scholarly journals Differential pulsatile secretagogue control of GH secretion in healthy men

2013 ◽  
Vol 304 (9) ◽  
pp. R712-R719 ◽  
Author(s):  
Catalina Norman ◽  
John Miles ◽  
Cyril Y. Bowers ◽  
Johannes D. Veldhuis
Keyword(s):  
Body Mass Index ◽  
Growth Hormone ◽  
Regression Analysis ◽  
Body Mass ◽  
Older Men ◽  
Regulatory Mechanisms ◽  
Double Blind ◽  
Healthy Men ◽  
Gh Secretion ◽  
Integrated Regulation

Pulsatile growth hormone (GH) secretion putatively reflects integrated regulation by GH-releasing hormone (GHRH), somatostatin (SST), and GH-releasing peptide (GHRP). GHRH and SST secretion is itself pulsatile. However, how GHRH and SST pulses act along with GHRP to jointly determine pulsatile GH secretion is unclear. Moreover, how testosterone (T) modulates such interactions is unknown. These queries were assessed in a prospectively randomized, placebo-controlled double-blind cohort comprising 26 healthy older men randomized to testosterone (T) vs. placebo supplementation. Pulses of GHRH, SST, or saline were infused intravenously at 90-min intervals for 13 h, along with either continuous saline or ghrelin analog (GHRP-2). The train of pulses was followed by a triple stimulus (combined l-arginine, GHRH, and GHRP-2) to estimate near-maximal GH secretion over a final 3 h. Testosterone vs. placebo supplementation doubled pulsatile GH secretion during GHRH pulses combined with continuous saline (GHRH/saline) ( P < 0.01). Pulsatile GH secretion correlated positively with T concentrations (270–1,170 ng/dl) in the 26 men during saline pulses/saline ( P = 0.015, R2 = 0.24), GHRH pulses/saline ( P = 0.020, R2 = 0.22), and combined GHRH pulses/GHRP-2 ( P = 0.016, R2 = 0.25) infusions. Basal nonpulsatile GH secretion correlated with T during saline pulses/GHRP-2 drive ( P = 0.020, R2 = 0.16). By regression analysis, pulsatile GH secretion varied negatively with body mass index (BMI) during saline/GHRP-2 infusion ( P = 0.001, R2 = 0.36), as well as after the triple stimulus preceded by GHRH/GHRP-2 ( P = 0.013, R2 = 0.23). Mean (10-h) GH concentrations under GHRP-2 were predicted jointly by estradiol (positively) and BMI (negatively) ( P < 0.001, R2 = 0.520). These data indicate that estradiol, T, and BMI control pulsatile secretagogue-specific GH-regulatory mechanisms in older men.

scholarly journals Regulated recovery of pulsatile growth hormone secretion from negative feedback: a preclinical investigation

2011 ◽  
Vol 301 (4) ◽  
pp. R1143-R1152 ◽  
Author(s):  
Johannes D. Veldhuis ◽  
Cyril Y. Bowers
Keyword(s):  
Body Mass Index ◽  
Growth Hormone ◽  
Body Mass ◽  
Negative Feedback ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Gh Secretion ◽  
Model Free ◽  
Preclinical Investigation ◽  
Igf I

Although stimulatory (feedforward) and inhibitory (feedback) dynamics jointly control neurohormone secretion, the factors that supervise feedback restraint are poorly understood. To parse the regulation of growth hormone (GH) escape from negative feedback, 25 healthy men and women were studied eight times each during an experimental GH feedback clamp. The clamp comprised combined bolus infusion of GH or saline and continuous stimulation by saline GH-releasing hormone (GHRH), GHRP-2, or both peptides after randomly ordered supplementation with placebo (both sexes) vs. E2 (estrogen; women) and T (testosterone; men). Endpoints were GH pulsatility and entropy (a model-free measure of feedback quenching). Gender determined recovery of pulsatile GH secretion from negative feedback in all four secretagog regimens (0.003 ≤ P ≤ 0.017 for women>men). Peptidyl secretagog controlled the mass, number, and duration of feedback-inhibited GH secretory bursts (each, P < 0.001). E2/T administration potentiated both pulsatile ( P = 0.006) and entropic ( P < 0.001) modes of GH recovery. IGF-I positively predicted the escape of GH secretory burst number and mode ( P = 0.022), whereas body mass index negatively forecast GH secretory burst number and mass ( P = 0.005). The composite of gender, body mass index, E2, IGF-I, and peptidyl secretagog strongly regulates the escape of pulsatile and entropic GH secretion from autonegative feedback. The ensemble factors identified in this preclinical investigation enlarge the dynamic model of GH control in humans.

