scholarly journals Two-Month Treatment of Obese Subjects with the Oral Growth Hormone (GH) Secretagogue MK-677 Increases GH Secretion, Fat-Free Mass, and Energy Expenditure1

1998 ◽  
Vol 83 (2) ◽  
pp. 362-369 ◽  
Author(s):  
J. Svensson ◽  
L. Lönn ◽  
J.-O. Jansson ◽  
G. Murphy ◽  
D. Wyss ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Fat Free Mass ◽  
Gh Secretion ◽  
Obese Subjects

Pyridostigmine enhances, but does not normalise, the GH response to GH-releasing hormone in obese subjects

1990 ◽  
Vol 122 (3) ◽  
pp. 385-390 ◽  
Author(s):  
R. C. Castro ◽  
J. G. H. Vieira ◽  
A. R. Chacra ◽  
G. M. Besser ◽  
A. B. Grossman ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Acetylcholinesterase Inhibitor ◽  
Random Order ◽  
Normal Subjects ◽  
Obese Patients ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Obese Subjects ◽  
Higher Doses ◽  
Hormone Responsiveness

Abstract Obese patients are characterised by several neuroendocrine abnormalities, including characteristically a decrease in growth hormone responsiveness to GH-releasing hormone. In normal subjects, the GH response to GHRH is enhanced by the acetylcholinesterase inhibitor, pyridostigmine. We have studied the effect of this drug on GH secretion in gross obesity. Twelve obese patients were studied (mean weight 156% of ideal) and compared with a group of 8 normal volunteers. Each subject was initially studied on two occasions, in random order, with GHRH (1–29) NH2 100 μg iv alone and following pretreatment with pyridostigmine 120 mg orally one hour prior to GHRH. In obese patients, the GH response to GHRH was significantly blunted when compared to controls (GH peak: 20 ± 4 vs 44 ± 16 μg/l; mean ± sem). After pyridostigmine, the response to GHRH was enhanced in the obese subjects, but remained significantly reduced compared to non-obese subjects treated with GHRH and pyridostigmine (GH peak: 30 ± 5 vs 77 ± 20 μg/l, respectively). In 6 subjects, higher doses of GHRH or pyridostigmine did not further increase GH responsiveness in obese patients. Our results suggest that obese patients have a disturbed cholinergic control of GH release, probably resulting from increased somatostatinergic tone. This disturbed regulation may be responsible, at least in part, for the blunted GH responses to provocative stimuli.

scholarly journals Baseline Body Composition in Prepubertal Short Stature Children with Severe and Moderate Growth Hormone Deficiency

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Pawel Matusik ◽  
Marta Klesiewicz ◽  
Karolina Klos ◽  
Martyna Stasiulewicz ◽  
Aleksandra Barylak ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Body Composition ◽  
Growth Hormone Deficiency ◽  
Peak Level ◽  
Fat Free Mass ◽  
Hormone Deficiency ◽  
Entire Group ◽  
Composition Analysis ◽  
Gh Secretion ◽  
Moderate Growth

Objective.To compare body composition parameters in short children with severe versus moderate and no growth hormone deficiency (GHD).Design and Method.61 children (40 boys) were studied. Height SDS, BMIZ-score, waist/height ratio (W/HtR), and body composition parameters (BIA) as fat tissue (FAT%), fat-free mass (FFM%), predicted muscle mass (PMM%), and total body water (TBW%) were evaluated. GH secretion in the overnight profile and two stimulation tests and insulin-like growth factor 1 (IGF-1) level were measured.Results.Overall, in 16 (26%) moderate (7.0 > peak GH < 10 ng/mL) and in 11 (18%) severe (GH ≤ 7.0 ng/mL) GHD was diagnosed. In children with sGHD BMIZ-score, W/HtR and FAT% were significantly higher, while FFM%, PMM%, and TBW% were significantly lower versus mGHD and versus noGHD subgroups. No significant differences between mGHD and noGHD were found. There were no differences in height SDS and IGF-1 SDS between evaluated subgroups. Night GH peak level correlated significantly with FAT%, FFM%, PMM%, and TBW%, (p<0.05) in the entire group.Conclusions.Only sGHD is associated with significant impairment of body composition. Body composition analysis may be a useful tool in distinguishing between its severe and moderate form of GHD.

scholarly journals Growth Hormone Status In Obese Subjects and Correlation With Age

2020 ◽  
Vol 9 (2) ◽  
pp. 368-373
Author(s):  
Mufarrihul Ihsan ◽  
Lilik Herawati ◽  
Purwo Sri Rejeki
Keyword(s):  
Growth Hormone ◽  
Body Mass ◽  
Body Fat ◽  
Pearson Correlation ◽  
Fasting Blood Glucose ◽  
Cross Sectional Study ◽  
Female Adolescent ◽  
Cross Sectional ◽  
Gh Secretion ◽  
Obese Subjects

Obesity also increases the risk of decreased Growth Hormone (GH) secretion. Decreased GH secretions have an impact on increasing body fat and decreasing lean body mass. This study aims to analyze the status of Growth Hormone (GH) in obese subjects and the correlation of GH with age. This study used a cross sectional study method using 30 obese female adolescent Body Mass Index (BMI) subjects 25-35 kg/m2, Percentage of Body Fat (PBF) above 30% and fasting blood glucose (FBG) below 100 mg/dL. Measurement of GH levels used the Enzym Link Immunosorbent Assay (ELISA) method. Data analysis techniques used the Pearson Correlation test with the Statistical Package for Social Science. Results obtained mean GH levels (761.119±504.627) pg/mL and average age (20.863±1.082) years (r =-0.483) and (p=0.023). Based on the results of the study, it can be concluded that there is a negative correlation between GH status and age in obese subjects

scholarly journals Suppression in growth hormone during overeating ameliorates the increase in insulin resistance and cardiovascular disease risk

