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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human growth hormone release is affected by a variety of pharmacological and physiological stimuli. We have studied the effect of oral clonidine, insulin hypoglycemia, and exercise on plasma hGH and GHRH levels in 31 healthy short-stature children. Thirteen underwent an oral clonidine test (0.15 mg/m2), 12 an iv. insulin test (0.1 U/kg), and 6 performed exercise (running for 10 min in a defined route). GHRH-1-44 was extracted from plasma on silica columns and determined by RIA. Although all three stimuli induced a marked increase in plasma hGH levels, only clonidine induced a significant increase in plasma GHRH levels. Maximal increment in GHRH during clonidine was 6.82 +/- 1.05 pmol/l (mean +/- SEM) as compared with 0.51 +/- 0.28 and 0.53 +/- 0.62 during hypoglycemia and exercise (p less than 0.0005 and p less than 0.005), respectively. An additional 24 subjects received TRH 0.2 mg/kg iv: 8 TRH alone, 8 TRH and insulin, and 8 TRH and clonidine. Only insulin potentiated the TRH-induced TSH response with a peak of 22.0 +/- 3.2 vs 16.0 +/- 0.8 and 15.3 +/- 1.5 mU/l (p less than 0.025) for TRH alone and TRH and clonidine, respectively. It is suggested that clonidine stimulates hGH secretion mainly through an enhancement of GHRH release, whereas stress stimuli such as hypoglycemia and exercise achieve hGH release by a different mechanism, possibly inhibition of somatostatin.
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PMID:Effect of oral clonidine, insulin-induced hypoglycemia and exercise on plasma GHRH levels in short-stature children. 210 91

To determine whether differential response to growth hormone-releasing hormone (GHRH) could cause the developmental changes seen in growth hormone (GH) secretion, we administered 10 micrograms/kg GHRH (1-44 NH2) to a group of four unanesthetized, fasted, rhesus monkeys via acutely placed venous catheters at 1, 7, 14, and 28 d postnatal age. Serum GH was assayed by hGH RIA in sera collected at -60, -30, 0, 15, 30, 45, 60, and 90 min relative to the GHRH bolus. Serum cortisol was measured by ELISA in the 0-, 30-, and 60-min samples. Differences between age groups were analyzed by repeated measures analysis of variance and paired t tests. Mean basal GH levels were higher at 1 d (9.4 +/- 1.2 micrograms/L, mean +/- SEM) than at 7 (5.5 +/- 0.4), 14 (5.6 +/- 0.5), and 28 d (5.3 +/- 0.5) of age. There were no other significant differences in mean basal GH values between the age groups. Mean post-GHRH GH concentrations decreased significantly with each age after 1 d (22.6 +/- 1.6): 7 d (16.4 +/- 1.3); 14 d (11.3 +/- 1.0); and 28 d (7.9 +/- 0.9). Similarly, mean delta-GH values decreased with each increase in age from 1 d (15.0 +/- 1.9): 7 d (10.9 +/- 1.6); 14 d (5.9 +/- 1.1); and 28 d (2.7 +/- 0.8). Serum cortisol was not correlated with serum GH at any age. Our study demonstrates decreasing basal GH concentration and GH responses to GHRH with advancing age from 1 to 28 d in the rhesus monkey.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Longitudinal changes in growth hormone response to growth hormone-releasing hormone in neonatal rhesus monkeys. 211 88

Hypothalamo-pituitary function in children with optic glioma may be impaired by the tumour itself and by the high cranial radiation doses used in treatment. This study evaluates the effect of optic glioma and its treatment on patient growth and pubertal development. Twenty-one patients (13 boys, 8 girls), treated for optic glioma by cranial irradiation (45-55 Grays) at a mean age of 5.4 years, were evaluated before (n = 10) and/or after (n = 21) irradiation. Growth hormone (GH) deficiency was present in only 1 patient tested before irradiation and in all patients after irradiation. Precocious puberty occurred in 7/21 cases, before irradiation in 5 patients and after irradiation in 2 patients. The cumulative height loss during the 2 years after irradiation was 0.2 +/- 0.2 SD (m +/- SEM) in 7 patients with precocious puberty and 1.1 +/- 0.2 SD in 14 prepubertal patients (P less than 0.01). The corresponding bone age advance over chronological age, evaluated 1-3 years after irradiation, was 1.1 +/- 0.5 and -0.7 +/- 0.3 year in the two groups (P less than 0.01). The mean height loss between time of irradiation and the final height was 2.3 +/- 0.6 SD (n = 6). Primary amenorrhoea, associated with low oestradiol levels, occurred in two of the three girls of pubertal age. These data indicate that the high dose of cranial radiation used to treat optic glioma invariably results in GH deficiency within 2 years and that hGH therapy is required when GH deficiency is documented.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Growth and endocrine disorders in optic glioma. 222 66

