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

Insulin, proinsulin and glucagon extracted from lean rat pancreases were studied in radioimmunoassay, radioreceptorassay and bioassay systems. Extracted insulin behaved identically to a rat insulin used as a reference standard in radioimmunoassay. On the basis of its immunoreactivity, extracted insulin was slightly less potent (about 70%) than the rat standard insulin in competing with the binding of 125I-insulin to rat liver membranes (radioreceptorassay) and in stimulating glucose oxidation by rat fat cells (bioassay). Extracted glucagon and a pork glucagon used as a reference standard were indistinguishable in two radioimmunoassay systems for glucagon, in competing with the binding of 125I-glucagon to rat liver membranes (radioreceptorassay) and in stimulating adenylate cyclase in rat liver membranes (bioassay). Genetically obese rats (Zucker, "fatty") were compared to their lean littermates with respect to insulin, proinsulin and glucagon extracted from their pancreases. Proinsulin represented the same proportion of total immunoreactive insulin in both types of rats. In the radioimmunoassays, the radioreceptorassays and the bioassays, insulin, proinsulin and glucagon from obese rats were indistinguishable from insulin, proinsulin and glucagon from lean rats. It is concluded that the pancreatic hormones of obese ("fatty") rats possess the same immunoreactivity and biological potency as those of nonobese rats. This excludes the possibility that some alteration in the biological properties of pancreas insulin and/or glucagon of fatty rats could explain the metabolic abnormalities observed in this type of obesity.
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PMID:Glucagon and insulin from lean rats and genetically obese fatty rats: studies by radioimmunoassay, radioreceptorassay and bioassay. 120 22

Glucagon concentration and regulation were examined in the Zucker rat, in which obesity and hyperlipemia are phenotypic expressions of an autosomal recessive gene. Using littermate animals which are phenotypically thin and normolipemic as controls, we observed reduced basal plasma glucagon levels in the obese lipemic rats. In response to fasting, obese lipemic animals inappropriately demonstrated a further reduction in plasma glucagon concentration. In response to pharmacologic glucagon stimulation (arginine), a subnormal rise in plasma glucagon concentration was observed in the obese, lipemic animals. Glucagon suppressibility with exogenous glucose remained intact. The reduced secretion of glucagon may be a consequence of the abnormal elevation in concentration of plasma insulin, free fatty acids, and glucose, which are characteristic of the obese, lipemic animal. A possible role of glucagon deficiency in the evolution or maintenance of the lipemic state is suggested.
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PMID:Endogenous glucagon regulation in genetically hyperlipemic obese rats. 127 76

Fifty-eight patients with biochemical reactive hypoglycemia (blood glucose 45 mg% or less after a 100 g OGTT) were tested, of whom 11 subjects were obese with normal glucose tolerance, 9 were obese with chemical diabetes, 9 had chemical diabetes without obesity, 6 had undergone gastrectomy, 7 had renal glycosuria and 16 were apparently isolated. An exaggerated insulin response to oral glucose was associated with reactive hypoglycemia in the post-gastrectomy syndrome, in normal-weight patients with chemical diabetes and 44% of the patients with the isolated syndrome. In contrast, plasma-insulin values cannot account for the reactive hypoglycemia observed in obese patients (with or without chemical diabetes), in subjects with renal glycosuira and in 56% of the patients with the isolated syndrome. A study of pancreatic-glucagon secretion in a group of twelve subjects with "isolated normoinsulinemic reactive hypoglycemia" failed to demonstrate any significant abnormality in the secretion of this hormone during oral glucose tolerance test or intravenous insulin tolerance test. As suggested by Permutt et al. (1973) biguanide therapy may be useful in the treatment of patients presenting severe and symptomatic reactive hypoglycemia which does not respond to classical dietary management.
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PMID:Studies on the pathogenesis of reactive hypoglycemia: role of insulin and glucagon. 127 43