scholarly journals MON-113 The Effect of Body Mass Index on the Peak Growth Hormone Level After Growth Hormone Stimulation Test in Children with Short Stature

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Nayeong Lee ◽  
Wonkyoung Cho ◽  
Yoonji Lee ◽  
Seulki Kim ◽  
Seonhwa Lee ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Growth Hormone ◽  
Regression Analysis ◽  
Short Stature ◽  
Body Mass ◽  
Multivariate Regression ◽  
Standard Deviation Score ◽  
Multivariate Regression Analysis ◽  
Stimulation Test ◽  
Peak Growth Hormone

Abstract Objective: The aim of this study is to evaluate the effect of body mass index (BMI) on peak growth hormone (GH) response after GH stimulation test in children with short stature. Methods: Data was obtained from retrospective review of medical records who visited the pediatric endocrinology at St. Vincent hospital of catholic university for short stature from January 2010 to June 2019. We studied 115 children (aged 3-17 years old) whose height was less than 3percentile for one’s age and sex and who underwent GH stimulation test {GH deficiency (GHD) = 47, Idiopathic short stature (ISS) = 68)}. Peak GH response was stimulated by dopamine (n=111), clonidine (n=7), glucagon (n=19), insulin (n=56) and arginine (n=32). Birth weight, parental height, chronologic age, bone age, height SDS (standard deviation score), weight SDS, BMI SDS hemoglobin, fT4, T3 TSH, cortisol, ACTH, GH, IGF-1 SDS, IGF-BP3 SDS and peak stimulated GH were analyzed. Results: In the characteristics of subject, weight SDS and BMI SDS in GHD group were increased than ISS group (p&lt;0.000, p=0.000). Free T4 was decreased in GHD group than ISS group (p=0.012). In total group, BMI SDS was associated negatively with peak GH level stimulated by dopamine (r=-0.419, p&lt;0.000), insulin (r=-0.271, p=0.044) and arginine (r=-0.368, p=0.038), but did not showed correlation with peak GH level stimulated by glucagon. In GHD group, BMI SDS showed negative correlation with peak GH level using dopamine (r=-0.356, p=0.015) and arginine (r=-0.509, p=0.022). In ISS group, BMI SDS was correlated negatively with peak GH using dopamine (r=-0.330, p=0.007). In multivariate regression analysis of GHD group, weight SDS and BMI SDS were the only two significant predictors of peak GH response in stimulation test stimulated by dopamine (ß=-0.576, p=0.015) and arginine (ß=-0.097, p=0.022). In ISS group, only mother’s height (ß=0.474, p=0.000) and TSH (ß=-2.251, p&lt;0.000) were demonstrated statistically significant predictors of peak GH stimulated by dopamine in multivariate regression analysis. In case of using insulin as a stimulant in ISS group, there is nothing which has statistical significance as a predictor of peak GH response in multivariate regression analysis. Conclusion: BMI was associated negatively with peak GH response after GH stimulation test in children with short stature, especially in GHD group.

