15 children with kwashiorkor, 15 with marasmic-kwashiorkor, and 21 with marasmus, before and in the survivors, after nutritional rehabilitation, as well as in 10 underweight and eight normal Egyptian children. We also evaluated arginine-induced insulin and GH secretion. IGF-I concentrations were reduced in the three severely malnourished groups (0.07 +/- 0.03, 0.05 +/- 0.03, and 0.09 +/- 0.09 U/ml, respectively) but returned to normal after refeeding. IGF-II concentrations were low in the kwashiorkor (175 +/- 79 ng/ml), marasmic-kwashiorkor (111 +/- 57 ng/ml), and marasmic children (128 +/- 70.9 ng/ml) and returned to normal after nutritional rehabilitation. Basal GH levels were high in the three severely malnourished groups (21.9, 28.8, and 16.6 ng/ml, respectively) and returned to normal after refeeding (8.1, 6.5, and 6.0 ng/ml, respectively). GH responses to arginine were depressed in the three malnourished groups and improved significantly in marasmic-kwashiorkor and marasmic children after nutritional rehabilitation. Insulin responses to arginine were impaired in kwashiorkor, and marasmic-kwashiorkor children and improved significantly after refeeding. IGF-I levels correlated significantly with percent of expected weight (r = 0.52, p less than 0.001), percent of expected height (r = 0.42, p less than 0.001), and weight/(height)2 index (r = 0.34, p less than 0.01). IGF-I levels correlated positively with insulin levels (r = 0.421, p less than 0.001) and negatively with cortisol concentrations (r = -0.400, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Language of Publication

English

Unique Identifier

87091314

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MeSH Heading (Major)

Insulin|*BL/SE; Insulin-Like Growth Factor I|*BL; Insulin-Like Growth Factor II|*BL; Kwashiorkor|*BL/DH/ME; Protein-Energy Malnutrition|*BL/DH/ME; Somatomedins|*BL; Somatotropin|*BL/SE

MeSH Heading

Anthropometry; Arginine|PD; Child, Preschool; Human; Hydrocortisone|BL; Infant; Serum Albumin|AN; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE

ISSN

0031-3998

Country of Publication

UNITED STATES

CAS Registry/EC Number

0 (Serum Albumin); 0 (Somatomedins); 11061-68-0 (Insulin); 50-23-7 (Hydrocortisone); 67763-96-6 (Insulin-Like Growth Factor I); 67763-97-7 (Insulin-Like Growth Factor II); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin)

Record 28 from database: MEDLINE
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Title

Differential effects of 18- and 24-Gy cranial irradiation on growth rate and growth hormone release in children with prolonged survival after acute lymphocytic leukemia.

Author

Cicognani A; Cacciari E; Vecchi V; Cau M; Balsamo A; Pirazzoli P; Tosi MT; Rosito P; Paolucci G

Address

Second and Third Pediatric Clinics, University of Bologna, Italy.

Source

Am J Dis Child, 1988 Nov, 142:11, 1199-202

Abstract

To evaluate the effects of two different doses of cranial irradiation on growth and growth hormone (GH) release, we studied 61 children with acute lymphocytic leukemia who had survived at least five years in continuous complete remission. Forty-three children received 24 Gy (group 1) and 18 children received 18 Gy (group 2). Height was evaluated at diagnosis, at the end of treatment, and 6, 12, and 24 months later. Growth hormone release was evaluated by arginine and levodopa tests after the end of treatment. After diagnosis, the height SD score decreased significantly in both groups; two years after the end of treatment, only group 1 showed an SD score for height that was still significantly lower than at diagnosis. Group 1 showed impaired GH responses to the tests and, compared with controls, group 1 in fact included a percentage of subjects with a normal response to levodopa (ie, greater than 8 micrograms/L) that was significantly lower (56.4% vs 83.3%) and a percentage of nonresponders to both tests that was significantly higher (21.6% vs 0%). These data indicate that only patients treated with lower cranial irradiation dosage (18 Gy) had complete growth recovery and normal GH responses to pharmacologic tests.

Language of Publication

English

Unique Identifier

89022995

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MeSH Heading (Major)

Brain|*RE; Growth|*RE; Leukemia, Lymphocytic, Acute|ME/*PP; Somatotropin|*SE

MeSH Heading

Arginine|DU; Central Nervous System Diseases|PC; Child; Child, Preschool; Comparative Study; Female; Human; Levodopa|DU; Male; Radiation Dosage

Publication Type

JOURNAL ARTICLE

ISSN

0002-922X

Country of Publication

UNITED STATES

CAS Registry/EC Number

0 (Levodopa); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin)

Record 29 from database: MEDLINE
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Title

Arginine-induced insulin and growth hormone secretion in children with nutritional rickets.

Author

Soliman AT; Aref MK; Rogol AD

Address

Department of Pediatrics, Alexandria University Faculty of Medicine, Egypt.

Source

J Pediatr Gastroenterol Nutr, 1987 Jul-Aug, 6:4, 589-92

Abstract

We evaluated arginine-induced insulin and growth hormone (GH) secretion in ten children with vitamin D deficiency rickets and compared these values with those of eight age-matched control children. All rachitic children had biochemical (increased serum alkaline phosphatase activity and decreased calcium x phosphate product) and clinical evidence for rickets. After an intravenous infusion of arginine-HCl (10% solution, 0.5 g/kg), blood samples were obtained for the measurement of serum insulin and GH concentrations. The mean insulin level 30 min after the start of the infusion was 22.2 +/- 17.1 microU/ml for the rachitic children. This value is significantly below that for the normal children, 63.4 +/- 38.7 microU/ml (p = 0.004). Neither the fasting insulin level nor any others after the arginine infusion differed significantly from those for the control children. There were no significant differences in the fasting or the arginine-stimulated GH levels between the rachitic and control children. The concentrations of insulin-like growth factors did not differ between the two groups.

Language of Publication

English

Unique Identifier

88118070

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MeSH Heading (Major)

Arginine|*DU; Insulin|BL/*SE; Rickets|*BL; Somatotropin|BL/*SE

MeSH Heading

Alkaline Phosphatase|BL; Blood Glucose|ME; Calcium|BL; Human; Infant; Infusions, Intravenous; Insulin-Like Growth Factor I|BL; Insulin-Like Growth Factor II|BL; Phosphorus|BL; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE

ISSN

0277-2116

Country of Publication

UNITED STATES

CAS Registry/EC Number

EC 3.1.3.1 (Alkaline Phosphatase); 0 (Blood Glucose); 11061-68-0 (Insulin); 67763-96-6 (Insulin-Like Growth Factor I); 67763-97-7 (Insulin-Like Growth Factor II); 7004-12-8 (Arginine); 7440-70-2 (Calcium); 7723-14-0 (Phosphorus); 9002-72-6 (Somatotropin)

Record 30 from database: MEDLINE
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Title

Constitutional delay in growth: comparison of linear growth with serum growth hormone response to provocative tests in 26 children.

