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PubMed1977

Collaborative study of the effects of human growth hormone in growth hormone deficiency: IV. Treatment with low doses of human growth hormone based on body weight.

In order to define the minimum effective dose of human growth hormone (GH) in growth hormone deficient children, GH was administered to three groups of patients based on their body weight. Five children who received 0.01 International Unit (IU) GH/kg three times a week (tiw) failed to respond with a significant increase in their rate of growth. A dose of 0.03 IU GH/kg tiw increased the growth rate of 12 patients from 3.5 +/- 0.4 (SE) cm/year to 6.4 +/- 0.4 (SE) cm/year (P less than 0.001) during the first 12 months of therapy. Eight children (67%) larger than or equal to 6.0 cm/year. A similar increase growth rate from 3.6 +/- 0.4 (SE) cm/year to 7.3 +/- 0.4 (SE) cm/year (P less than 0.001) was observed over the first 12 months of therapy in 16 growth hormone deficient children who were given 0.06 IU GH/kg tiw. Thirteen children (81%) grew larger than or equal to 6.0 cm/year. During a second year of treatment, children receiving either 0.03 or 0.06 UI GH/kg tiw again showed a significant increase in their rate of growth. However, the response was significantly less than that observed during the first year of treatment. Comparison of these results with those available in the literature suggests that the most efficient, although not necessarily the optimal, initial dose of GH in children with growth hormone deficiency is 0.06 IU GH/kg administered three times a week.

Adolescent↗
PubMed1989

Conserved and unique amino acid residues in the domains of the growth hormones. Flounder growth hormone deduced from the cDNA sequence has the minimal size in the growth hormone prolactin gene family.

Growth hormone (GH), prolactin (PRL), and placental lactogen (PL) constitute a protein family whose genes are considered to have evolved from a common ancestral gene. GHs isolated from various vertebrate species are known to possess highly conserved structural and functional features. In the present study we have cloned and sequenced flounder growth hormone (fGH) cDNA to predict the primary structure of the hormone. The preprotein of fGH is composed of 190 amino acids, and mature fGH is found to be extraordinarily small, having 171 or 173 amino acid residues. The estimated molecular masses of mature fGH are 19.4 to 19.7 kDa. This minimal size of fGH enabled an extended analysis of the essential domains and of amino acid residues required in hormone-specific activities. fGH conserves and shares 37 residues with 20 other vertebrate GHs. These common residues are seen to cluster in five distinct domains (GD1 to GD5). In human PL (hPL), which has low growth-promoting activity, 35 of these 37 residues are conserved, while the other 2 residues in the GD1 domain (Arg-16 and Leu-20) are replaced by Gln and Ala, respectively. In a less active variant of human GH, hGH-V, only 1 residue (His-21) of the 37 residues is replaced by Tyr. Besides these 3 residues, 6 other residues unique to the GHs and some PLs, that is, Ala-24 (GD1), Ser-54 (GD2), Ser-78 (GD3), Leu-106, Leu-116, and Asp-122 (GD4), appear to be important for specific binding of the GHs. The GD5 domain, at the carboxyl-terminal ends of the GHs is considered to be involved mainly in the formation and stabilization of GH molecules.

Amino Acid Sequence↗
PubMedDate not supplied

[Genetic engineering of peptide hormones. III. Cloning of the swine growth hormone cDNA and construction of the gene for expression of the hormone in bacteria].

The clones containing cDNA of porcine growth hormone were obtained using poly(A)-RNA from porcine pituitary as a template for reverse transcriptase. The analysis of their nucleotide sequences revealed that these cDNAs have differences not only on the nucleotide level but also on the amino acid level, i. e. the polymorphism of mRNA and protein occurs in the case of porcine growth hormone. To create the construction for expression of porcine growth hormone in E. coli, the 5'-part of cDNA, coding the first 15 amino acids of the mature hormone, was substituted by the artificial sequence.

Amino Acid Sequence↗
PubMed1996

[Growth hormone therapy in childhood. Growth hormone therapy in small children without growth hormone deficiency].