Effects of glucose load and/or arginine on insulin and growth hormone secretion in hyperprolactinemia and obesity

1996 ◽  
Vol 135 (2) ◽  
pp. 205-210 ◽  
Author(s):  
Mauro Maccario ◽  
Silvia Grottoli ◽  
Paola Razzore ◽  
Massimo Procopio ◽  
Salvatore Endrio Oleandri ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Growth Hormone ◽  
Insulin Secretion ◽  
Body Mass ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Insulin Response ◽  
Glucose Load ◽  
Gh Secretion ◽  
Glucose Levels

Maccario M, Grottoli S, Razzore P, Procopio M, Oleandri SE, Ciccarelli E, Camanni F, Ghigo E. Effects of glucose load and/or arginine on insulin and growth hormone secretion in hyperprolactinemia and obesity. Eur J Endocrinol 1996;135:205–10. ISSN 0804–4643 In hyperprolactinemic patients an exaggerated glucose-induced insulin secretion has been reported, but these results have not been confirmed by other researchers. On the other hand, there are few data concerning somatotrope secretion in this condition. In order to clarify these points, in seven normal weight hyperprolactinemic female patients (HP: age 18–46 years, body mass index = 21.8 ± 0.6 kg/m2, basal prolactin = 91.7 ± 16.5 μg/l) we studied the effects of glucose load (100 g orally) and/or arginine (0.5 g/kg infused over 30 min on insulin glucose and growth hormone (GH) levels. These results were compared with those obtained in seven patients with simple obesity (OB: age 23–48 years, body mass index = 38.3 ± 2.6 kg/m2) in whom exaggerated insulin and low GH secretion are well known. Seven normal women (NS: age 26–32 years, body mass index = 20.6 ± 1.9 kg/m2) were studied as controls. The insulin response to glucose in HP (area under curve = 11460.8 ± 1407.5 mU·min·1−1) was not significantly different from NS (7743.7 ±882.9 mU·min·1−1) and OB (14 504.8 ± 1659.9 mU·min·1−1). The arginine-induced insulin release in HP and OB was similar (4219.4 ± 631.7 and 4107.3 ± 643.2 mU·min·1−1. respectively), both being higher (p < 0.02) than in NS (2178.1 ± 290.9 mU·min·1−1). Glucose and arginine had an additive effect on insulin release in HP and NS (19 769.1 ± 3249.6 and 10996.6 ± 1201.0 mU·min·1−1, respectively) and a synergistic effect in OB (28117.3± 5224.7 mU·min·1−1). In HP the insulin response to the combined administration of glucose and arginine was not significantly different from the one in OB, and both were higher (p < 0.05) than in NS. The increase in glucose levels after glucose administered on its own or combined with arginine was higher (p < 0.02) and longer lasting in OB than in NS and HP. After arginine in OB, the glucose levels did not show the late decrease under baseline values observed in HP and NS. Glucose inhibited GH secretion both in HP and NS (p < 0.05), while arginine stimulated it in all groups, although the GH response in HP and NS was higher (p < 0.03) than in OB. The arginine-induced GH secretion was inhibited by glucose in HP and NS but not in OB. These results demonstrate that both in hyperprolactinemic patients and in obesity there is a clear increase in insulin secretion. The insulin hyperresponsiveness in hyperprolactinemia is more clearly demonstrated by combined stimulation with glucose and arginine. In spite of similar insulin hypersecretion in hyperprolactinemic and obese patients, GH secretion is reduced only in the latter; with these data the hypothesis that somatotrope insufficiency in obesity is due to hyperinsulinism is unlikely. Ezio Ghigo, Divisione di Endocrinologia, Ospedale Molinette, C.so Dogliotti 14, 10126 Torino, Italy

scholarly journals Gonadal Status and Body Mass Index Jointly Determine Growth Hormone (GH)-Releasing Hormone/GH-Releasing Peptide Synergy in Healthy Men

2008 ◽  
Vol 93 (3) ◽  
pp. 944-950 ◽  
Author(s):  
Remberto C. Paulo ◽  
Mihaela Cosma ◽  
Cacia Soares-Welch ◽  
Joy N. Bailey ◽  
Kristi L. Mielke ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Growth Hormone ◽  
Body Mass ◽  
Healthy Men ◽  
Releasing Hormone ◽  
Gonadal Status

Growth hormone secretion in primary adrenal Cushing's syndrome is disorderly and inversely correlated with body mass index