Author

McArthur RG; Bala RM; Rademaker AW

Address

 

Source

Clin Invest Med, 1986, 9:1, 6-11

Abstract

The peak levels of serum growth hormone (GH) obtained in response to administration of insulin and arginine in 26 children with constitutional delay in growth (CDG) are compared to similar test results in 7 normal children. Heights at the time of testing, and follow-up linear growth, are documented in all subjects. Most patients with constitutional delay in growth could be identified on the basis of history, physical examination, bone age radiograph, and yearly follow-up of growth. Only two patients exhibited growth of less than 4 cm per year; both had normal responses to provocative testing. In response to provocative testing, individual patients with constitutional delay in growth revealed peak levels of serum GH which were within the normal range, but the group mean peak value was less (p less than 0.05) than in normal children. One child with clinical constitutional delay in growth revealed a subnormal response to both provocative tests. The results suggest that children with constitutional delay in growth may have a diminished reserve for secreting growth hormone.

Language of Publication

English

Unique Identifier

86162452

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MeSH Heading (Major)

Arginine|*DU; Growth Disorders|BL/*PP; Insulin|*DU; Somatotropin|*BL

MeSH Heading

Adolescence; Blood Glucose|AN; Body Height; Child; Child, Preschool; Comparative Study; Female; Human; Male; Reference Values

Publication Type

JOURNAL ARTICLE

ISSN

0147-958X

Country of Publication

CANADA

CAS Registry/EC Number

0 (Blood Glucose); 11061-68-0 (Insulin); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin)

Record 31 from database: MEDLINE
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Title

Beta-adrenergic modulation of growth hormone (GH) autofeedback on sleep-associated and pharmacologically induced GH secretion.

Author

Kelijman M; Frohman LA

Address

Department of Internal Medicine, University of Cincinnati, College of Medicine, Ohio 45267.

Source

J Clin Endocrinol Metab, 1989 Dec, 69:6, 1187-94

Abstract

To determine whether GH feedback affects both induced and spontaneous GH secretion and to explore its neurotransmitter mediation, we assessed the effects of 6-h GH infusions (0.55-5.5 micrograms/m2/min) on sleep-associated and GH-releasing hormone (GHRH)-, insulin hypoglycemia-, and arginine-stimulated GH secretion and their modulation by beta-adrenergic blockade in normal men. GH infusions initiated 2 h before the expected onset of sleep produced a dose-dependent inhibition of GH secretion. GH infusions (0.55 micrograms/m2/min) initiated 4 h before the stimuli inhibited the GH response to each, but did not alter the TSH response to TRH. Propranolol infusion (80 micrograms/min) started 2 h before the onset of sleep or the stimulus enhanced GH responses to GHRH and insulin alone and in the presence of GH. In contrast, propranolol neither enhanced the GH responses to arginine or sleep nor reversed the inhibitory effects of GH. The negative feedback effect of GH to both physiological and pharmacological stimuli of GH secretion indicates that it is most likely mediated by both stimulation of somatostatin and inhibition of GHRH release. The effects of beta-adrenergic blockade suggest an inhibition of somatostatin release, although the complex interaction of GH and propranolol implies that they act through dissimilar mechanisms.

Language of Publication

English

Unique Identifier

90062420

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MeSH Heading (Major)

Propranolol|*PD; Receptors, Adrenergic, beta|DE/*PH; Sleep|DE/*PH; Somatotropin|*PD/PH/SE

MeSH Heading

Adult; Arginine|PD; Feedback; Human; Hypoglycemia|PP; Insulin|PD; Insulin-Like Growth Factor I|PD; Male; Protirelin|PD; Somatostatin|PD; Somatotropin-Releasing Hormone|PD; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE

ISSN

0021-972X

Country of Publication

UNITED STATES

CAS Registry/EC Number

0 (Receptors, Adrenergic, beta); 11061-68-0 (Insulin); 24305-27-9 (Protirelin); 51110-01-1 (Somatostatin); 525-66-6 (Propranolol); 67763-96-6 (Insulin-Like Growth Factor I); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin); 9034-39-3 (Somatotropin-Releasing Hormone)

Record 32 from database: MEDLINE
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Title

Circulating serum phenylalanine concentrations and the effect of arginine infusion on plasma levels of growth hormone and insulin in treated phenylketonuric children.

Author

Rosskamp R; Mallmann R; Liappis N; Soetadjii S

Address

 

Source

Acta Endocrinol (Copenh), 1987 Apr, 114:4, 483-7

Abstract

According to desired phenylalanine (Phe) levels of 50-80 mg/l during treatment, three groups of patients with classical phenylketonuria (PKU) (5.3-17.1 years) were formed. They were investigated for their growth hormone (GH) and insulin response to arginine infusion: Group I (N = 5) had Phe levels below (22 +/- 4 mg/l), group II (N = 3) within (61 +/- 6 mg/l), and group III (N = 3) above therapeutic limits (156 +/- 3 mg/l). Nine children (5.2-14.5 years) with short stature served as controls. Whereas group I and II PKU children showed normal GH response to arginine infusion, group III children exhibited impaired GH response expressed as integrated GH response (218 +/- 38.6 micrograms X 1(-1) X 2 h vs 911 +/- 145 micrograms X 1(-1) X 2 h; P less than 0.01) or peak GH response (6.6 +/- 1.2 micrograms/l vs 18.7 +/- 2.3 micrograms/l; P less than 0.05). Integrated insulin responses did not differ between the three PKU groups but were significantly higher in all PKU patients compared with controls (4903 +/- 421 mU/l vs 2750 +/- 378 mU/l; P less than 0.01). However, this reflects impaired insulin secretion in children with constitutional delay of growth and adolescence rather than hyperinsulinism in PKU patients.

Language of Publication

English

Unique Identifier

87208756

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MeSH Heading (Major)

Arginine|*AD; Insulin|*BL; Phenylalanine|*BL; Phenylketonuria|BL/*DT; Somatotropin|*BL

MeSH Heading

Adolescence; Child; Child, Preschool; Female; Human; Infant; Infusions, Intravenous; Insulin-Like Growth Factor I|BL; Male

Publication Type

JOURNAL ARTICLE

ISSN

0001-5598

Country of Publication

DENMARK

CAS Registry/EC Number

11061-68-0 (Insulin); 3617-44-5 (Phenylalanine); 67763-96-6 (Insulin-Like Growth Factor I); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin)

Record 33 from database: MEDLINE
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Title

Growth hormone deficiency due to GH-N gene deletion in an Austrian family.