Serum growth hormone binding protein (GHBP) activity was estimated in healthy neonates (n = 6), children and adolescents (n = 97) and young adults (n = 19). GHBP activity was measured by incubating 125I-hGH (human growth hormone) (approximately 25,000 c.p.m.) with serum (100 microliters) in the presence and in the absence of excess unlabelled hGH, followed by separation of specifically bound 125I-hGHBP complexes from free 125I-hGH by gel filtration on Ultrogel AcA44 minicolumns. The results are expressed as the percentage specific binding relative to an adult reference serum (%RSB), after correction for endogenous hGH of the unknown serum. The between-assay coefficients of variation for two sera of %RSB activity of 51.2 and 115.4% were 6.0 and 7.0% respectively. In neonates, low values of serum GHBP were found (%RSB = 27.1 +/- 5.0 SEM) followed by a major rise during the first 6 years of life to a mean value (%RSB = 68.3 +/- 4.1 SEM) which more than doubled that of neonates. Thereafter, values rose progressively throughout childhood and puberty to reach maximum values in young adults (%RSB = 95.0 +/- 3.1 SEM). A novel observation was that serum GHBP activity correlated significantly with height standard deviation score (SDS) (males: r = 0.77, P less than 0.001; females: r = 0.56, P = 0.01) and weight SDS (P less than 0.001) for both sexes before puberty. During puberty GHBP correlated only with weight SDS in males (r = 0.60, P less than 0.01). In all age groups studied, no correlation could be found between serum GHBP and height velocity.
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PMID:Serum growth hormone binding protein activity in healthy neonates, children and young adults: correlation with age, height and weight. 262 Apr 62

Nocturnal urinary growth hormone values were measured by a sensitive enzyme immunoassay in normal adults, patients with GH deficiency, patients with Turner's syndrome, normal but short children who had normal plasma GH responses to provocative tests, and patients with acromegaly. The mean nocturnal urinary GH values in patients with acromegaly were significantly greater than those in normal adults (1582.3 +/- 579.8 vs 53.5 +/- 8.6 pmol/mmol creatinine (+/- SEM); p less than 0.05). In the normal but short children and patients with Turner's syndrome, the mean nocturnal urinary GH values were 83.1 +/- 5.2 and 79.8 +/- 29.5 pmol/mmol creatinine, respectively. In patients with GH deficiency, the nocturnal urinary GH values were undetectable (less than 5.3 pmol/mmol creatinine) except in one patient where the value was 6.3 pmol/mmol creatinine. The nocturnal urinary GH values of the patients with GH deficiency were significantly lower than those of the other groups (p less than 0.05). In normal but short children, the nocturnal urinary GH values correlated significantly with mean plasma nocturnal GH concentrations (r = 0.76, p less than 0.001), and 24-hour urinary GH values (r = 0.84, p less than 0.001), respectively. In 4 patients with GH deficiency who had circulating anti-hGH antibody, the urinary GH values were also undetectable. These data indicate that nocturnal urinary GH value reflects endogenous GH secretion during collection time, and that measurement of the nocturnal urinary GH values is a useful method for screening of patients with GH deficiency and acromegaly.
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PMID:Measurement of nocturnal urinary growth hormone values. 267 89

