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PubMed1987

Changing pituitary reactivity to follicle-stimulating hormone and luteinizing hormone-releasing hormone after induced ovulatory cycles and after anovulation in patients with polycystic ovarian disease.

Pituitary reactivity to GnRH, characteristic of polycystic ovarian disease (PCOD), has been attributed both to a primary ovarian cause and to hypothalamic-pituitary dysfunction. If the heightened pituitary reactivity characteristic of PCOD patients is secondary to chronic anovulation, ovulatory cycles should produce changes in the LH to FSH ratio and reduce the augmented response to GnRH. In a randomized cross-over study of 10 women with PCOD, GnRH (100 micrograms) was injected iv on the fifth day of 2 consecutive cycles, 1 of them following anovulation and progesterone withdrawal bleeding and the other following an induced ovulatory cycle. Mean basal plasma 17 beta-estradiol, progesterone, and FSH levels were similar after ovulatory and anovulatory cycles. However, mean basal serum testosterone (P less than 0.05) and LH (P less than 0.01) levels were significantly lower, as were LH levels 30, 60, and 90 min (P less than 0.01) and FSH levels 60 and 90 min (P less than 0.05) after GnRH injection, after an ovulatory cycle than after an anovulatory cycle. The pituitary response to GnRH in those PCOD patients, therefore, was more normal after an ovulatory cycle than after an anovulatory cycle. We conclude that the heightened pituitary reactivity characteristic of PCOD patients is associated with chronic anovulation.

Adult↗
PubMed1988

Maintenance of the ratio of bioactive to immunoreactive follicle-stimulating hormone in normal men during chronic luteinizing hormone-releasing hormone agonist administration.

Chronic administration of LHRH agonist analogs to humans reduces gonadal function through pituitary desensitization. Serum immunoreactive gonadotropin levels are modestly reduced, whereas serum bioactive LH levels are drastically suppressed. The effects on bioactive FSH levels, however, are not known. In this study, serum bioactive FSH was measured using an in vitro granulosa cell aromatase bioassay in four normal men given a LHRH agonist, [D-Trp6,Pro9-NEt]LHRH (LHRHA; 500 micrograms/day for 16 weeks), by sc infusion and testosterone enanthate (TE; 100 mg, im every 2 weeks) and in five men given 500 micrograms/day LHRHA by daily sc injection for 20 weeks and TE (100 mg every 2 weeks) from weeks 10 through 20. During the first study, serum immunoreactive FSH levels (IR-FSH) decreased by 56.5 +/- 4.8% (+/- SEM), and serum bioactive FSH (Bio-FSH) level decreased by 57.6 +/- 6.4%. The ratio of Bio-FSH to IR-FSH did not change. During the second study, both serum IR-FSH and Bio-FSH levels followed a triphasic pattern, decreasing slightly but not significantly immediately after initiation of LHRHA administration, progressively increasing to a peak (P less than 0.5 vs, baseline) at week 10, and then, after addition of TE to this regimen, decreasing slightly again. The Bio-FSH to IR-FSH ratio, as in the first study, did not change. When serum obtained at week 10 during the second study, just before initiation of TE, was chromatographed on a Sephadex G-100 column, IR-LH eluted in two distinct peaks, while IR-FSH eluted as a single peak. These results demonstrate that in normal men chronic LHRHA administration alone for up to 10 weeks or LHRHA plus TE for up to 16 weeks does not alter the qualitative characteristics of secreted FSH, since there was no dissociation between serum IR- and Bio-FSH levels.

Adult↗
PubMed1989

Specific, time-dependent actions of low-dose ethinyl estradiol administration on the episodic release of growth hormone, follicle-stimulating hormone, and luteinizing hormone in prepubertal girls with Turner's syndrome.