2012 ◽  
Vol 303 (10) ◽  
pp. E1264-E1272 ◽  
Author(s):  
Andrea S. Cornford ◽  
Ariel L. Barkan ◽  
Alexander Hinko ◽  
Jeffrey F. Horowitz
Keyword(s):  
Insulin Resistance ◽  
Growth Hormone ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Fat Free Mass ◽  
Gh Treatment ◽  
Gh Secretion ◽  
Isotope Tracer ◽  
Fractional Synthetic Rate ◽  
Plasma Gh

Previously, we reported that overeating for only a few days markedly suppressed the secretion of growth hormone (GH). The purpose of the present study was to determine the role of this reduction in GH concentration on key metabolic adaptations that occur during 2 wk of overeating. Nine nonobese, healthy adults were admitted to the hospital for 2 wk, during which time they ate ∼4,000 kcal/day (70 kcal·kg fat-free mass−1·day−1; 50% carbohydrate, 35% fat, and 15% protein), and their plasma GH concentration was allowed to decline naturally (control). An additional eight subjects underwent the same overeating intervention and received exogenous GH treatment (GHT) administered in four daily injections to mimic physiological GH secretion throughout the 2-wk overeating period. We measured plasma insulin and glucose concentrations in the fasting and postprandial state as well as fasting lipolytic rate, proteolytic rate, and fractional synthetic rate (FSR) using stable-isotope tracer methods. GHT prevented the fall in plasma GH concentration, maintaining plasma GH concentration at baseline levels (1.2 ± 0.2 ng/ml), which increased fasting and postprandial assessments of insulin resistance ( P < 0.05) and increased fasting lipidemia (all P < 0.05 vs. control). In addition, preventing the suppression in GH with overeating also blunted the increase in systemic proteolysis ( P < 0.05 GHT vs. control). However, GHT did not alter lipolysis or FSR in response to overeating. In conclusion, our main findings suggest that the suppression in GH secretion that naturally occurs during the early stages of overeating may help attenuate the insulin resistance and hyperlipidemia that typically accompany overeating.

The effect of atenolol on the growth hormone response to growth hormone-releasing hormone in obese children

1992 ◽  
Vol 126 (2) ◽  
pp. 124-127 ◽  
Author(s):  
Sandro Loche ◽  
Stefano Pintus ◽  
Daniela Carta ◽  
Anna Carla Muntoni ◽  
Gabriella Congiu ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Area Under The Curve ◽  
Acute Administration ◽  
Adrenergic Blockade ◽  
Obese Children ◽  
Gh Secretion ◽  
Adrenergic Antagonist ◽  
Significant Augmentation ◽  
Obese Subjects ◽  
Β Adrenergic Receptors

We have evaluated the effect of acute administration of atenolol, a selective β-adrenergic antagonist, on the GH response to GHRH in nine obese children and in eight age-matched controls. The GH response to GHRH (1–29, 1 μg/kg iv), evaluated both as the GH peak and as integrated area under the curve, was significantly lower in the obese children than in the controls. Pretreatment with atenolol (50 or 100mg orally in subjects with body weight <or >40 kg, respectively, administered 120 min before the GHRH injection) significantly increased the GH response to GHRH in the obese subjects, such that their mean peak GH levels and mean integrated area under the curve after atenolol plus GHRH were similar to those of the control children after GHRH. Also in control children, atenolol caused a significant augmentation of the GH response to GHRH. Mean peak GH levels and mean integrated area under the curve after atenolol plus GHRH were significantly higher in the controls than in the obese children given the same treatment. These data show that inhibition of central β-adrenergic receptors counteracts the blunted GH response to GHRH present in the obese children. In view of the alleged mechanism of action of β-adrenergic blockade (inhibition of endogenous SRIH release), our data suggest that the somatostatinergic system is intact in obesity, and that the suppressed GH secretion is due to other causes.

GROWTH HORMONE RESPONSES TO FRUCTOSE IN DIABETES MELLITUS

1974 ◽  
Vol 75 (3) ◽  
pp. 497-502
Author(s):  
Mayer B. Davidson ◽  
Roger M. Steele
Keyword(s):  
Diabetes Mellitus ◽  
Growth Hormone ◽  
Fasting Glucose ◽  
Area Under The Curve ◽  
Oral Glucose ◽  
Gh Secretion ◽  
Significant Difference ◽  
Duration Of Disease ◽  
Hormone Responses

ABSTRACT Since fructose is normally metabolized in diabetics and has recently been shown to stimulate GH secretion, it was used to assess GH responses in diabetics. Fourteen diabetics (9 on insulin) and 8 controls matched for weight were studied. Fructose, infused over 10 min, was compared to arginine, infused over 30 min, both at 0.5 g/kg. Samples were collected at 0, 30, 60, 90 and 120 min and GH responses assessed as area under the curve minus the fasting area. There was no significant difference between the GH responses in diabetics and controls to either agent. Responses to arginine and fructose were significantly correlated (r = 0.60, P < 0.01) in all subjects, but not related to therapy, duration of disease or fasting glucose (75–287 mg/100 ml) in the diabetics. Oral glucose blunted the GH response to fructose in 2 controls. It is concluded that 1) fructose can stimulate GH secretion in male diabetics; 2) however, fructose-stimulated GH responses are not increased in diabetes mellitus.

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