2005 ◽  
Vol 288 (1) ◽  
pp. E63-E70 ◽  
Author(s):  
Maarten O. van Aken ◽  
Alberto M. Pereira ◽  
Marijke Frölich ◽  
Johannes A. Romijn ◽  
Hanno Pijl ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Growth Hormone ◽  
Body Mass ◽  
Approximate Entropy ◽  
Cushing's Syndrome ◽  
Control Group ◽  
Cortisol Secretion ◽  
Age And Gender ◽  
Gh Secretion ◽  
And Gender

To evaluate the impact on the somatotropic axis of endogenous cortisol excess in the absence of primary pituitary disease, we investigated spontaneous 24-h growth hormone (GH) secretion in 12 adult patients with ACTH-independent hypercortisolism. Plasma GH concentration profiles (10-min samples) were analyzed by deconvolution to reconstruct secretion and approximate entropy to quantitate orderliness of the release process. Comparisons were made with a body mass index (BMI)-, age-, and gender-matched control group and an age- and gender-matched lean control group. GH secretion rates did not differ from BMI-matched controls but were twofold lower compared with lean subjects, mainly due to a 2.5-fold attenuation of the mean secretory burst mass ( P = 0.001). In hypercortisolemic patients, GH secretion was negatively correlated with BMI ( R = −0.55, P = 0.005) but not cortisol secretion. Total serum IGF-I concentrations were similar in the three groups. Approximate entropy (ApEn) was increased in patients with Cushing's syndrome compared with both control groups (vs. BMI-matched, P = 0.04; vs. lean, P = 0.001), denoting more irregular GH secretion patterns. ApEn in patients correlated directly with cortisol secretion ( R = 0.77, P = 0.003). Synchrony between cortisol and GH concentration series was analyzed by cross-correlation, cross-ApEn, and copulsatility analyses. Patients showed loss of pattern synchrony compared with BMI-matched controls, but copulsatility was unchanged. We conclude that hyposomatotropism in primary adrenal hypercortisolism is only partly explained (∼30%) by increased body weight and that increased GH secretory irregularity and loss of synchrony suggest altered coordinate regulation of GH release.

Pyridostigmine treatment selectively amplifies the mass of GH secreted per burst without altering GH burst frequency, half-life, basal GH secretion or the orderliness of GH release

1997 ◽  
pp. 377-386 ◽  
Author(s):  
K Friend ◽  
A Iranmanesh ◽  
IS Login ◽  
JD Veldhuis
Keyword(s):  
Body Mass Index ◽  
Growth Hormone ◽  
Body Mass ◽  
Half Life ◽  
Approximate Entropy ◽  
Burst Frequency ◽  
Release Process ◽  
Assay Sensitivity ◽  
Deconvolution Analysis ◽  
Gh Secretion