To investigate the actions of acute and chronic low doses of ethinyl estradiol (EE) on the pulsatile characteristics of GH and gonadotropin release we studied seven girls with Turner's syndrome [mean age, 7.5 +/- 0.75 (+/- SE) yr] on 3 separate study days. At baseline (study I), blood was drawn every 20 min from 2000-0800 h for GH, LH, and FSH determinations. One month after study I the patients were started on 100 ng/kg EE, orally, daily, and an identical study was repeated 1 week (study II) and 5 weeks (study III) from the initiation of low dose EE therapy. A pulse detection algorithm, Cluster, was used to objectively analyze pulsatility profiles. There were consistent and significant increases in all seven patients after 5 weeks of low dose EE therapy in mean GH concentrations (study I, 7.0 +/- 1.1 micrograms/L; study III, 13.4 +/- 1.7; P = 0.008), mean area under the GH pulse (study I, 602 +/- 52 micrograms/L.min; study III, 1350 +/- 261; P = 0.026), and mean GH pulse amplitude (study I, 14.0 +/- 2.2 micrograms/L; study III, 32.8 +/- 6.0; P = 0.018); with no detectable changes in GH pulse frequency (study I, 5.3 +/- 0.6 pulses/12 h; study III, 5.3 +/- 0.4). These findings were not accompanied by any significant changes in plasma somatomedin-C or serum estradiol concentrations or urinary cytological maturation indexes. Conversely, the amount of radioimmunoassayable FSH activity was suppressed after low dose EE therapy, with a decrease in mean FSH concentrations (study I, 23.5 +/- 6.6 IU/L; study III, 5.9 +/- 1.2; P = 0.035) and mean pulse amplitude (study I, 28.6 +/- 8.6 IU/L; study III, 8.2 +/- 1.8; P = 0.038), with no detectable changes in FSH pulse frequency (study I, 7.6 +/- 0.6 pulses/12 h; study III, 7.3 +/- 0.6). Similar qualitative changes in LH pulsatility were observed after low dose estradiol administration. In conclusion, our results demonstrate that low dose EE therapy results in a significant augmentation of pulsatile GH activity, with reciprocal decreases in gonadotropin concentrations in girls with Turner's syndrome. Such observations indicate an exquisite sensitivity of gonadotrope and somatotrope function to low dose estrogen action in this prepubertal hypogonadal model.

Adolescent↗
PubMed1990

Pyridostigmine blocks the inhibitory effect of glucocorticoids on growth hormone-releasing hormone stimulated growth hormone secretion in normal man.

Glucocorticoids have been shown to inhibit GH secretion in normal man when acutely and chronically administered in pharmacological amounts. Pyridostigmine (PD), an acetylcholinesterase inhibitor, is able to elicit GH secretion when administered alone and to enhance the GH response to GHRH in normal subjects probably via a decrease in the hypothalamic release of somatostatin. The aim of the present study was to investigate the influence of glucocorticoids on the GH response to PD administered either alone or in combination with GHRH in normal adult subjects. Six healthy adult volunteers underwent six experimental protocols. They received 1) human (h) GHRH(1-29)NH2, 100 micrograms injected as an iv bolus; 2) cortisone acetate, 50 mg administered orally (po) 60 min before an hGHRH iv bolus injection; 3) PD, 120 mg administered po, 60 min before an hGHRH iv bolus injection; 4) PD and cortisone acetate, administered po 60 min before an hGHRH iv bolus injection; 5) PD, administered po 60 min before a saline iv bolus injection; 6) PD and cortisone acetate administered po 60 min before a saline iv bolus injection. Mean GH levels, peak GH levels, and GH area under the curves (AUCs) were significantly lower after GHRH + cortisone as compared to GHRH alone. However, these parameters were not significantly different after PD + GHRH + cortisone when compared to PD + GHRH and after PD + cortisone when compared to PD alone. We conclude that acute administration of pharmacological amounts of glucocorticoids cannot inhibit the GH response to PD alone or in combination with GHRH. Thus, we hypothesize that the inhibitory action of glucocorticoids on the GH response to GHRH in man may be mediated by an enhancement of either somatostatin release by the hypothalamus or somatostatin action on the pituitary.