Author

Frisch H; Phillips JA 3d

Address

 

Source

Acta Endocrinol Suppl (Copenh), 1986, 279:, 107-12

Abstract

An 11 year old Austrian boy with isolated growth hormone deficiency type I A is described. On institution of GH therapy at the age of 2 2/12 years there was only a short growth response and anti-GH-antibodies with high binding capacity were detected, and growth was inhibited. Examination of the nuclear DNA by restriction endonuclease analysis demonstrated a defect of the GH-N gene in the patient. The results suggest the deletion in this Austrian family is different from that seen in other patients. The parents were heterozygous for the deletion and had a subnormal GH response to stimulation with arginine, but their somatomedin-C concentrations and their heights were normal. The patients' sister was of normal height, hormone analyses were normal, and the GH-N gene was not affected.

Language of Publication

English

Unique Identifier

87044832

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MeSH Heading (Major)

Chromosome Deletion|*; Growth Disorders|DT/*GE; Somatotropin|BL/*DF/GE/IM/TU

MeSH Heading

Antibodies|AN; Arginine|DU; Austria; Case Report; DNA|GE; Human; Infant; Insulin|DU; Male; Nucleic Acid Hybridization

Publication Type

JOURNAL ARTICLE

ISSN

0300-9750

Country of Publication

DENMARK

CAS Registry/EC Number

0 (Antibodies); 11061-68-0 (Insulin); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin); 9007-49-2 (DNA)

Record 34 from database: MEDLINE
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Title

Exogenous growth hormone treatment alters body composition and increases natural killer cell activity in women with impaired endogenous growth hormone secretion.

Author

Crist DM; Peake GT; Mackinnon LT; Sibbitt WL Jr; Kraner JC

Address

Department of Medicine, University of New Mexico School of Medicine, Albuquerque 87131.

Source

Metabolism, 1987 Dec, 36:12, 1115-7

Abstract

In order to assess the potential relationship between human growth hormone (GH) and body composition (BC) and natural immunity (NI), we measured the effects of exogenous GH on fat weight (FW), fat-free weight (FFW), and the cytotoxic activity of natural killer (NK) cells in women with impaired GH secretion. Mean peak serum concentrations of GH in response to L-dopa/arginine stimulation were 6.2 +/- 1.1 (SEM) ng/mL in 6 untreated subjects (US) and 5.4 +/- 1.5 ng/mL in 6 GH-treated subjects (TS). Moreover, the pretreatment circulating levels of IGF-I were low in both groups (US 684 +/- 121 mU/mL and TS 583 +/- 83 mU/mL), and they correlated with pretest levels of NK cell activity (r = .59, P less than .05) when both groups were combined. The TS were given 700 micrograms of human GH IM for an average of 14 days while the US were studied in parallel without GH treatment. As measured by hydrodensitometry or skinfold anthropometry, FW decreased (26.1 +/- 6.8 kg to 23.8 +/- 6.3 kg, P less than .05) and FFW increased (44.9 +/- 3.3 kg to 46.2 +/- 3.8 kg, P less than .05) in the TS. In the US, there were no significant (P less than .05) changes in either FW or FFW. Using a standard 51Cr release assay to measure the specific lytic (SL) activity of NK cells, mean SL activity increased from 24.4 +/- 7.0% to 44.1 +/- 8.9% (P less than .05) in the TS, whereas levels in the US were not altered significantly (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Language of Publication

English

Unique Identifier

88065053

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MeSH Heading (Major)

Body Composition|*DE; Insulin-Like Growth Factor I|*DF; Killer Cells, Natural|*DE; Somatomedins|*DF; Somatotropin|DF/PD/*TU

MeSH Heading

Adult; Arginine|DU; Female; Human; Levodopa|DU; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE

ISSN

0026-0495

Country of Publication

UNITED STATES

CAS Registry/EC Number

0 (Levodopa); 0 (Somatomedins); 67763-96-6 (Insulin-Like Growth Factor I); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin)

Record 35 from database: MEDLINE
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Title

Resolution of apparent growth hormone-dependent growth failure during puberty: a case report.

Author

Weissberger AJ; Ho KY; Lazarus L

Address

Garvan Institute of Medical Research, St Vincent's Hospital, Sydney, Australia.

Source

Horm Res, 1989, 32:4, 148-50

Abstract

A prepubertal boy with apparent growth hormone (GH)-dependent growth failure displayed a marked increase in growth velocity, normal GH responses to arginine/insulin infusion and a fourfold increase in spontaneous 24-hour GH secretion following the onset of normal puberty. The case supports earlier observations of a transient form of GH insufficiency in some short prepubertal children, but represents the first evidence that puberty restores spontaneous as well as stimulated GH secretion in such patients.

Language of Publication

English

Unique Identifier

90169832

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MeSH Heading (Major)

Growth Disorders|*PP; Puberty|*PH; Somatotropin|BL/*PH

MeSH Heading

Adolescence; Arginine|PD; Blood Glucose|ME; Case Report; Human; Insulin|BL/PD; Male; Radioimmunoassay; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE

ISSN

0301-0163

Country of Publication

SWITZERLAND

CAS Registry/EC Number

0 (Blood Glucose); 11061-68-0 (Insulin); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin)

Record 36 from database: MEDLINE
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Title

Ectopic growth hormone-releasing hormone (GHRH) syndrome in a case with multiple endocrine neoplasia type I.

Author

Yamasaki R; Saito H; Sano T; Kameyama K; Yoshimoto K; Hosoi E; Matsumura M; Harada K; Saito S

Address

Department of Internal Medicine, School of Medicine, University of Tokushima, Japan.

