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

We have recently reported an impaired growth hormone (GH) response to a single i.v. bolus dose of growth hormone releasing factor (1 microgram/kg body weight) in obese women. We have now investigated whether the i.v. administration of low dose GHRF(1-29)NH2 (0.33 microgram/kg/h) by 15 min pulsed injections for 3 h followed by an i.v. bolus (1 microgram/kg) to four normal weight women and six obese women results in an enhancement of GH release. In the control women low dose GHRF, given either as a single 10 microgram injection or in pulses of equivalent total dosage, produced a GH response identical to that seen after a single bolus of 60 micrograms (mean peak GH low dose 30 +/- 2 mU/l, peak GH large dose 30 +/- 0.5 mU/l). In the obese women GH release was significantly less than the controls after low doses of GHRF (P less than 0.01) and the peak was delayed compared to that following a single large bolus dose (peak GH 7 +/- 1.2 mU/l). However, three of the obese women who previously showed no response to a large dose of GHRF did release GH after low dose pulsed injections. The final bolus of GHRF after 3 h of pulsed injections did not elicit any additional GH release in the subjects irrespective of body weight. We conclude that obesity may be characterized by impaired GH release to i.v. GHRF. The finding that some obese women do not respond to a single large dose injection of GHRF but do release GH after low dose pulsed injections supports the hypothesis of a hypothalamic disorder in these women.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Growth hormone response to low dose intravenous injections of growth hormone releasing factor in obese and normal weight women. 287 50

The effects of chronic growth hormone deficiency on the growth hormone-dependent, sexually dimorphic hepatic drug-metabolizing enzymes were studied in adult rats of both sexes. Neonatal administration of monosodium L-glutamate produced the expected syndrome characterized by stunted growth, obesity, prolonged vaginal estrus, and an inhibition in the growth of the pituitaries, adrenals, gonads, sexual accessory organs, and kidneys. Associated with these abnormalities was a 90% reduction in the concentration of serum growth hormone in male and female rats. In contrast, the activities of hepatic aniline hydroxylase, total cytochrome P-450, and the Michaelis constants and maximal velocities for hexobarbital hydroxylase and UDP-glucuronosyltransferase were unaffected by the profound deficiency in growth hormone.
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PMID:Normal levels of hepatic drug-metabolizing enzymes in neonatally induced, growth hormone-deficient adult male and female rats. 287 66

Young and mature, genetically obese and non-obese, spontaneously hypertensive rats (SHR) were injected with saline (controls) or naloxone for 12 weeks. Naloxone stilled the hyperphagia to a normal intake in the obese SHR (Obese/SHR) so that young Obese/SHR did not develop their usual massive obesity and mature Obese/SHR that had become massively obese were reduced to leanness. The naloxone-treated young, obese and non-obese SHR (controls) exhibited marked reduction of the weight of their pituitary and adrenal glands, whereas the pituitary and adrenal glands of naloxone-treated mature, obese and non-obese/SHR were greatly increased in weight. The elevated systolic blood pressure of the obese and non-obese rats was reduced after chronic treatment with naloxone. Naloxone treatment caused reduction of blood ACTH, corticosterone, and beta endorphin levels but elevated growth hormone levels. The characteristic hyperinsulinemia, hyperlipidemia, hyperglycemia, elevated BUN levels, and the Cushingoid spectrum of degenerative changes found in Obese/SHR did not appear in naloxone-treated rats.
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PMID:Anti-opiate (naloxone) suppression of Cushingoid degenerative changes in obese/SHR. 299 79

Opiates stimulate the growth hormone and prolactin responses to stimuli in non-obese humans. Obese patients, however, show lowered growth hormone and prolactin responses and raised beta-endorphin levels. We therefore investigated the effect of the opiate antagonist naloxone on the stimulated growth hormone and prolactin secretions in a controlled double-blind study in obese patients. All patients received 200 micrograms TRH and 0.5 g/kg b.w. arginine together with 2 mg of naloxone or placebo i.v. in a randomized sequence. The TRH- and arginine-induced increases in prolactin and growth hormone were significantly greater after administration of naloxone (p less than 0.05). Naloxone also produced a significant increase in ACTH, cortisol and beta-endorphin when compared with placebo. TSH, triiodothyronine, thyroxine, insulin, glucagon and blood glucose showed no significant differences between both days of the trial. The effect of naloxone on growth hormone and prolactin secretions in obese humans can thus be regarded as a partial normalization. We therefore conclude that the hypothalamic regulatory disturbance of growth hormone and prolactin secretions in the obese could be caused by raised opiate levels.
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PMID:Naloxone increases the response of growth hormone and prolactin to stimuli in obese humans. 303 2