The availability of unlimited amounts of recombinant human growth hormone (rhGH) has now made it possible to investigate its growth-promoting effect in children in whom growth hormone production is not deficient. In girls suffering from the Ullrich Turner syndrome, treatment with rhGH increases final height by some 6 to 8 cm. An increase in growth rate has also been observed in children with renal insufficiency, and in children with intrauterine growth retardation. Favourable results have also been reported in children receiving glucocorticoids for such chronic conditions as rheumatoid arthritis, and in youngsters with hypochondroplasia. In a further group of children with various disorders an improvement in the growth rate has been observed, although nothing can yet be said about the outcome in terms of final height. To achieve an increase in growth rate, pharmacological doses of growth hormone higher than those used in children with growth hormone deficiency are necessary. For this reason, the risk of unwanted side effects might be higher than in the latter.

Adolescent↗
PubMed1976

Studies on the disulfide bonds of glycoprotein hormones. Course of reduction of bovine luteinizing hormone, bovine thyroid-stimulating hormone, and their subunits.

The five disulfide bonds of isolated alpha subunits of luteinizing hormone (LH) and thyroid-stimulating hormone (TSH) are completely reduced at pH 8.5 in 15 min with no denaturant required and with only a slight excess of reducing agent. At pH 7.0, reduction is complete after 6 to 10 h. These results together with an earlier study concerning the positions of the two most readily reduced bonds (Cornell J.S., and Pierce, J.G. (1974) J. Biol. Chem. 249, 4166-4174) show that, in the isolated alpha subunit, all disulfides are readily accessible, although it is possible that a change in conformation, after rapid initial reduction of two disulfides, makes the remaining three more susceptible to reduction. No partially reduced and S-carboxymethylated intermediates were found at pH 7.0 other than those seen at pH 8.5, nor were additional intermediates found at pH 8.5 when reduction was initiated in the presence of alkylating agent. In contrast, reduction of the beta, hormone-specific, subunits of LH and TSH, while complete at pH 8.5 after 2 to 6 h, does not proceed to completion at pH 7.0 even after 24 h or upon addition of 6 M urea or large concentrations of reducing agent, and partially reduced intermediates useful in location of disulfide bridges can be trapped (e.g. Reeve, J.R., Cheng, K.-W., and Pierce, J.G. (1975) Biochem. Biophys. Res. Commun. 67, 149-155). Little or no reduction of the intact hormones is found at pH 7.0 in the absence of denaturing agents. This protection by the intact structure shows that the two most readily reduced disulfides of the alpha subunit and the single most readily reduced sidulfide of the beta subunits are either in regions of subunit-subunit contact or that these bonds become more reactive in the isolated subunits because of different influences by neighboring groups. At pH 8.5, intact LH is completely reduced after 6 h, but intact TSH is more resistant to reduction, which may reflect a higher affinity between subunits than exists in LH.

Animals↗
PubMed1978

Hormonal control of implantation in the rat: inhibition by luteinizing hormone-releasing hormone and its analogues.

Chronic treatment of pregnant rats with luteinizing hormone-releasing hormone (LH-RH) and its analogues (Analogue I: des-Gly10-LH-RH-ethylamide; Analogue II: des-Gly10-[D-Ala6]-LH-RH-ethylamide) inhibited implantation of the ovum. Analogues I and II were 4.5 and 173 times potent than native LH-RH in inhibiting implantation respectively. On Day 8 of the treatment with Analogue II, the pituitary glands of the pregnant rats contained approximately 10% of the amount of LH and FSH found in intact pregnant rats. By contrast, serum levels of LH were significantly higher and those of FSH significantly lower in Analogue II-treated rats than in control rats. The ovaries of Analogue II-treated rats were lighter than those of control rats because of smaller corporalutea and less developed follicles. Peripheral serum concentrations of progesterone in rats treated with LH-RH and its analogues were significantly lower than those in control rats. The peripheral serum concentration of progesterone declined earlier in rats treated with LH-RH and Analogue I than it did in rats treated with Analogue II. The inhibitory affect of Analogue II was overcome by concurrent treatment with the following combinations of hormones: progesterone + oestradiol; progesterone + human chorionic gonadotropin (hCG); prolactin + oestradiol; and prolactin + hCG. Treatment with progesterone or prolactin alone did not overcome the effect of Analogue II. These results indicate that Analogue II stimulates the production and release of LH and release of FSH to cause high ratios of LH/prolactin and LH/FSH. The induced imbalance of gonadotropins suppresses the development of ovarian follicles and corpora lutea and reduces secretion of both oestrogen and progesterone. The resulting low levels of ovarian steroids cause a delay in implantation.