Source

Endocrinol Jpn, 1988 Feb, 35:1, 97-109

Abstract

A 36-yr-old man with multiple endocrine neoplasia (MEN) type I had an ectopic growth hormone-releasing hormone (GHRH) syndrome due to a GHRH-secreting pancreatic tumor. The immunoreactive (IR)-GHRH concentration in his plasma ranged from 161 to 400 pg/ml (299 +/- 61 pg/ml, mean +/- SD; normal, 10.4 +/- 4.1 pg/ml), and a significant correlation was found between his plasma IR-GHRH and GH (r = 0.622, p less than 0.02). After removal of the pancreatic tumor, the high plasma GH concentration returned to nearly the normal range (42.2 +/- 31.3 to 9.6 +/- 3.8 ng/ml). These changes paralleled the normalization of his plasma IR-GHRH (16.1 +/- 3.8 pg/ml) and some of his symptoms related to acromegaly improved. However, plasma GH (7.7 +/- 1.3 ng/ml) and IGF-I (591 +/- 22 ng/ml) concentrations were high at 12 months after surgery, suggesting adenomatous changes in the pituitary somatotrophs. Before surgery, exogenous GHRH induced a marked increase in plasma GH, and somatostatin and its agonist (SMS201-995) completely suppressed GH secretion, but not IR-GHRH release. No pulsatile secretion of either IR-GHRH or GH was observed during sleep. An apparent increase in the plasma GH concentration was observed in response to administration of TRH, glucose, arginine or insulin, while plasma IR-GHRH did not show any fluctuation. However, these responses of plasma GH were reduced or no longer observed one month and one year after surgery. These results indicate that 1) a moderate increase in circulating GHRH due to ectopic secretion from a pancreatic tumor stimulated GH secretion resulting in acromegaly, and evoked GH responses to various provocative tests indistinguishable from those in patients with classical acromegaly, and 2) the ectopic secretion of GHRH may play an etiological role in the pituitary lesion of this patient with MEN type I.

Language of Publication

English

Unique Identifier

88283591

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MeSH Heading (Major)

Multiple Endocrine Neoplasia|*SE; Neoplastic Endocrine-Like Syndromes|DI/*PA; Pancreatic Neoplasms|*SE; Somatotropin-Releasing Hormone|BL/*SE

MeSH Heading

Acromegaly|ET; Adult; Arginine|PD; Case Report; Glucose|PD; Human; Insulin|PD; Male; Protirelin|PD; Radioimmunoassay; Somatostatin|PD; Somatotropin|BL/SE; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE

ISSN

0013-7219

Country of Publication

JAPAN

CAS Registry/EC Number

11061-68-0 (Insulin); 24305-27-9 (Protirelin); 50-99-7 (Glucose); 51110-01-1 (Somatostatin); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin); 9034-39-3 (Somatotropin-Releasing Hormone)

Record 37 from database: MEDLINE
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Title

Growth hormone and carbohydrate intolerance in cirrhosis.

Author

Shankar TP; Solomon SS; Duckworth WC; Jerkins T; Iyer RS; Bobal MA

Address

Department of Medicine, VA Medical Center, Memphis, Tennessee.

Source

Horm Metab Res, 1988 Sep, 20:9, 579-83

Abstract

Patients with cirrhosis of the liver often have insulin resistance and elevated circulating growth hormone levels. This study was undertaken (a) to evaluate glucose intolerance, insulin resistance and abnormal growth hormone secretion and (b) to determine if GH suppression improves insulin resistance. Glucose tolerance tests (GTT), intravenous insulin tolerance tests (IVITT), arginine stimulation tests (AST) and glucose clamp studies before and during GH suppression with somatostatin were performed in a group of patients with alcohol-induced liver cirrhosis. During GTT cirrhotic subjects had a 2-hour plasma glucose of 200 +/- 9.8 ng/dl (N = 14) compared to 128 +/- 8.0 ng/dl in normal controls (N = 15), P less than 0.001. Basal GH was elevated in cirrhotic patients and in response to arginine stimulation reached a peak of 17.0 +/- 5.4 ng/ml (N = 7), compared to a peak of 11.3 +/- 1.8 ng/ml in 5 normal controls (P = NS). During IVITT patients with cirrhosis had a glucose nadir of 60.0 +/- 4.0 mg/dl (N = 9), compared to 29.0 +/- 7.0 mg/dl in controls (N = 5), P less than 0.001. Peak GH levels during IVITT were not significantly different in cirrhotics and controls. Glucose utilization rates in 4 patients with cirrhosis of the liver before somatostatin mediated GH suppression was 3.1 +/- 0.5 mg/kg/min and 6.5 +/- 1.5 mg/kg/min during somatostatin infusion, P less than 0.025. We conclude that patients with alcohol induced cirrhosis have sustained GH elevations resulting in insulin resistance which improves after GH suppression.

Language of Publication

English

Unique Identifier

89065585

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MeSH Heading (Major)

Blood Glucose|*ME; Liver Cirrhosis|BL/*PP; Somatotropin|*BL

MeSH Heading

Adult; Arginine|PD; Glucose Clamp Technique; Glucose Tolerance Test; Human; Insulin Resistance; Middle Age; Support, U.S. Gov't, Non-P.H.S.; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE

ISSN

0018-5043

Country of Publication

GERMANY, WEST

CAS Registry/EC Number

0 (Blood Glucose); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin)

Record 38 from database: MEDLINE
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Title

Somatostatin analogue SMS 201-995 reduces serum IGF-I levels in patients with neoplasms potentially dependent on IGF-I.

Author

Pollak MN; Polychronakos C; Guyda H

Address

Department of Oncology, McGill University, Montreal, Quebec, Canada.

Source

Anticancer Res, 1989 Jul-Aug, 9:4, 889-91

Abstract

Tumors of several organs have been shown to bear cell surface receptors for insulin-like growth factor I (IGF-I), and to exhibit dependence on this mitogen for optimum proliferation both in vivo and in vitro. To investigate the feasibility of a novel form of endocrine therapy that would exploit such dependence, we treated 8 patients with non-endocrine solid tumours with the somatostatin analogue SMS 201-995, in an effort to reduce growth hormone-stimulated IGF-I production. Significant decreases in basal and arginine-stimulated serum growth hormone and serum IGF-I were noted. This approach deserves evaluation as a potentially useful form of palliative endocrine therapy for certain cancers.

Language of Publication

English

Unique Identifier

90055032

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MeSH Heading (Major)

Insulin-Like Growth Factor I|*AN/PH; Neoplasms|*DT/PP; Octreotide|*TU; Somatomedins|*AN; Somatotropin|*BL

MeSH Heading

Adult; Aged; Arginine|DU; Breast Neoplasms|DT; Colonic Neoplasms|DT; Female; Human; Kidney Neoplasms|DT; Middle Age; Ovarian Neoplasms|DT; Pancreatic Neoplasms|DT; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE

ISSN

0250-7005

Country of Publication

GREECE

CAS Registry/EC Number

0 (Somatomedins); 67763-96-6 (Insulin-Like Growth Factor I); 7004-12-8 (Arginine); 83150-76-9 (Octreotide); 9002-72-6 (Somatotropin)

Record 39 from database: MEDLINE
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Title

Arginine induced growth hormone (hGH) response and paradoxical hGH secretion stimulated by TRH in diabetes mellitus.