Adult↗
PubMed1990

Pulsatile growth hormone secretion in patients with acromegaly and normal men: the effects of growth hormone-releasing hormone infusion.

Twenty-four GH secretory patterns were studied before and during continuous infusions of GHRH in six patients with active acromegaly and in six normal adult men. GH release was episodic in both groups. Control subjects showed a normal diurnal variation in GH release, with the majority of GH released at night (2200-0800 h); mean levels were 1.5 +/- 0.4 (SE) ng/mL (day) and 4.2 +/- 0.8 ng/mL (night). Acromegalics had no diurnal variation in GH; levels were 45.3 +/- 13.7 ng/mL (day) and 39.8 +/- 12.2 ng/mL (night). Acromegalics demonstrated an increased frequency of GH pulses compared to normals (11.8 +/- 0.8 vs. 2.2 +/- 0.3/24 h). During continuous 24-h infusions of GHRH, the normal subjects continued to show a diurnal variation in GH release, but GH pulse frequency increased to a rate (11.7 +/- 1.4 pulses/24 h) very similar to that of the patients with acromegaly. In contrast, GHRH infusion did not alter the GH pulse frequency in the acromegalics. GHRH increased the mean levels of GH in both groups (patients 80.2 +/- 20.3 vs. 41.0 +/- 12.1 ng/mL, x +/- SE. P less than 0.05; controls 10.2 +/- 2.0 vs. 3.33 +/- 0.5 ng/mL, P less than 0.01). Some of the patients with acromegaly showed a progressive decline in GH levels during the infusion period, suggesting desensitization or exhaustion of releaseable stores; however, GH levels remained above basal values in all patients. After the 24-h GHRH infusions, the GH response to a bolus of GHRH was diminished in the normal subjects (2.1 +/- 0.9 vs. 16.8 +/- 5 ng/mL, x +/- SE; P less than 0.01) but not in the acromegalic patients (30.2 +/- 8.9 vs. 35.5 +/- 12.5 ng/mL; NS). These results indicate that GH release is episodic under basal conditions and during continuous GHRH infusion in both acromegalic and normal subjects, indicating the importance of other modulators of GH release, such as somatostatin, which may remain pulsatile even in acromegaly.

Acromegaly↗
PubMed1992

Differing responses of plasma bioactive and immunoreactive follicle-stimulating hormone and luteinizing hormone to gonadotropin-releasing hormone antagonist and agonist treatments in postmenopausal women.

Plasma bioactive (B) and immunoreactive (I) FSH and LH were measured every 10 min for 8 h in the same postmenopausal women in a three-phase study: 1) during normal pulsatile gonadotropin secretion (basal study; n = 8), 2) 8 h after a single injection of a GnRH antagonist (5 mg Nal-Glu, sc; n = 5), and 3) 21 days after a GnRH agonist injection (D-Trp6, 3.75 mg depot preparation, im; n = 7). I-FSH and I-LH were measured by monoclonal antibody immunoradiometric assays. B-FSH and B-LH were measured in selected samples with the immature rat granulosa cell and mouse interstitial cell assays, respectively. Significant pulsatility of B- and I-FSH and LH was demonstrated in the basal samples, but only the B/I ratio of LH was slightly elevated within the secretion peaks. After GnRH antagonist treatment, I-FSH decreased from a mean pretreatment level of 55.7 +/- 7.8 IU/L by 26% (P less than 0.001), and B-FSH from 313.8 +/- 61.9 IU/L by 44% (P less than 0.01). The B/I ratio decreased from 6.4 +/- 1.7 to 4.5 +/- 1.0 (P less than 0.05). After agonist treatment, the I- and B-FSH levels decreased by 92% and 83% (P less than 0.0001), respectively, but the B/I ratio increased to 17.3 +/- 4.7 (P less than 0.05). The concentrations of I- and B-LH decreased by 75% and 80%, respectively (P less than 0.001), after antagonist treatment. After agonist treatment, I-LH decreased by 92%, and B-LH by 93% (P less than 0.0001). No changes in the B/I ratios of LH were found after either treatment. In conclusion, no changes were found in the quality of circulating LH during the treatments, whereas the antagonist treatment decreased and the agonist treatment increased the B/I ratio of FSH. These findings provide further evidence that the qualitative responses of FSH and LH to treatment with the same GnRH analog are different, and that the suppressive mechanisms of GnRH antagonist and agonist action on gonadotropin secretion are different.