Animals↗
PubMed1991

Immunocytochemical localization of growth hormone and growth hormone-releasing hormone immunoreactivity in the brain and pituitary of the little brown bat.

Anterior pituitary cells exhibiting growth hormone (GH) immunoreactivity and forebrain neurons containing growth hormone-releasing hormone (GHRH) immunoreactivity were identified in little brown bats (Myotis lucifugus) using light microscopic immunocytochemistry. Pituitary somatotropes appeared as ovoid or polyhedral cells that were distributed throughout most of the pars distalis, with the exception of its most rostral region where this cell type was scarce. GH-immunoreactive cells occupied approximately one-third of the total volume of the pars distalis; this proportion did not differ significantly between males and females or in bats collected at different times of year. Neuronal perikarya containing immunoreactive GHRH were observed in the hypothalamic arcuate and suprachiasmatic nuclei, as well as in the cortical and subcortical telencephalon. Fibers were most evident in the median eminence, paraventricular and periventricular nuclei, and molecular layer of the cerebral cortex. Fine fibers were also accumulated in the bed nucleus of the stria terminalis and in the amygdala.

Animals↗
PubMedDate not supplied

Potential therapeutic indications for growth hormone and growth hormone-releasing hormone in conditions other than growth retardation.

Growth hormone (GH) previously was available in limited supply and only for the treatment of GH-deficient children. The recent production of GH by recombinant DNA technology has provided a potential surfeit of this hormone and raises the possibility of its use in other conditions. In addition, the isolation, characterization, and synthesis of GH-releasing hormone (GRH) provides an opportunity to use this peptide in conditions in which increased circulating levels of GH are desired. Both GH and GRH have potential therapeutic uses in conditions other than growth retardation.

Aging↗
PubMed1991

Biological activity of luteinizing hormone in uraemic children: spontaneous nocturnal secretion and changes after administration of exogenous pulsatile luteinizing hormone-releasing hormone--preliminary observations.

Normal pubertal progression is associated with quantitative and qualitative changes in gonadotrophin release. Uraemic children show a delayed or disturbed puberty. We have therefore examined nocturnal gonadotrophin and sex steroid secretion in seven males and three females [age 11-15 years, pubertal stage (PS) 1-3] with chronic renal failure on conservative treatment. In addition to immunoreactive luteinizing hormone (i-LH) we have measured the biological activity of LH (b-LH). Nine children aged 12-17 years with PS 1-3 and normal renal function served as a control group. In two uraemic children, i-LH, b-LH, follicle stimulating hormone and sex steroids were evaluated before and 7 days after pulsatile LH-releasing hormone (LHRH) administration (150 ng/kg body weight subcutaneously every 120 min). Mean i-LH levels were higher in uraemic children than in controls. An increase in i-LH during sleep was found in all controls and in eight of ten uraemic subjects. Mean b-LH levels were lower during sleep and the b/i LH ratio was reduced in uraemic children with PS 2-3 whether asleep or awake compared with controls. Pulsatile administration of LHRH provoked a rise of i-LH and b-LH levels with an increased b/i LH ratio, suggesting an intact pituitary responsiveness. These preliminary data indicate that the gonadotrophin control of LH is abnormal in uraemic children, and that biopotency of LH secretion might be improved after short-term pulsatile LHRH administration.

Adolescent↗
PubMed1990

The growth hormone response to growth hormone releasing hormone in patients previously treated with bilateral adrenalectomy alone for Cushing's disease.

Human growth hormone releasing hormone (GHRH) fails to stimulate human growth hormone (GH) in hypercortisolism. In order to study whether the responsiveness to GHRH stimulation returns after cure of the hypercortisolism, the GH response to GHRH was examined in 8 patients at least 5 yr after they had undergone bilateral adrenalectomy as their sole treatment for Cushing's disease. None had current evidence of a pituitary macroadenoma. A group of 8 healthy subjects matched for age and sex formed the control group. All patients and subjects received an iv injection of GHRH 1 microgram/kg, after an overnight fast, blood samples were taken before and at 15, 30, 45, 60, 90 and 120 min. There was no statistical difference between the peak GH or area under curve (AUC) response (median, range) in the two groups studied (adrenalectomized peak GH 9.2 (4.6-32.0) vs 16.5 (7.5-63) mU/l, adrenalectomized AUC response 647.5 (344.2-1489.5) vs 1103.5 (339.7-5188.5) mU/l. Patients with Cushing's disease once cured of hypercortisolism, have a GH response to GHRH.