Author

Winkler G; Gerö L; Halmos T; Grósz A; Gefferth G; Varga P; Tamás G Jr

Address

 

Source

Acta Diabetol Lat, 1987 Apr-Jun, 24:2, 109-17

Abstract

Growth hormone (hGH) reserve following arginine administration and the paradoxical hGH response to thyrotropin-releasing hormone (TRH) were studied in 30 diabetics without evidence of vascular complications. The diabetics were divided into 4 groups according to the type of their disease and to the metabolic condition within the IDDM group (insulin-dependent: IDDM, in acceptable response and in poor metabolic control; non-insulin-dependent: NIDDM, and juvenile diabetics not requiring insulin at least for two years after diagnosing their disease: NIDDY). The results were compared with controls of identical age and normal weight. A paradoxical hGH response to TRH stimulation was found only in IDDM patients in poor metabolic control. In this group the hGH reserve revealed by arginine was significantly larger than in the others. It was shown that the induced hGH release was independent of the sex distribution of the groups and of the basal hGH values. Magnitude of the hGH reserve and appearance of the paradoxical hGH response were not necessarily correlated but the substantial reserve was frequently associated with a paradoxical response. It can be assumed that the unfavorable metabolic condition is of decisive importance in giving rise to these anomalies. Our observations seem to confirm the need for good metabolic control if the pathological hGH secretion in diabetics is to be prevented.

Language of Publication

English

Unique Identifier

87322111

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MeSH Heading (Major)

Arginine|*PD; Diabetes Mellitus|*BL; Protirelin|*PD; Somatotropin|*BL

MeSH Heading

Adult; Blood Glucose|ME; Diabetes Mellitus, Insulin-Dependent|BL; Diabetes Mellitus, Non-Insulin-Dependent|BL; Female; Human; Insulin|TU; Male; Middle Age

Publication Type

JOURNAL ARTICLE

ISSN

0001-5563

Country of Publication

ITALY

CAS Registry/EC Number

0 (Blood Glucose); 11061-68-0 (Insulin); 24305-27-9 (Protirelin); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin)

Record 40 from database: MEDLINE
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Title

Growth without growth hormone: the "invisible" GH syndrome.

Author

Bistritzer T; Chalew SA; Lovchik JC; Kowarski AA

Address

Department of Pediatrics, University of Maryland School of Medicine, Baltimore 21201.

Source

Lancet, 1988 Feb 13, 1:8581, 321-3

Abstract

Growth hormone (GH) deficiency, diagnosed by radioimmunoassay (RIA) measurements of GH in blood after provocation or in continuous 24 h samples of venous blood, is usually associated with growth failure. 4 non-obese boys have been identified who had normal linear growth despite apparent GH deficiency by standard RIA. All 4 patients had normal GH concentrations as measured with an IM-9 cell radio-receptor assay (RRA). The RRA/RIA ratio of the 4 patients significantly exceeded that of controls. Thus, these patients secrete a molecule with normal GH receptor binding and bioactivity which is "invisible" to the standard GH RIA. This variant GH is possibly expressed from the human GH-V gene or a mutant allele.

Language of Publication

English

Unique Identifier

88120824

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MeSH Heading (Major)

Growth|*/DE; Somatotropin|BL/*DF/PD

MeSH Heading

Acromegaly|BL; Adolescence; Arginine|DU; Child; Human; Insulin|DU; Radioimmunoassay; Radioligand Assay|MT; Receptors, Somatotropin|ME; Recombinant Proteins|PD; Support, Non-U.S. Gov't; Syndrome

Publication Type

JOURNAL ARTICLE

ISSN

0140-6736

Country of Publication

ENGLAND

CAS Registry/EC Number

0 (Receptors, Somatotropin); 0 (Recombinant Proteins); 11061-68-0 (Insulin); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin)

Record 41 from database: MEDLINE
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Title

Total deficiency of growth hormone and prolactin, and partial deficiency of thyroid stimulating hormone in two Dutch families: a new variant of hereditary pituitary deficiency.

Author

Wit JM; Drayer NM; Jansen M; Walenkamp MJ; Hackeng WH; Thijssen JH; Van den Brande JL

Address

Department of Pediatrics, University Hospital for Children and Youth, Utrecht, The Netherlands.

Source

Horm Res, 1989, 32:5-6, 170-7

Abstract

Four out of 10 children in two unrelated families presented with a total pituitary growth hormone (GH) and prolactin deficiency and a partial thyrotropin (TSH) deficiency. The GH gene was intact in family I. The pituitaries, visualized by magnetic resonance imaging, were normal. All children responded well to GH and L-thyroxine therapy. Baseline plasma somatostatin and its peak response to arginine infusion were elevated in family I and they had a milder TSH deficiency than family II. Plasma insulin showed a poor response to arginine infusion. This hereditary combination of pituitary deficiencies suggests a deficiency of a common positive transcription factor.

Language of Publication

English

Unique Identifier

90236416

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MeSH Heading (Major)

Family|*; Hypopituitarism|BL/*GE; Prolactin|BL/*DF; Somatotropin|BL/*DF/TU; Thyrotropin|*DF

MeSH Heading

Adult; Arginine|DU; Case Report; Child; Child, Preschool; Dwarfism, Pituitary|DT/GE; Female; Human; Hypothyroidism|DT/GE; Infant; Male; Thyroxine|TU

Publication Type

JOURNAL ARTICLE

ISSN

0301-0163

Country of Publication

SWITZERLAND

CAS Registry/EC Number

7004-12-8 (Arginine); 7488-70-2 (Thyroxine); 9002-62-4 (Prolactin); 9002-71-5 (Thyrotropin); 9002-72-6 (Somatotropin)

Record 42 from database: MEDLINE
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Title

Growth hormone-releasing effect of oral growth hormone-releasing peptide 6 (GHRP-6) administration in children with short stature.

Author

Bellone J; Ghizzoni L; Aimaretti G; Volta C; Boghen MF; Bernasconi S; Ghigo E

Address

Department of Clinical Pathophysiology, University of Turin, Italy.