A soluble GH-binding protein, which cross-reacted with a monoclonal antibody (Mab) to the rabbit liver membrane GH receptor, has been identified in cytosol preparations from both fetal and maternal portions of rabbit placenta. Structural studies using gel filtration chromatography and chemical covalent cross-linking techniques have shown that the GH-binding protein in fetal/maternal placental cytosol has a native mol wt of 104,000 and a denatured subunit of about 57,000 mol wt (with or without dithiothreitol). Very low levels of GH-specific [125I]human (h) GH binding were observed in membrane preparations from the corresponding placentae, even after desaturation of any endogenously bound hormone by 5 M MgCl2. No PRL-specific binding was observed in placental membranes or cytosols. Scatchard analysis of [125I]hGH binding to fetal and maternal placental cytosol revealed linear plots with Ka values of 6.1 +/- 1.1 nM-1 (fetal) and 5.31 +/- 0.63 nM-1 (maternal; mean +/- SEM; n = 5). The binding capacity of maternal placental cytosol, when expressed as femtomoles per mg protein (170 +/- 10.10) or femtomoles per g tissue (3245 +/- 123), was about 3-fold higher than that for fetal placental cytosol. Northern blot analysis of fetal and maternal placental mRNA probed with a GH receptor oligonucleotide probe revealed hybridization to a 4.4 to 4.7-kilobase and a 2.2-kilobase species in fetal placenta only. The level of GH-specific binding observed in fetal and maternal placental cytosol did not correlate directly with the level of mRNA expression. A GH-binding protein has also been shown to be present in fetal rabbit serum and is known to be structurally and immunologically related to the rabbit placental and liver cytosolic GH-binding proteins. Scatchard analysis of [125I]hGH binding to fetal serum GH-binding protein revealed a single class of high affinity sites with a Ka of 4.64 +/- 1.29 nM-1 and a capacity of 338 +/- 167 fmol/ml serum (mean +/- SEM; n = 4). Given the relative binding capacities and the demonstration of GH receptor mRNA in fetal placental cytosol, it is highly unlikely that contamination of fetal placental cytosol by fetal serum accounts for all of the placental binding capacity observed. However, no such definitive conclusion regarding contamination by maternal rabbit serum of maternal placental cytosol can be made. The presence of GH-binding proteins in placental cytosol has not been described previously, and these observations suggest that GH may have a role in placental metabolism.
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PMID:Binding sites for growth hormone in rabbit placental cytosol. 275 89

The growth response to two years of GH treatment was studied in fifteen children after radiotherapy for a cranial tumor. The growth response was compared to that of short children (-2 SD) and that of children with idiopathic growth hormone deficiency (GHD) of similar ages. All children were treated with hGH 0.1 IU/kg/day s.c.; which is a higher dose and frequency than previously reported for irradiated children. On this protocol the growth rate increased 5.0 +/- 0.5 cm/y (mean +/- SEM) the first year and 3.8 +/- 0.7 cm/y the second year compared to the growth rate the year before GH-treatment. Although the net gain in growth was higher than previously reported, the first year growth response was significantly reduced (p less than 0.05) compared to that of GHD-children (7.6 +/- 0.5 cm/y) but exceeded (p less than 0.05) that of short children (3.4 +/- 0.3 cm/y). The median spontaneous 24 h-GH secretion was 209 mU/l in the short children, 52 mU/l in the irradiated children and 16 mU/l in the idiopathic GHD children. Thus the growth increment varied inversely to the spontaneous GH secretion observed in the three groups.
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PMID:Improved growth response to GH treatment in irradiated children. 278 71

We studied the metabolic clearance rate (MCR) serum half-time (t1/2) and apparent distribution space (DS) of unlabelled, authentic, biosynthetic human growth hormone (B-hGH) in 9 GH-deficient patients by means of the constant iv infusion to equilibrium technique. B-hGH was infused for 3 h at a rate of 33 ng.kg-1.min-1 after which the disappearance from serum of GH was followed for 1 h. The mean +/- SEM values for MCR, t1/2 and DS were: 2.3 +/- 0.6 ml.kg-1.min-1, 21.1 +/- 1.7 min and 67.6 +/- 14.6 ml/kg, respectively. The disappearance of GH was monoexponential for the first 30 min, during which 75% of the GH had been cleared. The disappearance rate during the last 30 min of the observation period was somewhat lower, still approximately 90% of the GH had been eliminated after 60 min.
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PMID:The metabolic clearance rate, serum half-time and apparent distribution space of authentic biosynthetic human growth hormone in growth hormone-deficient patients. 291 43

