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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate whether the impaired growth hormone secretion associated with obesity is a result of a hypothalamic or a pituitary disorder and whether it is a cause or a consequence of obesity, we studied plasma growth hormone responses to growth hormone-releasing factor in morbidly obese patients before gastrointestinal surgical therapy, in formerly obese subjects who had lost considerable weight postoperatively, and in non-obese controls. Growth hormone secretion was also assessed in response to insulin-induced hypoglycemia (in seven patients preoperatively and four postoperatively). In patients studied preoperatively, growth hormone responses to growth hormone-releasing factor were markedly impaired (P less than 0.001 as compared with controls), whereas in patients studied postoperatively they were partially restored to normal (P less than 0.05 as compared with those studied preoperatively). Growth hormone responses to insulin-induced hypoglycemia were similarly diminished in obese patients studied before operation (P less than 0.02). The growth hormone response to growth hormone-releasing factor was inversely correlated with the percentage of ideal body weight (P less than 0.01) and directly correlated with the growth hormone response to insulin (P less than 0.01). The impaired responsiveness to growth hormone-releasing factor suggests that the diminished response to insulin hypoglycemia is mediated by an impaired pituitary response to endogenous growth hormone-releasing factor. The reversibility of the defect after weight reduction suggests that it is a consequence rather than a cause of obesity.
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PMID:Impaired growth hormone responses to growth hormone-releasing factor in obesity. A pituitary defect reversed with weight reduction. 643 6

Growth hormone (GH) and somatomedin (Sm) are the main factors of human growth. Sm is GH-dependent, but Sm increase after hGH injection in hypopituitary dwarfs is slow, and preceded by a decrease. The liver and kidneys are the main places of Sm production in vivo, the liver having probably also a regulatory effect. In vitro, GH-dependent production of Sm may be obtained from fibroblasts as well as from liver cells. Sm activates thymidine uptake by cultured human fibroblasts and by activated human lymphocytes, this effect needing cofactors from serum. Discrepant correlations between growth, GH and Sm are found in some pathological situations, such as obesity, craniopharyngioma, celiac disease, infantile malnutrition. Moreover, transferrin, a plasma protein, correlates also with growth.
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PMID:[Relationships between growth, and plasma growth hormone and growth factors under normal physiological conditions and during pathological states (author's transl)]. 701 77

Growth hormone (GH) secretion is reduced in girls with Turner's syndrome (TS) at pubertal age. We have recently proposed that the impairment of GH release in TS girls might be secondary to obesity. In the present study, we assessed the influence of overweight-related insulin status on spontaneous GH secretion in a group of 15 TS girls. Eighteen age-matched short normal subjects and six short obese prepubertal children were chosen as controls. Anthropometry, spontaneous GH secretion, insulin-like growth factor-I (IGF-I) serum levels, basal fasting insulin, and glucose concentrations were determined. The percentage of ideal body weight (IBW) was used as an index of nutritional status. Baseline fasting glucose (milligrams per deciliter) to insulin (milliunits per liter) ratio (G/I) was chosen as an index of insulin resistance. GH secretion was significantly lower in TS girls than in non-obese children (P < .005), whereas no significant difference was seen between TS and obese subjects. IGF-I levels were not statistically different in all groups. GH secretion was confirmed to be related to the degree of overweight (r = -.52, P < .05 in TS girls and r = -.74, P < .0001 in control group). G/I was closely related to both the percentage of IBW (r = -.59, P = .02) and GH level (r = .57, P = .03) in TS patients. These results confirm that the blunted GH secretion in TS patients is dependent on nutritional status, and suggest that insulin resistance secondary to overweight might represent the pathophysiologic link between the obesity-related metabolic status and impaired GH secretion.
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PMID:Is obesity-related insulin status the cause of blunted growth hormone secretion in Turner's syndrome? 763 44