Adrenalectomy↗
PubMed1991

Effect of gestational mastectomy on postpartum gonadotropin releasing hormone and thyrotropin releasing hormone-induced luteinizing hormone and prolactin response in first lactation Holstein cattle.

First lactation Holstein cows were divided into two treatment groups to evaluate thyrotropin releasing hormone (TRH, 0.25 microgram/kg body weight) and gonadotropin releasing hormone (GnRH; 200 micrograms) induced secretion of prolactin (PRL) and luteinizing hormone (LH) on days 7 and 16 postpartum. Disregarding treatment, LH response was greater (p less than 0.01) on day 16 than day 7 postpartum (7.5 +/- 0.3 ng/ml on day 7 vs 10.2 +/- 0.3 ng/ml serum on day 16). Mastectomized cattle had similar time for initiation of LH increase, but peak concentrations were achieved later. Peak PRL concentrations were reached 12 to 15 min after injection and returned to baseline within 2.5 h in both groups. However, intact cows had higher (p less than 0.01) mean serum PRL than the mastectomized cows for 1 h following injection. Peak PRL concentration was 83.3 +/- 17.6 ng/ml for mastectomized cows vs 128.0 +/- 24.7 ng/ml for intact cows. It appears that udder removal allows for greater pituitary responsiveness to GnRH but diminishes PRL response to TRH suggesting the mammary gland differentially affects pituitary secretion of LH and PRL.

Animals↗
PubMedDate not supplied

Intrasubject reproducibility of growth hormone-releasing hormone-stimulated growth hormone in older women, older men, and younger men.

Intrasubject reproducibility of growth hormone (GH) response to growth hormone-releasing hormone (GHRH) was studied in healthy older women (n = 9), older men (n = 8), and younger men (n = 10). Subjects received IV injections of 0.1 ml/kg saline, 1 micrograms/kg GHRH, and 2 micrograms/kg GHRH, three times each, and blood was sampled at 0, 15, 30, 45, 60, and 120 min for GH concentration. There was no significant difference in peak GH response between the 1- and 2-micrograms/kg GHRH dosages. GH responsiveness, group variance of peak GH, and intrasubject variability were greatest for younger men, less for older men, and least for older women at both dosages of GHRH. Because of the large intrasubject variability observed in this study, it appears necessary to test subjects more than once to obtain a valid characterization of GH responsiveness.

Adult↗
PubMed1994

Growth hormone response to growth hormone releasing hormone and to clonidine stimulation in peripubertal patients with major depressive disorder.

The responses of growth hormone (GH) to administration of growth hormone-releasing hormone (GHRH-1 micrograms/kg b.w.) and of clonidine (clon-2.5 micrograms/kg b.w.) and basal levels of somatomedin C (SmC) were measured in nine peripubertal patients with Major Depressive Disorder (MDD) and in 9 age- and gender-matched controls. Basal GH and SmC levels, and GH response to GHRH did not differ in patients and controls, whereas responses to clonidine were significantly higher in some and lower in other patients than in controls.

Adolescent↗
PubMed1985

The influence of thyrotropin releasing hormone on in vivo prolactin release and in vitro prolactin, luteinizing hormone, and growth hormone release from dispersed pituitary cells of the young turkey (Meleagris gallopavo).

Intravenous administration of 0.025, 0.25, or 2.5 micrograms/kg thyrotropin releasing hormone (TRH) to 4-week-old female turkeys induced a dose-dependent increase (P = 0.004) in serum prolactin (PRL) 15 min post-treatment. Dispersed anterior pituitary cell cultures were utilized to determine the effect of TRH on cellular release of PRL, luteinizing hormone (LH), and growth hormone (GH). In the first experiment, cells from 13-week-old male turkeys were initially incubated for 24 hr in Medium 199 (M-199) plus 10% turkey serum and then placed in M-199 plus 10(-10) to 10(-4) M TRH for 5 hr. Incubation with TRH produced no change in PRL release from that of spontaneous release (P = 0.854). However, 10(-5) and 10(-4) M TRH induced LH release (P less than 0.0001). The TRH-induced GH response was parabolic (P less than 0.0001), with the maximal release at 10(-8) M. The second experiment, utilizing pituitary cells from 7-week-old females, studied these responses on 3, 5, and 7 days of monolayer incubation. TRH failed to induce a PRL release in all tests (P greater than 0.162), although hypothalamic extract induced a large release (P less than 0.0001) of PRL each time. Both 10(-6) and 10(-4) M TRH induced a LH release on Day 3 while only 10(-4) M did so on Day 5, and none of the doses elicited a release on Day 7. The parabolic GH response generally persisted in all tests.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Pharmacokinetics of growth hormone secretion in humans induced by growth hormone releasing hormone.