Adult↗
PubMed1994

Recombinant human follicle-stimulating hormone stimulates multiple follicular growth, but minimal estrogen production in gonadotropin-releasing hormone antagonist-treated monkeys: examining the role of luteinizing hormone in follicular development and steroidogenesis.

The two-cell theory predicts that follicular steroidogenesis requires the coordinate actions of both FSH and LH; however, the role of LH in follicular growth is less clear. The present study was designed to investigate the relative importance of LH and FSH in follicular growth and steroidogenesis. Cynomolgus monkeys were treated with a GnRH antagonist (antide; 3 mg/kg.day) for 20 days beginning in the midluteal phase of the menstrual cycle. After 10 days of antide administration, monkeys were injected with recombinant human FSH (rhFSH; 10 IU; n = 3), human menopausal gonadotropin (hMG; 10 IU; n = 3), or FSH plus 0.5 IU LH (n = 3) twice daily for 10 days. rhFSH stimulated multiple follicular development; however, peak serum estradiol levels were only 943 +/- 195 pmol/L. In contrast, monkeys treated with the same dose of hMG had significantly higher (P < 0.05) peak estradiol levels (6013 +/- 1322 pmol/L). The addition of 0.5 IU LH to the rhFSH treatment resulted in serum estradiol levels similar to those in monkeys treated with rhFSH only. Importantly, no differences in follicle number or size were evident among these treatment groups. Follicular fluid estradiol levels were consistent with serum levels (rhFSH, 187 +/- 11 nmol/L; hMG, 1531 +/- 173 nmol/L). Even larger proportional differences in follicular fluid androstenedione (rhFSH 13.6 +/- 1.4 nmol/L; hMG, 307 +/- 97.7 nmol/L) levels were found. The results in this LH-deficient primate model suggest that FSH alone is capable of stimulating ovarian follicular growth; however, the resulting follicles manifest minimal estradiol production, probably due to deficiencies in the LH-induced precursors to estradiol.

Androstenedione↗
PubMed1994

Reciprocal relationship between the level of circulating cortisol and growth hormone secretion in response to growth hormone-releasing hormone in man: studies in patients with adrenal insufficiency.

The aim of our study was to elucidate the relationship between the level of circulating cortisol and the GH responsiveness to GHRH in six hypoadrenal patients (one male and five females; age range, 35-67 yr; body mass index range, 18-31 kg/m2). Twenty-four hours after taking the last dose of replacement therapy, each patient underwent the following experimental trials on nonconsecutive days: 1) saline, and 2) 12.5 mg, or 3) 25 mg, or 4) 250 mg hydrocortisone hemisuccinate in 250 mL saline constant iv infusion from 0-180 min. On each occasion, 1 micrograms/kg human GHRH-(1-29)NH2 was injected as an iv bolus at 60 min. During GHRH and saline infusion, serum cortisol levels were always less than the detection limit of the assay (55 nmol/L). During 12.5-, 25-, and 250-mg hydrocortisone infusions (from 15-180 min), serum cortisol averaged 413.8 +/- 19.3, 772.5 +/- 46.9, and 1520.2 +/- 110.4 nmol/L, respectively. The GH peaks after GHRH treatment during the various infusions of hydrocortisone were compared to the GH peaks observed after saline, which were normalized to 100% in each subject. GH peaks after GHRH and 25 mg hydrocortisone (70 +/- 11%) and GHRH and 250 mg hydrocortisone (69 +/- 7%) were significantly (P < 0.05) lower than the GH peaks after GHRH and saline or GHRH and 12.5 mg hydrocortisone (83 +/- 15%). No significant differences were observed between the GH peaks after GHRH and 12.5 mg hydrocortisone or GHRH and saline. Our data demonstrate that in hypoadrenal patients, the acute absence of circulating cortisol does not impair the GH secretory response to GHRH with respect to the eucortisolemic state. Moreover, our data suggest that 700 nmol/L is the approximate threshold serum cortisol concentration above which a decrease in the GH responsiveness to GHRH is observed in humans. Further increases in serum cortisol levels above this threshold value do not cause a proportional decrease in the GH responsiveness to GHRH.