Growth hormone (GH) secretion in response to all provocative stimuli is decreased in patients with obesity. Recently, we found that the combined administration of GH-releasing hormone (GHRH) and the hexapeptide GH-releasing peptide-6 (GHRP-6) induced a large increase in plasma GH levels. To gain further insight into the disrupted mechanism of GH regulation in obesity, we investigated whether the inhibition of somatostatinergic tone with pyridostigmine could further increase the GH response to combined administration of GHRH and GHRP-6. In normal subjects, administration of GHRH plus GHRP-6 induced a marked increase in plasma GH with a peak at 30 minutes (mean +/- SEM, 76.7 +/- 9.7 micrograms/L), which was similar to that obtained after pretreatment with pyridostigmine (74.7 +/- 9.4 micrograms/L). In obese patients, combined administration of GHRH plus GHRP-6 induced a clear increase in GH secretion with a peak at 15 minutes of 42.2 +/- 10.0 micrograms/L, which was also unaffected after pretreatment with pyridostigmine (38.4 +/- 5.8 micrograms/L). The GH response was lower in obese patients than in controls as assessed by the area under the curve after administration of both GHRH plus GHRP-6 (1,846 +/- 396 v 4,773 +/- 653, P < .01) and pyridostigmine plus GHRH plus GHRP-6 (1,989 +/- 372 v 5,098 +/- 679, P < .005). In conclusion, these data suggest that GHRP-6 can behave as a functional somatostatin antagonist, and that somatotrope responsiveness to the combined administration of GHRH plus GHRP-6 is largely independent of somatostatinergic tone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of combined administration of growth hormone (GH)-releasing hormone, GH-releasing peptide-6, and pyridostigmine in normal and obese subjects. 778 58

The purpose of this study was to evaluate growth hormone (GH) secretion and clarify the factors influencing GH secretion in obesity. Nine obese subjects and eight controls were recruited. We compared the GH response to L-dopa with or without pyridostigmine pretreatment in obese and control subjects. Plasma glucose, insulin, insulin-like growth factor I (IGF-I) and free fatty acid (FFA) were also measured. Growth hormone responses and GH area under the response curve (AUC) to L-dopa were significantly lower in obese subjects than those in controls. Pyridostigmine significantly enhanced the GH response to L-dopa in both obese and control subjects. However, enhanced GH responses in obese subjects were attenuated biologically and lower than those in controls with L-dopa only. Plasma levels of insulin insulin and FFA were significantly higher in obese subjects than those in controls. Body mass index had a positive correlation with the levels of insulin and FFA. However, GH AUC had an inverse correlation with insulin and FFA in obese subjects and controls. Stepwise multiple regression analysis showed a highly significant effect of FFA on GH AUC, but no independent influence of other factors on GH AUC. The reduced GH secretion found in this study suggests an increase in somatostatinergic tone and a diminished release of GHRH from the hypothalamus in obesity. However, other factors including hyperinsulinemia and increased plasma FFA may play an important additional role in the secretory dysfunction of GH in obesity.
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PMID:Reduced growth hormone response to L-dopa and pyridostigmine in obesity. 792 Aug 71

Growth hormone (GH) secretion is regulated by a complex system of central and peripheral signals. Recently, a new GH-releasing hexapeptide (His-D-Trp-Ala-Trp-D-Phe-Lys-NH2) called GHRP-6 which specifically releases GH has been studied. In the present work the mechanism of action of GHRP-6 has been addressed in experimental animal models as well as in obese subjects. GHRP-6 releases GH independently of the hypothalamic factors GHRH and somatostatin and is a powerful GH releaser in obesity.
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PMID:Regulation of growth hormone secretion by the growth hormone releasing hexapeptide (GHRP-6). 792 Sep 95

Growth hormone (GH) secretion is markedly blunted in obesity. Reportedly, genetically obese Zucker rats show a reduced GH secretion due to an impaired function of hypothalamic neurons producing the GH-releasing hormone (GHRH). The aim of this work was: (1) to compare the in vitro GH responsiveness to GHRH in genetically obese female versus male Zucker rats and, (2) to evaluate the function of hypothalamic GHRH and somatostatin and of pituitary receptors for these neurohormones as assessed by the effectiveness of GHRH and somatostatin on adenylate cyclase (AC) activity. Baseline GH secretion of pituitaries obtained from male and female obese rats was not different and similar to that present in lean counterparts. Stimulation with 10(-7) M GHRH elicited a significantly lower GH secretion from the pituitaries of obese male rats but induced a similar GH secretion from the pituitaries of lean and obese female rats. In these pituitaries, GH concentration was similar in obese versus lean male and female rats [corrected]. A sex-related difference was also evidenced when plasma concentrations of somatomedin C (IGF-I) were evaluated. Obese male rats had lower IGF-I concentrations than lean counterparts, while this was not the case for obese versus lean female rats. Evaluation of AC activity following GHRH disclosed a lower activation in obese than in lean male rats, whereas in the females the enzyme activation was higher in obese than in lean animals. Conversely, the inhibitory effect of somatostatin on forskolin-stimulated AC was similar in pituitary membranes of obese and lean rats of both sexes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Growth hormone secretion is differently affected in genetically obese male and female rats. 810 99