Administration of monosodium glutamate to neonate rats causes hypothalamic lesions in the region of the nucleus arcuatus and the eminentia mediana, followed by massive accumulation of triglycerides, diminished secretion of growth hormone, reduced body length and organ weights and diminished number of adipocytes (hypoplastic-hypertrophic obesity). Locomotor activity of obese animals is reduced by about 50%. Food intake is increased by about 10% during growth and development of obesity but decreased beneath the level of that in control animals in the stationary phase of obesity. Hyperinsulinemia coupled with insulin resistance develops in the stationary phase of obesity, i.e. when adipocyte diameter has reached approximately 100 microns. The effects of reduced secretion of growth hormone are considered to be a main factor of fat accumulation in this type of obesity.
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PMID:Development of hypothalamic obesity in growing rats. 306 67

Although, in many respects and from a metabolic point of view, obesity and AN are clearly two opposite pathological conditions, the available data concerning insulin sensitivity in these two syndromes are not so obviously opposite. Indeed, whereas everybody is convinced that obesity is characterized by an increased insulin resistance, the papers reporting insulin sensitivity parameters in AN contain some apparently contradictory results. The observations of simultaneously low fasting blood glucose and plasma-insulin levels in anorectic patients could suggest increased insulin sensitivity in AN. However, if this is the case, it would be present despite other metabolic and hormonal changes (increased plasma concentrations of free fatty acids, cortisol, and growth hormone) which are known factors of insulin resistance. During an oral glucose-tolerance test, an impaired glucose-tolerance occurring despite sustained insulin response to glucose is usually found in anorectic patients before treatment; these abnormalities are, at least partially, reversed after successful refeeding. From these results, such conclusive, if indirect, evidence exists for relative insulin insensitivity in untreated AN. Similar results were initially reported with the intravenous glucose-tolerance test. Typically, the coefficient of glucose assimilation K was reduced in anorectic patients before treatment and increased after realimentation. This seemed to occur despite a relative increase in insulin response to glucose, which again may be related to insulin resistance in these undernourished subjects. However, more recent data demonstrated that the early insulin response is significantly lower in anorectic patients than in controls and that more than half of these patients have normal glucose-tolerance despite decreased peripheral plasma insulin levels. These latter observations, on the contrary, suggest an increased insulin sensitivity, at least in some patients with AN. Only the recently developed minimal model method allows us to discriminate between changes in insulin secretion and action after intravenous glucose injection and thus to infer accurately the sensitivity of the tissues to insulin. Unfortunately, this technique has not been applied to anorectic patients, until now, to solve the controversy. The simplest way to assess the action in vivo of insulin is to perform an intravenous insulin-tolerance test. However, the initial findings with this test, which showed exaggerated fall in plasma-glucose values and delayed return to basal levels after intravenous injection of insulin in AN, do not necessarily mean increased insulin sensitivity in these self-starved patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Insulin sensitivity in anorexia nervosa: a mirror image of obesity? 306 98