Addison Disease↗
PubMed1994

Arginine and growth hormone-releasing hormone restore the blunted growth hormone-releasing activity of hexarelin in elderly subjects.

Although both spontaneous and stimulated GH secretion undergo an age-related decline, the secretory capacity of somatotrope cells is preserved in human aging. In the present study we compared the GH responses to hexarelin, GHRH, and the combined administration of hexarelin and GHRH or arginine in young and elderly subjects. Thirteen young (24- to 30-yr-old) and 16 elderly (65- to 84-yr-old) normal males were divided into 2 groups. The first group (7 young and 8 elderly subjects) received the following as single iv injections during 3 different treatment sessions: hexarelin (2 micrograms/kg), GHRH (2 micrograms/kg), or hexarelin (2 micrograms/kg) plus GHRH (2 micrograms/kg). The second group (6 young and 8 elderly subjects) was administered single iv injections of hexarelin (2 micrograms/kg) or hexarelin (2 micrograms/kg) plus arginine (0.5 g/kg) during 2 different treatment sessions. In both groups basal IGF-I levels in the elderly were lower than those in young subjects (114.5 +/- 18.7 vs. 211.5 +/- 19.1 micrograms/L; P < 0.001). In the first group the GH response to hexarelin was greater in young compared to elderly subjects (area under the curve from 0-120 = 4849 +/- 601 vs. 2112 +/- 683 micrograms.min/L; P < 0.001). GHRH elicited a lower GH response than that induced by hexarelin in both young (1455 +/- 102 micrograms/h.L; P < 0.02) and elderly subjects (563 +/- 87 micrograms/min.L; P < 0.02). GHRH potentiated the somatotrope response to hexarelin in both young (7725 +/- 503 micrograms/min.L; P < 0.02) and elderly subjects (3895 +/- 612 micrograms/min.L; P < 0.02), but to a lesser extent in the latter (P < 0.001). In the second group, the GH response induced by hexarelin was also higher in young subjects than in elderly subjects (4819 +/- 668 vs. 1649 +/- 459 micrograms/min.L; P < 0.001). The GH response to hexarelin was potentiated by arginine in elderly (4139 +/- 1057 micrograms/min. L; P < 0.001), but not in young subjects (4743 +/- 774 micrograms/min.L). This study shows that the maximal effective dose of hexarelin releases more GH than the maximal effective dose of GHRH in both normal young and elderly subjects. The effect of hexarelin on GH secretion is age dependent, and the GH response to the combined administration of hexarelin and GHRH was significantly higher in young subjects compared to elderly subjects. Arginine does not potentiate the GH response to hexarelin in young subjects, whereas it significantly enhances it in elderly subjects.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1995

Melatonin enhances the luteinizing hormone and follicle-stimulating hormone responses to gonadotropin-releasing hormone in the follicular, but not in the luteal, menstrual phase.

Exogenous melatonin enhances LH pulse amplitude and mean LH levels in women during the follicular, but not the luteal, menstrual phase. In this study we investigated whether an increased pituitary response to GnRH is involved in the stimulatory effect of melatonin. Eight normal cycling women were studied on 2 consecutive days during the follicular stage (days 4-6), and eight were studied during the luteal phase (days 19-21) of the menstrual cycle. On 2 consecutive days, each women received, randomly and in a double blind fashion, placebo or 3 mg melatonin (1 mg at 0800, 1000, and 1200 h), whereas the pituitary LH and FSH responses to GnRH were tested by the iv administration of three submaximal doses of GnRH (1 microgram at 0900 h, 5 micrograms at 1100 h, and 10 micrograms at 1300 h). In the follicular phase, melatonin administration enhanced the LH and FSH responses to all three GnRH stimuli, whereas in the luteal phase, melatonin administration was ineffective. The present data indicate that an enhancing effect of melatonin on the LH and FSH responses to submaximal GnRH stimuli is evident in the follicular, but not the luteal, phase of the menstrual cycle and infer an endocrine window for the effect of melatonin on gonadotropin secretion.

