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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Following a standard mixed meal, plasma concentrations of growth hormone releasing hormone (GHRH), somatostatin (SMS) and growth hormone (GH) were measured every 30 min for 300 min in six young adults with type I insulin-dependent diabetes mellitus (IDDM) and five normal controls. Mean blood glucose concentrations were higher and mean free insulin levels lower in the diabetics compared with controls both in fasting specimens and at all times following the mixed meal. Basal concentrations (mean +/- SEM) of GHRH were similar in diabetic (12.7 +/- 1.8 pg/ml) and control subjects (11.8 +/- 1.1 pg/ml). Following ingestion of the mixed meal, a rise in GHRH was observed in the control subjects maximal between 30 and 240 min (P less than 0.025) but the response was blunted in the diabetics. Mean GHRH concentrations were greater in the controls than in the diabetic subjects at all stages during the test, the maximum difference being noted at 120 mins (P less than 0.04). Basal SMS concentrations and those observed after the mixed meal were similar in diabetic and control subjects. These results indicate that glucose and insulin may play a role in the regulation of GHRH release following a mixed meal but circulating levels of GHRH and SMS are unlikely to be relevant to the abnormal regulation of GH in IDDM.
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PMID:The growth hormone releasing hormone (GHRH) response to a mixed meal is blunted in young adults with insulin-dependent diabetes mellitus whereas the somatostatin response is normal. 197 74

We have studied the serum growth hormone (GH) response to two consecutive doses of growth hormone releasing hormone (GHRH) (50, 100, 200 micrograms) given 1, 2 or 3 h apart in seven adult males. The serum GH profile was analysed by deconvulution incorporating a variable half-life for GH. All three doses of GHRH stimulated maximal GH secretion: 50 micrograms, 146.0 mU/min (SEM 24.0); 100 micrograms, 128.1 mU/min (SEM 14.3); 200 micrograms, 134.1 mU/min (SEM 20.5) (one-way ANOVA, P = NS). The magnitude of the second secretory burst after the second dose of GHRH was less than that induced by the first injection of GHRH, particularly when doses of 200 micrograms were used. Factors influencing the response to the second dose were the GH secretory status at the point that the stimulus was applied and the time interval between administration of the first and second doses. These studies demonstrate that the pituitary gland is capable of responding to two consecutive doses of GHRH although the second response is always less than the first. The data demonstrate the importance of using methods of assessing GH secretion and not relying simply on measured serum GH concentration values.
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PMID:The pituitary gland is capable of responding to two successive doses of growth hormone releasing hormone (GHRH) 193 35

On forty-six fasting and resting children, aged 5-17 years, with short stature (below -2 SD) a growth hormone releasing hormone (GH-RH) stimulation test (2 micrograms/kg iv bolus, Sanofi) was performed. Twenty-two children were prepubertal, of which, 13 had a constitutional short stature (CSS), nine an idiopathic growth hormone deficiency (IGHD). Twenty-four subjects were pubertal, at the stage II or III of Tanner. Among them, six had a constitutional short stature (CSS) and 18 an idiopathic delayed puberty (IDP). Blood samples were taken for determination of plasma somatostatin-like immunoreactivity (SLI) in chilled test tubes containing EDTA + aprotinin. Plasma SLI levels were measured after extraction and concentration on C18 Sep Pack columns by radioimmunoassay using an antibody against 1-14 somatostatin. The sensitivity of this assay is around 3 pg/ml. After GH-RH stimulation the peak of GH (mean +/- SEM) was in prepubertal subjects: 25.3 +/- 9.1 micrograms/l in CSS, and 18.6 +/- 10.3 micrograms/l in IGHD. In pubertal subjects GH peaks were 17.6 +/- 8.4 micrograms/l in CSS and 15.6 +/- 3.8 micrograms/l in children with IDP. No significant differences was found between basal plasma SLI levels in the four groups of subjects, being respectively (mean +/- SEM) 11.9 +/- 1.8 pg/ml in prepubertal subjects with CSS, 9.6 +/- 2.6 pg/ml in IGHD, 7.6 +/- 1.7 pg/ml in pubertal children with CSS and 6.6 +/- 1.5 pg/ml in children with IDP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Negative correlation between peripheral plasma somatostatin levels and GH responses to GH-RH stimulation tests in children. 287 69