Source

Eur J Endocrinol, 1995 Oct, 133:4, 425-9

Abstract

Growth hormone-releasing peptide 6 (GHRP-6) is a synthetic hexapeptide with a potent GH-releasing activity after intravenous, subcutaneous, intranasal and oral administration in man. Previous data showed its activity also in some patients with GH deficiency. The aim of our study was to verify the GH-releasing activity of oral GHRP-6 administration on GH secretion in children with normal short stature. The effect of oral GHRP-6 (300 micrograms/kg) was compared with that of the maximally effective dose of intravenous GH-releasing hormone (GHRH-29, 1 microgram/kg). As the GHRH-induced GH rise in children is potentiated by arginine (ARG), even when administered by oral route at low dose (4 g), we studied also the interaction of oral GHRP-6 and ARG administration. We studied 13 children (nine boys and four girls aged 6.2-10.5 years, pubertal stage I) with normal short stature (height less than -2 SD score; height velocity more than -2 SD score; normal bone age; insulin-like growth factor I > 70 micrograms/l). In a first group of children (N = 7), oral GHRP-6 administration induced a GH response (mean +/- SEM; peak at 60 min vs baseline: 18.8 +/- 3.0 vs 1.1 +/- 0.3 micrograms/l, p < 0.0006; area under curve: 1527.3 +/- 263.9 micrograms l-1 h-1) which was similar to that elicited by GHRH (peak at 45 min vs baseline: 20.8 +/- 4.5 vs 2.2 +/- 0.9 micrograms/l, p < 0.007; area under curve: 1429.4 +/- 248.2 micrograms l-1 h-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Language of Publication

English

Unique Identifier

96038765

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MeSH Heading (Major)

Growth Disorders|*DT; Oligopeptides|AD/*PD/TU; Somatotropin|*SE

MeSH Heading

Administration, Oral; Arginine|AD/PD; Body Height; Child; Comparative Study; Female; Human; Insulin-Like Growth Factor I|ME; Kinetics; Male; Somatotropin-Releasing Hormone|AD/PD; Support, Non-U.S. Gov't

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE

ISSN

0804-4643

Country of Publication

NORWAY

Record 43 from database: MEDLINE
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Title

Direct analysis of growth factor requirements for isolated human fetal hepatocytes.

Author

Hoshi H; Kan M; McKeehan WL

Address

W. Alton Jones Cell Science Center, Inc., Lake Placid, New York 12946.

Source

In Vitro Cell Dev Biol, 1987 Oct, 23:10, 723-32

Abstract

Hepatocytes were isolated from human fetal liver in order to analyze the direct effects of growth factors and hormones on human hepatocyte proliferation and function. Mechanical fragmentation and then dissociation of fetal liver tissue with a collagenase/dispase mixture resulted in high yield and viability of hepatocytes. Hepatocytes were selected in arginine-free, ornithine-supplemented medium and defined by morphology, albumin production and ornithine uptake into cellular protein. A screen of over twenty growth factors, hormones, mitogenic agents and crude organ and cell extracts for effect on the stimulation of hepatocyte growth revealed that EGF, insulin, dexamethasone, and factors concentrated in bovine neural extract and hepatoma cell-conditioned medium supported attachment, maintenance and growth of hepatocytes on a collagen-coated substratum. The population of cells selected and defined as differentiated hepatocytes had a proliferative potential of about 4 cumulative population doublings. EGF and insulin synergistically stimulated DNA synthesis in the absence of other hormones and growth factors. Although neural extracts enhanced hepatocyte number, no effect on DNA synthesis of neural extracts or purified heparin-binding growth factors from neural extracts could be demonstrated in the absence or presence of defined hormones, hepatoma-conditioned medium or serum. Hepatoma cell-conditioned medium had the largest impact on both hepatocyte cell number and DNA synthesis under all conditions. Dialyzed serum protein (1 mg/ml) at 10 times higher protein concentration had a similar effect to hepatoma cell-conditioned medium (100 micrograms/ml). The results suggest that hepatoma cell conditioned medium may be a concentrated and less complicated source than serum for purification and characterization of additional normal hepatocyte growth factors.

Language of Publication

English

Unique Identifier

88032740

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MeSH Heading (Major)

Growth Substances|*PD; Hormones|*PD; Liver|CY/DE/*EM

MeSH Heading

alpha-Fetoproteins|AN; Albumins|AN; Arginine|PD; Blood|PH; Cell Adhesion|DE; Cell Division|DE; Cell Survival; Cells, Cultured; Comparative Study; Culture Media|PD; Drug Interactions; Human; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE

ISSN

0883-8364

Country of Publication

UNITED STATES

CAS Registry/EC Number

0 (alpha-Fetoproteins); 0 (Albumins); 0 (Culture Media); 0 (Growth Substances); 0 (Hormones); 7004-12-8 (Arginine)

Record 44 from database: MEDLINE
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Title

Insulin-like growth factors in patients with nonislet cell tumors and hypoglycemia.

Author

Merimee TJ

Address

 

Source

Metabolism, 1986 Apr, 35:4, 360-3

Abstract

Insulin-like growth factors (IGF) in serum from 3 patients with nonislet cell tumors and hypoglycemia were measured by radioimmunoassay and by means of a rat liver membrane assay (specific for IGF II). The concentration of IGF II by receptor assay was greater than normal when the samples were initially assayed, but subsequently decreased 48% to 80% over the next 8 to 15 weeks. In the same serum samples, concentrations of both IGF I and IGF II by radioimmunoassay were consistently less than normal. In all 3 patients growth hormone (GH) responses to intravenous arginine were depressed and in 2 of the 3 patients, a GH-dependent 150 K serum protein carrier of IGF was absent. None of these abnormalities were seen in 7 patients with insulinomas and chronic hypoglycemia. The data suggest that some patients with nonislet cell tumors and hypoglycemia produce a receptor-active, nonimmunoreactive IGF-II-like material. This material appears (a) more labile than normal IGF II and (b) capable of inhibiting GH secretion. The latter effect may decrease immunoreactive IGF I and II, as well as decrease the GH-dependent 150 K protein carrier of these factors. The extreme lability of the IGF-II-like material produced by tumors probably explains the previous contradictory reports on this topic.

Language of Publication

English

Unique Identifier

86174303

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MeSH Heading (Major)

Hypoglycemia|*BL; Insulin-Like Growth Factor I|*BL; Insulin-Like Growth Factor II|*BL; Neoplasms|*BL; Somatomedins|*BL

MeSH Heading

Arginine|PD; Carrier Proteins|AN; Human; Receptors, Cell Surface|AN; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE

ISSN

0026-0495

Country of Publication

UNITED STATES

CAS Registry/EC Number

0 (Carrier Proteins); 0 (Insulin-Like Growth-Factor-Binding Proteins); 0 (Receptors, Cell Surface); 0 (Receptors, Somatomedin); 0 (Somatomedins); 67763-96-6 (Insulin-Like Growth Factor I); 67763-97-7 (Insulin-Like Growth Factor II); 7004-12-8 (Arginine)

Record 45 from database: MEDLINE
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Title

Effect of fenfluramine on insulin/growth hormone ratio in obese subjects.