The effect of one of the new human pancreatic growth hormone releasing factors (hpGRFs) was assessed in children or young adults with different forms of growth retardation or endocrine-metabolic diseases. Intravenously administered synthetic hpGRF-40 (1 microgram/kg) induced a clear-cut and prompt rise in plasma growth hormone (GH) levels in 8 normal prepubertal children and a definite GH rise in 11 out of 14 children with isolated GH deficiency (IGHD) and one child with the Silver-Russel syndrome. In two out of three subjects with craniopharyngioma hpGRF-40 did not induce any plasma GH increase. In seven out of ten children with constitutional growth delay (CGD), hpGRF-40 induced a biphasic GH response, with a prompt small GH increment followed by a second, more consistent rise. Both in children with IGHD and with CGD the rise in plasma GH following hpGRF-40 was markedly lower than in controls. In children with CGD the GH response to hpGRF-40 was defective, despite the fact that in most of them the GH response to standard pharmacological stimuli was normal according to generally accepted criteria. hpGRF induced a small but sustained plasma GH rise in four hypothyroid subjects, while in three out of four children with idiopathic obesity the GH response to hpGRF was strikingly reduced. These data demonstrate that hpGRF is a potent stimulus of GH release in normal prepubertal children and a physiological means of investigating GH function in diseases associated with growth impairment.
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PMID:Growth hormone response to hpGRF-40 in different forms of growth retardation and endocrine-metabolic diseases. 308 39

The mechanisms whereby growth hormone (GH) secretion is decreased in human obesity remain obscure. We studied the response of plasma GH and prolactin (PRL) to an I.V. dose of 0.5 mcg/kg of growth hormone releasing factor (GRF) in three groups of children: lean (N = 12), obese (N = 15) and GRF-deficient, i.e. children with complete GH deficiency on the basis of conventional provocative testing and evidence of hypothalamic dysfunction on the basis of thyrotropin-releasing hormone testing (N = 7). Mean (+/- SEM) peak plasma GH after GRF was blunted to the same extent in obese and in GRF deficient children (11.1 +/- 2.2 and 8.3 +/- 2.8 ng/ml) as compared to lean control children (34.7 +/- 4.7 ng/ml). The pattern of PRL response to GRF was however different in GRF deficient children, whose high basal PRL levels increased further after GRF injection, and in obese and lean children, who had n alpha acute change in PRL levels after GRF. Baseline plasma somatomedin C concentrations were low for age in GRF deficient children and tended to be high for age in obese children. On the basis of these discrepant patterns of response of PRL to GRF and plasma somatomedin C concentrations, we conclude that GRF deficiency does not account for the decreased GH secretion observed in obese children.
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PMID:Evidence against growth hormone-releasing factor deficiency in children with idiopathic obesity. 309 43

To elucidate further the role of opioid systems in the neuroendocrine alterations associated with obesity, we investigated the effect of the synthetic enkephalin analogue DAMME in 11 obese subjects and 10 lean controls. Prolactin responses to DAMME were similar in lean and obese, even in those obese subjects who had absent prolactin responses to insulin-induced hypoglycaemia. The obese showed impaired growth hormone release after both DAMME and insulin-induced hypoglycaemia compared to the lean subjects. The discordance of prolactin responses to DAMME and insulin-induced hypoglycaemia in the obese suggests that altered opioid systems are unlikely to account for the hypothalamic dysfunction present in obesity.
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PMID:The effect of enkephalin analogue on pituitary hormone release in human obesity. 310 84

Growth hormone levels following an intravenous bolus injection of 1 micrograms/kg body weight growth hormone releasing hormone were measured in 21 non-obese and 26 obese patients with Type 2 (non-insulin-dependent) diabetes mellitus and in 13 control subjects. Growth hormone responses in non-obese Type 2 diabetic patients were not statistically different from control subjects. However, obese Type 2 diabetic patients had significantly decreased growth hormone responses to growth hormone releasing hormone when compared with non-obese Type 2 diabetic patients (p less than 0.02). In 9 Type 2 diabetic patients growth hormone releasing hormone tests were performed both during hyperglycaemia and after metabolic improvement by insulin treatment. Growth hormone responses before and after insulin treatment were not statistically different. Our data demonstrate that growth hormone responses to growth hormone releasing hormone in non-obese Type 2 diabetic patients do not differ significantly from control subjects; obesity blunts growth hormone responses to growth hormone releasing hormone in Type 2 diabetes mellitus; and growth hormone responses following growth hormone releasing hormone administration in Type 2 diabetes mellitus are not influenced by the state of metabolic control.
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PMID:Effect of growth hormone releasing hormone on growth hormone secretion in type 2 (non-insulin-dependent) diabetes mellitus. 310 23


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