The adult testis is a source of hypothalamic neuropeptides including TRH, GnRH, POMC and CRF. The role of these neuropeptides as paracrine regulators of gonadal function in the testis remains unknown. We postulated that growth hormone releasing hormone (GHRH) might also be measureable in rat testis. Testes from ten post pubertal rats (400-425g, approximately 90d) were extracted and assayed in an enzyme linked immunosorbent assay (ELISA) which utilized an anti-rat GHRH antiserum and had a sensitivity of 30 pg. We detected 1.62 +/- 0.17 (M +/- SEM) ng of GHRH-like substance per g testis. The GHRH content of hypothalamus from these animals was 2.70 +/- 0.24 ng/g (N = 7.6 hypothalami/N). Fat served as a negative control tissue in which no GHRH-like material was detectable. To confirm the finding and in attempt to determine if it represented local production of GHRH, we measured GHRH mRNA using a cRNA probe subcloned from a cDNA for rat GHRH. Abundant levels of hybridizing RNA were found in mature testis by dot-blot hybridization (319% +/- 30% of the mean hypothalamus value). Northern analysis revealed that the rat hypothalamic GHRH mRNA was 715 nucleotides. In contrast, testicular GHRH(-like) mRNA was 1750 nucleotides. We conclude that there are high levels of a GHRH-like substance in mature rat testis which is present both at the level of protein product and gene transcript. The mRNA for this GHRH-like substance is substantially larger than the GHRH transcript from hypothalamus.
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PMID:Identification of a rat GHRH-like substance and its messenger RNA in rat testis. 313 3

It is well established that the central alpha 2-adrenergic agonist clonidine can enhance growth hormone (GH) secretion in humans. This effect is most likely due to stimulation of hypothalamic growth hormone releasing hormone (GHRH) release. To determine the potency of the new I1-imidazoline receptor agonist moxonidine to release pituitary hormones, 12 normal volunteers received clonidine (0.3 mg), moxonidine (0.3 mg), or placebo orally according to a randomized, double-blind protocol. Blood was drawn prior and up to 180 min after drug administration for determination of GH, adrenocorticotropic hormone (ACTH), prolactin, thyrotropin (TSH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), glucose, clonidine, and moxonidine concentrations. The results were compared to those obtained in a standard GHRH stimulation test (1 microgram/kg i.v.). Serum GH levels increased significantly in response to GHRH, clonidine, and moxonidine. However, the increase was less pronounced in response to clonidine and moxonidine as compared to GHRH (mean +/- SEM): after clonidine, GH increased from 0.2 +/- 0.1 to 5.4 +/- 1.5 ng/ml, p < 0.05; moxonidine increased GH levels from 0.1 +/- 0.04 to 4.8 +/- 1.9 ng/ml (p < 0.05); GHRH caused an increase from 0.01 +/- 0.05 to 14.8 +/- 2.5 ng/ml (p < 0.05). No significant change was observed in the concentration of any other pituitary hormone. We conclude that the new I1-imidazoline receptor agonist moxonidine stimulates GH release to a similar extent as clonidine.
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PMID:Growth hormone secretion in response to the new centrally acting antihypertensive agent moxonidine in normal human subjects: comparison to clonidine and GHRH. 758 24

Ghrelin activates the somatotropic and the hypothalamic-pituitary-adrenal axes, being crucially involved in sleep regulation. Simplified, growth hormone releasing hormone (GHRH) increases slow-wave sleep and REM sleep in males, whilst corticotropin-releasing hormone (CRH) increases wakefulness and decreases REM sleep. Ghrelin's role in sleep regulation and particularly its interactions with GHRH and CRH are not entirely clear. We aimed to elucidate the interactions between ghrelin, GHRH and CRH in sleep regulation and the secretion of cortisol and GH. Nocturnal GH and cortisol secretion and polysomnographies were determined in 10 healthy males (25.7+/-3.0 years) four times, receiving placebo (A), ghrelin (B), ghrelin and GHRH (C), or ghrelin and CRH (D) at 22:00, 23:00, 00:00, and 01:00h, in this single-blind, randomized, cross-over study. Non-REM sleep was significantly (p<0.05) increased in all verum conditions (mean+/-SEM: B: 355.3+/-7.4; C: 365.4+/-8.1; D: 371.4+/-3.9min) compared to placebo (336.3+/-6.8min). REM sleep was decreased (B: 84.3+/-4.2 [p<0.1]; C: 74.2+/-7.0 [p<0.05]; D: 80.4+/-2.7min [p<0.05]) compared to placebo (100.9+/-8.3). CRH+ghrelin decreased the time spent awake and enhanced the sleep efficiency; furthermore, the REM latency was decreased compared to the other treatment conditions. CRH enhanced the ghrelin-induced cortisol secretion but had no relevant effect on GH secretion. In turn, GHRH enhanced the ghrelin-induced GH secretion but had no effect on cortisol secretion. In conclusion, ghrelin exhibited distinct sleep effects, which tended to be enhanced by both GHRH and CRH. CRH had sleep-improving and REM permissive effects when co-administered with ghrelin, being in contrast to the effect of CRH alone in previous studies.
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PMID:Ghrelin alone or co-administered with GHRH or CRH increases non-REM sleep and decreases REM sleep in young males. 1832 18