Growth hormone (GH) release from the anterior pituitary gland is predominantly regulated by the two antagonistic hypothalamic peptides, growth hormone-releasing hormone (GHRH) and somatostatin. Appraising endogenous GHRH action is thus made difficult by the confounding effects of (variable) hypothalamic somatostatin inhibitory tone. Accordingly, to evaluate endogenous GHRH actions, we used a clinical model of presumptively acute endogenous somatostatin withdrawal with concomitant GHRH release. To this end, we administered in randomized order placebo or the indirect cholinergic agonist, pyridostigmine, for 48 h to 13 healthy men of varying ages (29-77 years) and body mass indices (21-47 kg/m2). We sampled blood at 10-min intervals for 48 h during both placebo and pyridostigmine (60 mg orally every 6 h) administration, and used an ultrasensitive GH chemiluminescence assay (sensitivity 0.0002-0.005 microgram/l) to capture GH pulse profiles. Multiparameter deconvolution analysis was applied to quantitate the number, amplitude, mass, and duration of significant underlying GH secretory bursts, and simultaneously estimate the GH half-life and concurrent basal GH secretion. Approximate entropy was utilized as a novel regularity statistic to quantify the relative orderliness of the hormone release process. All measures of GH secretion/half-life and orderliness were statistically invariant across the two consecutive 24-h placebo sessions. In contrast, pyridostigmine treatment significantly increased the mean serum GH concentration from 0.23 +/- 0.054 microgram/l during placebo to 0.45 +/- 0.072 microgram/l during the first day of treatment (P < 0.01). There was also a significant rise in the calculated 24-h pulsatile GH production rate from 8.9 +/- 1.7 micrograms/l/day on placebo to 27 +/- 5.6 micrograms/l/day during active drug treatment (P < 0.01). Pyridostigmine significantly and selectively amplified GH secretory burst mass to 1.5 +/- 0.35 micrograms/l compared with 0.74 +/- 0.19 microgram/l on placebo (P < 0.01). This was attributable to stimulation of GH secretory burst amplitude (maximal rate of GH secretion attained within the release episode) with no prolongation of estimated burst duration. Basal GH secretion and approximate entropy were not altered by pyridostigmine. However, age was strongly related to more disorderly GH release during both days of pyridostigmine treatment (r = +0.79, P = 0.0013). During the second 24-h of continued pyridostigmine treatment, most GH secretory parameters decreased by 15-50%, but in several instances remained significantly elevated above placebo. Body mass index, but not age, was a significantly negative correlate of the pyridostigmine-stimulated increase in GH secretion (r = -0.65, P = 0.017). In summary, assuming that somatostatin is withdrawn and (rebound) GHRH release is stimulated via pyridostigmine administration, we infer that relatively unopposed GHRH action principally controls GH secretory burst mass and amplitude, rather than apparent GH secretory pulse duration, the basal GH secretion rate, or the serial regularity/orderliness of the GH release process in the human. Moreover, we infer that increasing age is accompanied by greater disorderliness of somatostatin-withdrawn GHRH, and hence rebound GH, release. The strongly negative correlation between pyridostigmine-stimulated GH secretion and body mass index (but not age) further indicates that increased relative adiposity may result in decreased effective (somatostatin-withdrawn) endogenous GHRH stimulus strength.

Influence of Age and Body Mass Index on Measures of Physical Fitness in U.S. Army Soldiers

1996 ◽  
Vol 4 (3) ◽  
pp. 234-250 ◽  
Author(s):  
Joseph J. Knapik ◽  
Bruce H. Jones ◽  
James A. Vogel ◽  
Louis E. Banderet ◽  
Michael S. Bahrke ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Regression Analysis ◽  
Physical Fitness ◽  
Regression Model ◽  
Body Mass ◽  
Age Groups ◽  
Healthy Male ◽  
Healthy Men ◽  
Age Related ◽  
And Performance

This study describes associations between age, body mass index (BMI), and performance on three common measures of physical fitness: maximum pushups in 2 min, maximum sit-ups in 2 min, and 3.2-km run for time. Subjects were 5,346 healthy male soldiers, ages 18 to 53 years. Before age 30, there were few age-related differences between the youngest and the older age groups on any test; after age 30, performance declined as age increased, averaging 16%, 17%, and 7% per decade for push-ups, sit-ups, and the run, respectively. Regression analysis showed that age accounted for 10%, 15% and 9% of the variance in push-up, sit-up, and run performances, respectively. When BMI was added to the regression model it increased the variance accounted for in the run to 16% (age plus BMI) but did not explain variance in push-ups or sit-ups. There are systematic age-related declines in the performance of push-ups, sit-ups, and 3.2-km running, with age alone accounting for only 9% to 15% of the total performance variance in this sample of healthy men.

Effect of body mass index and fat distribution on insulin sensitivity, secretion, and clearance in nonobese healthy men.

1992 ◽  
Vol 75 (1) ◽  
pp. 170-175 ◽  
Author(s):  
C Walton ◽  
I F Godsland ◽  
A J Proudler ◽  
C V Felton ◽  
V Wynn
Keyword(s):  
Body Mass Index ◽  
Insulin Sensitivity ◽  
Body Mass ◽  
Fat Distribution ◽  
Healthy Men
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