Author

Altomonte L; Zoli A; Ghirlanda G; Manna R; Greco AV

Address

Istituto di Clinica Medica, Università Cattolica del Sacro Cuore, Roma, Italy.

Source

Pharmacology, 1988, 36:2, 106-11

Abstract

Obesity is characterized by increased levels of insulin and by subnormal growth hormone (GH) release. Insulin/GH ratio is significantly higher in obese than in lean individuals. Fenfluramine, an anorectic drug, may have some effects on hypothalamic-pituitary function and on insulin secretion, possibly through a serotonergic stimulation. The aim of this work was to study the effects of fenfluramine on the insulin/GH ratio after arginine in obese subjects. Ten volunteer obese females were studied; 10 volunteer women were the normal weight controls. All subjects were given placebo and fenfluramine (60 mg p.o.) in a randomized order and after 120 min underwent arginine infusion (25 g i.v. for 30 min). Blood samples were taken every 30 min until 270 min for GH and insulin radioimmunoassay. In the obese group the GH response to arginine was significantly lower than in controls. Fenfluramine administration restored the subnormal GH response to arginine in obese subjects. Arginine infusion provoked a greater insulin secretion in obese subjects than in lean individuals. Fenfluramine administration diminished the insulin response to arginine. Fenfluramine did not modify the insulin/GH ratio in controls while it significantly lowered the insulin/GH ratio in obese subjects. Because insulin promotes fat and carbohydrate storage while GH stimulates lipolysis, the combination of high insulin and low GH concentrations may worsen the obese condition. A lower insulin/GH ratio can be useful in the treatment of obesity.

Language of Publication

English

Unique Identifier

88177065

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MeSH Heading (Major)

Fenfluramine|*PD; Insulin|*BL; Obesity|*BL; Somatotropin|*BL

MeSH Heading

Adult; Arginine|PD; Female; Human; Middle Age

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL

ISSN

0031-7012

Country of Publication

SWITZERLAND

CAS Registry/EC Number

11061-68-0 (Insulin); 458-24-2 (Fenfluramine); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin)

Record 46 from database: MEDLINE
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Title

Impaired insulin response to glucose but not to arginine in heroin addicts.

Author

Passariello N; Giugliano D; Ceriello A; Chiariello A; Sgambato S; D'Onofrio F

Address

 

Source

J Endocrinol Invest, 1986 Oct, 9:5, 353-7

Abstract

Plasma glucose, insulin, glucagon and growth hormone responses to both oral glucose and iv arginine were evaluated in 15 heroin addicts and 15 control subjects matched for age, sex and weight. The heroin users had an exaggerated rise in plasma glucose concentrations following oral sugar, which persisted until the end of the study (102 +/- 5 mg/dl in addicts vs 72 +/- 3 mg/dl in controls at 240 min, p less than 0.01) and significantly lower insulin responses (insulin peak 28 +/- 4 microU/ml in addicts vs 67 +/- 8 microU/ml in controls, p less than 0.01). The inhibitory effect of glucose on glucagon concentrations was less evident in addicts than in controls. The responses of plasma glucose, insulin and glucagon to arginine were not significantly different between addicts and controls, while the growth hormone rise was significantly greater in addicts. These results demonstrate that heroin users have impaired insulin secretion to oral glucose but not to arginine and suggest that: the impaired insulin secretion in heroin addicts is not dependent on beta-cell exhaustion, and a selective inhibition of glucose-induced insulin secretion is operative in these subjects, as it happens in patients with noninsulin-dependent diabetes mellitus.

Language of Publication

English

Unique Identifier

87084484

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MeSH Heading (Major)

Arginine|*DU; Glucose Tolerance Test|*; Heroin Dependence|*BL; Insulin|*BL

MeSH Heading

Adult; Blood Glucose|ME; Female; Glucagon|BL; Human; Male; Somatotropin|BL

Publication Type

JOURNAL ARTICLE

ISSN

0391-4097

Country of Publication

ITALY

CAS Registry/EC Number

0 (Blood Glucose); 11061-68-0 (Insulin); 7004-12-8 (Arginine); 9002-72-6 (Somatotropin); 9007-92-5 (Glucagon)

Record 47 from database: MEDLINE
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Title

Effect of fenfluramine on growth hormone and prolactin secretion in obese subjects.

Author

Altomonte L; Zoli A; Alessi F; Ghirlanda G; Manna R; Greco AV

Address

Istituto di Clinica Medica, Università Cattolica S. Cuore, Roma, Italia.

Source

Horm Res, 1987, 27:4, 190-4

Abstract

Obese subjects show a subnormal growth hormone (GH) and prolactin (PRL) release in response to a variety of stimuli. Fenfluramine, an anorexiant drug used in obesity therapy, may have some effects on hypothalamic-pituitary function mediated by serotoninergic stimulation. The present investigation in obese subjects was carried out to study the effects of fenfluramine (60 mg orally) on GH and PRL secretion after intravenous arginine infusion. Ten volunteer obese females were studied and compared with 10 volunteer normal weight controls. In the obese group the GH response to arginine was significantly lower than in control group. Fenfluramine administration restored the subnormal GH response to arginine in obese subjects. The PRL response to arginine in obese women was subnormal. Fenfluramine administration restored the response of PRL to arginine infusion to normal. In conclusion, fenfluramine--under acute circumstances--enhances the hypothalamic-pituitary response to arginine in obese subjects. The decreased GH and PRL output in obese subjects is not due to an absolute hormonal deficiency and this effect of fenfluramine on GH secretion may--due to its lipolysis stimulation--be useful in obesity treatment.

Language of Publication

English

Unique Identifier

88138245

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MeSH Heading (Major)

Fenfluramine|*TU; Obesity|*DT/PP; Prolactin|BL/*SE; Somatotropin|BL/*SE

MeSH Heading

Adult; Arginine|DU; Comparative Study; Female; Human; Kinetics; Middle Age; Reference Values

Publication Type

JOURNAL ARTICLE

ISSN

0301-0163

Country of Publication

SWITZERLAND

CAS Registry/EC Number

458-24-2 (Fenfluramine); 7004-12-8 (Arginine); 9002-62-4 (Prolactin); 9002-72-6 (Somatotropin)

Record 48 from database: MEDLINE
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Title

Arginine enhances the growth hormone-releasing activity of a synthetic hexapeptide (GHRP-6) in elderly but not in young subjects after oral administration.

Author

Ghigo E; Arvat E; Rizzi G; Bellone J; Nicolosi M; Boffano GM; Mucci M; Boghen MF; Camanni F

Address

Dipartimento di Fisiopatologia Clinica, UniversitÄa di Torino, Italy.