This investigation compares the age- and sex-related changes in growth hormone (GH) response to growth hormone releasing hormone (GHRH) in normal subjects using an appropriate pharmacokinetic model. Twenty-five subjects (14 males and 11 females) aged 23-89 yr received a single intravenous bolus dose (1 microgram/kg) of GHRH-40 solution. Plasma GH concentration-time profiles are best characterized by a biexponential equation (or one-compartment model) with first-order release and disappearance rates and an equilibration lag time. The harmonic mean release rate half-life is similar for both sexes (males: 12.6 min vs. females; 11.4 min) but significantly different across age groups (23-35 yr: 7.2 min vs. 50-89 yr: 16.8 min). The mean disappearance rate half-life and GHRH-equilibration time lag for females (33.6 and 20.4 min, respectively) and the higher age group subjects (32.4 and 21.6 min, respectively) are significantly longer than those of males (22.8 and 9 min, respectively) and the lower age-group subjects (21.6 and 8.4 min, respectively). The mean metabolic clearance rate of GH is significantly lower (p less than 0.02) for females than for males (3.1 vs. 4.83 ml/hr.m2). However, the production rate and the amount of GH released by the pituitary for our subjects appear to be very similar for both males (8.7 micrograms/hr.m2 and 4.65 micrograms/m2) and females (9.33 micrograms/hr.m2 and 5.11 micrograms/m2).

Adult↗
PubMed1995

Growth hormone secretion and activation of cyclic AMP by growth hormone releasing hormone and gamma-aminobutyric acid in the neonatal rat pituitary.

The effect of factors influencing pituitary growth hormone secretion may be mediated by a combination of several intracellular mechanisms. The involvement of cyclic AMP (cAMP) in the GH stimulatory effect of tau-aminobutyric acid (GABA) and of growth hormone releasing hormone (GHRH) was studied in neonatal rat pituitaries. In the pituitaries of the newborn rats GH secretion was stimulated by forskolin and by isobutylmethylxantine (IBMX). GHRH but not GABA elevated pituitary cAMP concentration, whereas both drugs increased GH secretion from 2-day old pituitaries. IBMX did not augment the cAMP stimulating effect of GHRH in 2-day old, but potentiated it in older (7, 14 and 21-day old) pituitaries. The results indicate the presence of a functioning, but relatively immature intracellular signal transmission system in the 2-day old rat pituitary.

1-Methyl-3-isobutylxanthine↗
PubMed1987

Selective beta 1-adrenergic receptor-blockade with atenolol enhances growth hormone releasing hormone and mediated growth hormone release in man.

The growth hormone (GH) responses to a single bolus injection of the growth hormone releasing hormone (GRH) were examined in the basal state and in the presence of beta-adrenergic receptor blocking agents of different specificity in ten normal men. During a constant five-hour infusion of 56 micrograms/min of propranolol (nonselective beta-adrenergic receptor-blocker) in seven subjects studied, there was a significant augmentation of the GH release in response to exogenous GRH compared to the GH response during saline infusion, as measured by the peak serum GH concentrations after GRH (P = 0.019) and the integrated GH values (P = 0.019). A similar significant enhancement of GH responses to exogenous GRH as compared to the control day was observed with the specific beta 1-adrenergic receptor-blocker atenolol in all seven subjects studied (four of whom also participated in the propranolol study). Both the peak GH response to a GRH bolus and the integrated GH values were significantly greater with atenolol (P = 0.019 for both). There was no difference in serum GH concentrations after beta-adrenergic receptor-blocking drugs during a three-hour sampling period before GRH administration compared to placebo. Our results support the concept that beta-adrenergic receptors may modulate either the release or action of hypothalamic somatostatin in the control of GH secretion in man. We suggest the effect is mediated by specific beta 1-adrenergic receptors.

Adrenergic beta-Antagonists↗