Using a combination of polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate and immunoblotting with antihuman GH (anti-hGH) serum, we quantitatively and independently measured the major 22,000-dalton form of hGH (hGH22K) and the 20,000-dalton form (hGH20K). This technique was equally effective in assaying cell culture media or human sera. We studied isolated human pituitary cell cultures during a 16-day incubation period with and without stimulation by GH-releasing hormone (GHRH). Under basal conditions, the cells released 2.83 +/- 0.24 (+/- SEM) microgram hGH22K/ml . day and 0.67 +/- 0.17 microgram hGH20K/ml . day. GHRH (10(-8) M) treatment resulted in stimulation of both hGH22K and hGH20K by 24 h. We also measured both hGH22K and hGH20K in the sera of normal subjects before and after an iv bolus injection of 100 micrograms GHRH. hGH20K increased as did hGH22K. Peak concentrations of both variants occurred 45 min after GHRH administration. The results of this study indicate that the combination of sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting is an accurate and effective means of separately assaying hGH22K and hGH20K. We also demonstrated that primary monolayer cultures of human pituitary cells are an excellent model system for study of the secretion of these two hGH variants.
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PMID:Release of the 22,000- and the 20,000-dalton variants of growth hormone in vivo and in vitro by human anterior pituitary cells. 308 69

FSH bioactivity was measured by means of FSH-dependent aromatase activity (conversion of androgen substrate to estradiol). Assay sensitivity was optimized by the use of immature (7-10 days old) rats as Sertoli cell donors, serum-free medium for incubation, phosphodiesterase inhibitor (methylisobutylxanthinine), serial dilution of FSH in medium containing 1% BSA, delayed addition of FSH for 72 h after cell plating, and 19-hydroxyandrostenedione (2.5 X 10(-6) M) as the aromatizable androgen substrate. The method consisted of subjecting the decapsulated immature rat testes to a 2-step collagenase dispersion, plating the cells in medium [Dulbecco's Modified Eagle's Medium-Ham's F-10 (1:1)] containing growth factors and methylisobutylxanthinine for 72 h, adding increasing doses of FSH to the standard curve or small volumes of serum to the test vials as well as 19-hydroxyandrostenedione for 24 h, and measuring estradiol by RIA in dilutions of the medium. Using NIAMDD human (h) FSH-2 as the bioassay standard, the useful range of the assay was 0.01-5.0 ng/ml. Specificity was determined by the addition of graded doses of hLH, hTSH, ACTH, hGH, hPRL, and hCG. The minor degree of FSH bioactivity observed in a few hormone preparations was accounted for by the degree of FSH contamination in them. Mean intra- and interassay coefficients of variation were 9% and 11%, and the index of precision was 0.049. This bioassay was used to determine the bioactive FSH content of pituitary extracts, tissue culture media, elutions from columns, and isoelectrically focused samples. More importantly, small quantities of human sera gave responses parallel to the standard curve in a minimum of two dilutions. The bio- to immunoreactive ratios, expressed as the mean +/- SEM (NIAMDD-hFSH-2), were 0.66 +/- 0.2 in boys (n = 6), 0.78 +/- 0.2 in pubertal girls (n = 6), 1.18 +/- 0.2 in men (n = 13), 1.24 +/- 0.1 in postmenopausal women (n = 30), 1.94 +/- 0.3 in the follicular phase (n = 19), 6.2 +/- 1.4 in the ovulatory phase (n = 19), and 1.6 +/- 0.4 in the luteal phase (n = 19) of the normal menstrual cycle. These results indicate that the bio- to immunoreactive hFSH ratio in the circulation, is dependent upon the hormonal milieu of the subject.
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PMID:An improved in vitro bioassay for follicle-stimulating hormone (FSH): suitable for measurement of FSH in unextracted human serum. 311 17


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