Adult↗
PubMed2001

Aromatization mediates testosterone's short-term feedback restraint of 24-hour endogenously driven and acute exogenous gonadotropin-releasing hormone-stimulated luteinizing hormone and follicle-stimulating hormone secretion in young men.

The present clinical study examines the neuroregulatory hypothesis that feedback restraint of LH and FSH secretion by testosterone requires in vivo aromatization. To test this postulate, we prospectively and randomly assigned 47 healthy young men to 1 of 5 parallel short-term (5-day) double-blind interventions with: 1) placebo; 2) high-dose ketoconazole (KTCZ, 400 mg orally 4 times daily) to block both Leydig-cell and adrenal steroidogenesis; 3) KTCZ and transdermal testosterone delivery (7.5 mg daily); 4) KTCZ and transdermal estradiol (0.05 mg daily); or 5) KTCZ, testosterone, and the selective and potent aromatase inhibitor, anastrazole (5 mg orally twice daily). Blood was sampled every 10 min for 27 h on the last day of intervention to quantitate 24-h mean spontaneous and 3-h post-GnRH-stimulated (100 ng/kg iv bolus) LH and FSH release. KTCZ administration lowered the serum total testosterone concentration markedly from (mean +/- SEM) 423 +/- 57 ng/dL (15 +/- 2.0 nmo/L) during placebo ingestion to 58 +/- 8.6 ng/dL (2.0 +/- 0.3 nmol/L) (P < 10(-3)). Transdermal androgen addback along with KTCZ blockade increased testosterone levels to 607 +/- 57 ng/dL (21 +/- 2.0 nmol/L). KTCZ exposure alone drove a 3-fold increase in serum LH concentrations (P < 10(-3)) and a 2.5-fold rise in FSH secretion (P = 0.015), as assessed by high-specificity immunoradiometric assays. Concomitant transdermal testosterone (or estradiol) delivery repressed the elevated secretion of both LH and FSH to mid-normal baseline values. A 3-fold administration of anastrazole, KTCZ, and testosterone completely opposed exogenous testosterone's suppression of 24-h LH and FSH secretion. Anastrazole coadministration likewise abolished testosterone-dependent inhibition of 3-h GnRH-stimulated LH and FSH release. In summary, assuming the specificity of anastrazole's inhibition of aromatase activity, we conclude that circulating testosterone in healthy men curtails endogenously driven as well as exogenous GnRH-stimulated LH and FSH secretion conditional on its in vivo aromatization.

Administration, Cutaneous↗
PubMedDate not supplied

Long-term therapy with a single daily subcutaneous dose of growth hormone releasing hormone (1-29) in prepubertal growth hormone deficient children. Venezuelan Collaborative Study Group.

As part of a multicenter study to evaluate the efficacy and safety of one daily subcutaneous dose of 30 micrograms/kg of GHRH, 16 prepubertal GH-deficient children with a mean chronological age of 9.0 +/- 2.3 years were treated for 12 to 24 months. After six months of therapy 11 children (68.7%) were considered good responders in that their growth velocity increased by greater than 2 cm/yr over baseline and were continued on GHRH, while five subjects (31.3%) were regarded as poor responders and switched to recombinant hGH for the following six months. Growth velocity increased significantly in responders from a baseline of 3.4 +/- 0.7 cm/yr (mean +/- SD) to 6.8 +/- 0.1 cm/yr, 6.2 +/- 0.9 cm/yr, 6.6 +/- 1.0 cm/yr and 6.5 +/- 0.7 cm/yr at 6, 12, 18 and 24 months respectively. Bone ages advanced by an amount equivalent to the months of treatment. GHRH antibodies were detected in 4/11 and 6/11 responders at six and 12 months of treatment and in 2/5 non-responders at six months, but seemed not to interfere with growth. No side effects or changes in glucose and lipid levels were noted during therapy. These results suggest that GHRH (1-29) at the dose and schedule used is generally effective in the treatment of GH deficiency.