Source

J Endocrinol Invest, 1994 Mar, 17:3, 157-62

Abstract

In man the GH-releasing hexapeptide His-DTrp-Ala-Trp-DPhe-Lys-NH2 (GHRP-6) has been shown to be active even after oral administration. On the other hand, it has been shown that arginine (ARG) totally restores the reduced somatotropic responsiveness to GHRH observed in aging. Based on the foregoing, in this study we verified the GH-releasing activity of oral GHRP-6 (300 micrograms/kg) in normal aging and the possible enhancing effect of 8 g oral ARG on the GH-releasing effect of GHRP-6. Eight young (age 24-32 yr) and 8 elderly (age 66-85 yr) subjects were studied. In all the GH response to GHRH (1 microgram/kg iv) was also studied. Both IGF-I levels and the GH response to iv GHRH were lower in elderly than in young subjects (mean +/- SE, IGF-I: 65.1 +/- 9.1 vs 142.9 +/- 9.4 micrograms/L, p < 0.0001; GH peak: 5.4 +/- 1.0 vs 13.6 +/- 0.8 micrograms/L, p < 0.0001). Oral GHRP-6 administration induced a GH rise in elderly which was lower, though not significantly, than that in young subjects (GH peak: 9.9 +/- 2.0 vs 16.2 +/- 5.4 micrograms/L). Oral ARG administration enhanced the GHRP-6-induced GH rise in elderly (GH peak: 22.1 +/- 3.3 micrograms/L, p < 0.01 vs GHRP-6 alone) while failed to modify it in young subjects (GH peak: 13.5 +/- 3.4 micrograms/L). The GH response to oral ARG+GHRP-6 in elderly was higher than that to all stimuli in young adults (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Language of Publication

English

Unique Identifier

94327857

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MeSH Heading (Major)

Aging|*ME; Arginine|AD/AE/*PD; Oligopeptides|AD/AE/*PD; Somatotropin|*BL; Somatotropin-Releasing Hormone|AD/AE/*PD

MeSH Heading

Administration, Oral; Adult; Aged; Aged, 80 and over; Amino Acid Sequence; Comparative Study; Drug Synergism; Human; Injections, Intravenous; Insulin-Like Growth Factor I|ME; Male; Molecular Sequence Data; Support, Non-U.S. Gov't

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE

ISSN

0391-4097

Country of Publication

ITALY

Record 49 from database: MEDLINE
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Title

Failure to confirm the existence of short-latency, short-loop feedback regulation (autoregulation) of growth hormone secretion in the human.

Author

Molitch ME; King LW; Moses AC; Gottesman S; Hlivyak L

Address

 

Source

Neuroendocrinology, 1986, 43:6, 651-6

Abstract

That growth hormone (GH) regulates its own secretion by negative feedback both directly and indirectly via somatomedins has been well-documented in the rat and assumed, on the basis of limited studies, to be true for man as well. Prior to proceeding with studies designed to investigate the nature of this feedback in various endocrine states, we sought first to confirm the existence of direct, short-latency GH feedback in normal individuals. Primed, continuous rate infusions of human GH in normal volunteers achieved a range of steady state GH levels. After 1 h of GH infusion, arginine HCl (500 mg/kg) was infused over 30 min and the GH response assessed. Seven of 8 subjects achieved steady state GH levels in the 8-21 ng/ml range with an infusion rate of 0.0045 U/min following a 0.277 U bolus. After arginine, there was a significant increment of GH levels (range 11.6-69.5 ng/ml) in all 7 subjects. With a higher infusion rate of 0.009 U/min following a 0.54 U bolus, 1 of 2 subjects reached a steady state of 31.0 ng/ml and no response to arginine was demonstrable. Two subjects reached steady state levels of 45.0 and 58 ng/ml during a 0.018 U/min infusion after a 1.08 U bolus and had increments of 26.2 and 25.9 ng/ml following arginine. In 3 subjects achieving levels of 64.5, 107.0 and 132.0 ng/ml, there were increments of 55.0, 61.7 and 13.0 ng/ml during infusions of 0.036 U/min following boluses of 2.16 U. However, only in the first of these 3 was a true steady state achieved.(ABSTRACT TRUNCATED AT 250 WORDS)

Language of Publication

English

Unique Identifier

87015144

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MeSH Heading (Major)

Homeostasis|*; Somatotropin|AD/DU/*SE

MeSH Heading

Arginine|DU; Feedback; Human; Kinetics; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE

ISSN

0028-3835

Country of Publication

SWITZERLAND

CAS Registry/EC Number

7004-12-8 (Arginine); 9002-72-6 (Somatotropin)

Record 50 from database: MEDLINE
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Title

Neuroendocrinological evidence of an anti-dopaminergic effect of flunarizine.

Author

Cortelli P; Santucci M; Righetti F; Pirazzoli P; Albani F; Baruzzi A; Sacquegna T; Cacciari E

Address

Institute of Neurology, University of Bologna, Italy.

Source

Acta Neurol Scand, 1988 Apr, 77:4, 289-92

Abstract

The effect of a one month treatment with flunarizine (5 mg/day) on pituitary responsiveness to gonadotrophin-releasing hormone (GnRH), thyrotrophin-releasing hormone (TRH) and arginine infusion was assessed in 17 adolescents (11 M, 6 F) treated with the drug to prevent migraine attacks. Basal prolactin concentrations as well as the prolactin response to TRH were significantly (p less than 0.05) increased after flunarizine treatment. Flunarizine had no effect on the folliclestimulating and luteinising hormone response to GnRH stimulation, growth hormone response to arginine infusion or thyrotrophin response to TRH stimulation. Our data suggest that flunarizine may interfere with the hypothalamic-pituitary-prolactin axis decreasing dopaminergic inhibitory tonus.

Language of Publication

English

Unique Identifier

88266620

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MeSH Heading (Major)

Dopamine|*AI; Flunarizine|BL/*PD

MeSH Heading

Adolescence; Arginine|PD; Child; Female; Gonadorelin|PD; Human; Male; Pituitary Gland|DE/SE; Prolactin|SE; Protirelin|PD; Somatotropin|SE; Thyrotropin|SE

Publication Type

JOURNAL ARTICLE

ISSN

0001-6314

Country of Publication

DENMARK

CAS Registry/EC Number

24305-27-9 (Protirelin); 33515-09-2 (Gonadorelin); 51-61-6 (Dopamine); 52468-60-7 (Flunarizine); 7004-12-8 (Arginine); 9002-62-4 (Prolactin); 9002-71-5 (Thyrotropin); 9002-72-6 (Somatotropin)

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