Growth hormone secretion is blunted in obesity. Recent studies have shown that the sub-group of obesity with preponderance of accumulation of fat in visceral depots is associated with endocrine abnormalities. We therefore measured IGF-I concentrations in serum in 27 men who also underwent computerized tomography measurements of regional and total body fat mass. Furthermore, euglycemic-hyperinsulinemic glucose clamps were used to determine insulin resistance, and established 'risk factors' for cardiovascular disease and non-insulin dependent diabetes mellitus were measured, i.e. blood pressure, plasma lipids, and blood glucose, as well as sex steroid hormones. Visceral fat mass systolic blood pressure and triglycerides were higher (P < 0.05) in the group with low (87 +/- 4 micrograms/l) IGF-I values, compared to those with high (126 +/- 6 micrograms/l) IGF-I values, divided after the median value. IGF-I was negatively correlated with visceral fat mass (r = 0.40), independently of subcutaneous and total fat mass. As described before visceral fat mass was directly associated to a majority of the measured 'risk factors', as well as indirectly to testosterone and sex hormone binding globulin (SHBG) concentrations. The latter were also strongly related statistically to the 'risk factors'. IGF-I concentrations showed, however, weaker correlations with the metabolic factors, blood pressure or sex steroid hormones. Multivariate analyses revealed that the correlations of visceral fat with the risk factors were not influenced by IGF-I, while testosterone or SHBG totally abolished these associations. The results indicate that low serum IGF-I concentrations, suggesting deficient growth hormone secretion, are associated with visceral but not with subcutaneous or total fat masses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low concentrations of insulin-like growth factor-I in abdominal obesity. 838 69

Growth hormone (GH)-releasing hormone (GHRH) and somatostatin have a dominant role in regulating GH secretion. However, results of studies using the new class of GH secretogogues, particularly GHRP-6, indicate that there may also be other, as yet undefined, hypothalamic mechanisms involved. Studies in adults with hypothalamopituitary disconnection (functional pituitary stalk transection), show GHRP-6-mediated GH release to be completely blocked, indicating a main action at the hypothalamic rather than the pituitary level. The synergistic effect of GHRH plus GHRP-6 administration on GH release seen in normal adults (and virtually unaffected by age, obesity, or sex) is also absent in these patients, providing further support for this conclusion. Studies of the effects of GHRP-6 in children with GH deficiency due to perinatal pituitary stalk transection have produced similar findings. It is suggested that the combined GHRH plus GHRH-6 test should be a promising tool for diagnosing GH deficiency states in both children and adults, and may identify a subgroup of patients with GH deficiency caused by interruption of the hypothalamopituitary connection.
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PMID:Role of the new growth hormone-releasing secretagogues in the diagnosis of some hypothalamopituitary pathologies. 876 5

Growth hormone (GH) secretion is reduced with age in normal subjects. Aging is furthermore associated with a decline in lean body mass and an increase in relative adiposity, and overt obesity is a negative determinant of GH secretion in all age groups. We tested the hypothesis that differences in body composition and physical fitness rather than age determine stimulated GH secretion in healthy adults. Forty-two clinically nonobese adults [22 women and 20 men, mean age 39.4 yr (range 27-59), mean +/- SE body mass index (BMI) = 23.9 +/- 0.5 kg/m2] underwent 2 GH stimulation tests (arginine and clonidine), determination of maximal oxygen consumption (VO2-max), and a number of anthropometric measurements: body mass index (BMI), waist to hip (W/H)-ratio, intraabdominal fat and thigh muscle to fat (M/F)-ratio (computed tomography scan), total body fat, and lean body mass (DEXA scan). Peak GH levels were lower with clonidine [mean +/- SE (micrograms/L): 9.79 +/- 1.29 (arginine) vs. 3.56 +/- 0.57 (clonidine) (P < 0.001)]. Arginine-stimulated GH peak levels correlated negatively with indices of adiposity and age [intraabdominal fat: r = -0.72, P < 0.001; W/H-ratio: r = -0.58, P < 0.001; age: r = -0.54, P < 0.001], and positively with VO2-max [r = 0.60, P < 0.001]. Clonidine-stimulated GH peak correlated negatively with intraabdominal fat [r = -0.60, P < 0.001] and age [r = -0.46, P = 0.008]. Multiple linear regression revealed multicollinearity among several of the independent variables. In all equations abdominal adiposity and physical fitness, rather than age, contributed significantly to predict changes in arginine stimulated GH secretion. Intraabdominal fat was a more important determinant of the clonidine evoked GH response than age. In clinically nonobese, healthy adults relative adiposity, in particular in the abdominal region, is a major negative determinant of stimulated GH secretion, and physical fitness is an important positive predictor. The cause-effect relationship of these observations remains to be elucidated, but our findings may have clinical implications in the diagnosing of GH-deficiency in adults.
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PMID:Abdominal adiposity and physical fitness are major determinants of the age associated decline in stimulated GH secretion in healthy adults. 896 53


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