Body Height↗
PubMed1987

Sex difference in growth hormone response to growth hormone-releasing hormone between pubertal tall girls and boys.

In adult rats and also in young adults, a sex difference in GH responsiveness to GHRH has been reported with the higher responses in males. In young rats, however, the reverse has been found, i.e. a higher GH response in females than in males. This discrepancy promoted us to compare GH responsiveness to GHRH in midpubertal tall girls (N = 10) and boys (N = 8). An iv bolus administration of 100 micrograms of GHRH to these adolescents disclosed a sex difference in GH responsiveness. At all time intervals up to 30 min after the bolus, the GH responses to GHRH in the girls were significantly higher than in the boys (P less than 0.025 - P less than 0.05), whereas the peak GH increments (34 +/- 4 vs 19 +/- 3 micrograms/l; P less than 0.02) were about twice as high in the former as in the latter. The data suggest that like in rats, also in humans, sex-related changes in pituitary GH sensitivity to GHRH may be an important factor in the pubertal growth and development at least in tall girls and boys.

Adolescent↗
PubMed1988

Exaggerated growth hormone response to growth hormone-releasing hormone in type I diabetes mellitus.

Excessive GH response to various stimuli has been frequently described in diabetes mellitus. We studied the GH response to a synthetic GHRH in a group of 16 non-obese Type I diabetic patients. GHRH (1-44) given as iv bolus at a dose of 50 micrograms induced a markedly greater GH response in the diabetic than in the normal subjects with peak values of 39.5 and 14.7 micrograms/l, respectively, and the differences were significant from 15 to 60 min. Peak GH level was 44.6 micrograms/l in diabetic patients without retinopathy and 34.2 micrograms/l in patients with retinopathy, but the difference was not significant. Peak GH levels did not correlate with metabolic control of disease estimated by basal glucose and HbA1 levels nor with age, weight of the patients, and duration of the disease. It is concluded that Type I diabetic patients show an exaggerated GH response to GHRH and this response does not correlate with the metabolic control of diabetes.

Adult↗
PubMed1989

Pyridostigmine counteracts the blunted growth hormone response to growth hormone-releasing hormone of obese children.

We have evaluated the effect of acute administration of pyridostigmine bromide, a cholinesterase inhibitor, on the GHRH-induced GH rise in 11 obese children and in 8 age-matched controls. The GH response to GHRH (hpGRF 1-40, 1 microgram/kg iv), evaluated both as maximum GH peak and as integrated area under the curve, was significantly lower in the obese children than in the controls. Pretreatment with pyridostigmine bromide (60 mg orally 60 min before the GHRH injection) significantly increased both baseline GH levels and the GH response to GHRH in all the obese subjects, so that their mean baseline GH, peak GH levels and integrated area under the curve after pyridostigmine bromide plus GHRH were similar to those of the control children after GHRH. Also in control children pyridostigmine bromide increased (though not significantly) baseline GH levels. and caused a significant augmentation of the GH response to GHRH. Mean peak GH levels and mean integrated area under the curve after pyridostigmine bromide plus GHRH were significantly higher in the controls than in the obese children given the same treatment. Mean baseline Sm-C levels were significantly higher in the obese than in control children. These data show that enhancement of cholinergic neurotransmission, likely in the hypothalamus, counteracts the blunted GH response to GHRH present in the obese children, and that in simple obesity the potential of the pituitary to make a secretory response to a direct GH secretagogue is preserved.

Adolescent↗