The chronology of changes in body weights, food intakes and plasma concentrations of selected metabolic hormones and metabolites were determined in sheep during the induction (dynamic) and static phases of diet-induced obesity. Lean adult Dorset ewes weighing 47 kg were fed a pelleted hay-grain diet at maintenance (lean; n = 7) or were fed the same diet ad libitum to a maximum intake of 3 kg.sheep-1.d-1 (obese; n = 8) for 78 wk. Body weight of obese sheep doubled (97 vs. 47 kg) by wk 42 of ad libitum intake. Average daily intakes of dry matter (12.8 g/kg) and digestible energy (165 kJ/kg) were comparable in maintenance-fed lean sheep and ad libitum-fed obese sheep consuming maintenance after wk 50, which began the static phase of obesity. Fasting plasma concentrations of insulin in the obese sheep increased steadily from 50 +/- 6 pmol/L at wk 0 to a sustained plateau of 249 +/- 21 pmol/L after wk 30. Plasma levels of glucose, immunoreactive glucagon and thyroid hormones were consistently greater (P less than 0.05) in obese sheep than in lean sheep after wk 2, 3 and 25, respectively, of the experiment. Concentration of lipid (49 vs. 25%) in the carcass stripped of internal fat was greater (P less than 0.01) in obese sheep than in lean sheep, but concentration of protein (10.4 vs. 15.3%) was less in the heavier carcass (58 vs. 24 kg) of the obese sheep. We conclude that hyperinsulinemia and abnormal fuel metabolism are early events during dynamic obesity and these defects persist throughout the static phase of obesity. Maintenance energy requirements relative to unit body weight (W1.0) seem similar in lean and dietary obese sheep.
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PMID:Dynamic and static phases of severe dietary obesity in sheep: food intakes, endocrinology and carcass and organ chemical composition. 154 7

This study was initiated to elucidate the mechanisms behind valproate-induced weight gain. Eight patients with epilepsy were studied with identical examination programs before and during the end of the first month of treatment with sodium valproate (VPA). The measurements included registration of food intake, indirect calorimetry, and determination of pancreatic and thyroid hormones, catecholamines, albumin, electrolytes, glycerol, and free fatty acids. Measurements were performed both at the basal condition and during a 3-hour oral glucose tolerance test (OGTT). After the start of VPA treatment, the mean levels during the OGTT of plasma glucose and catecholamines were significantly decreased by 7% and 25%, respectively (P less than .05). The mean ratio of insulin to glucagon decreased by 37% (P less than .01). During the glucose load, the decreases in free fatty acids were less pronounced after the start of VPA treatment, whereas the mean levels of glycerol were found to be unchanged. We detected no differences between the two periods with regard to total energy intake or macronutrient selection, energy expenditure, or thyroid hormones. As VPA is known to affect the concentration of carnitine in humans, it is hypothesized that a possible VPA-induced deficiency of the beta-oxidation of fatty acids is important for the development of obesity in epileptic patients in long-term treatment with VPA, but changes in catecholamines or other hormones might also be of importance.
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PMID:Metabolic changes during treatment with valproate in humans: implication for untoward weight gain. 164 Aug 53

Neuropeptide Y (NPY) concentrations were measured by radioimmunoassay in eight microdissected hypothalamic regions of obese (fa/fa) and lean (Fa/?) Zucker rats. Freely fed obese rats showed significant (40-100%) increases in NPY concentrations in several regions, notably the paraventricular, ventromedial, and dorsomedial nuclei and the arcuate nucleus/median eminence, compared with lean rats. Hypothalamic NPY concentrations were not affected in either obese or lean rats by food restriction, which caused 25% weight loss over 3 wk. Refeeding to initial weight significantly increased NPY levels in the ventromedial and dorsomedial nuclei in lean rats but did not significantly alter NPY concentrations in any hypothalamic region in obese rats. These observations indicate fundamental differences in the regulation of hypothalamic NPY between obese and lean Zucker rats. NPY injected into the paraventricular nucleus and other regions causes hyperphagia, obesity, and increased secretion of insulin, glucagon, ACTH, and corticosterone. These behavioral and neuroendocrine abnormalities all occur in the obese Zucker syndrome and may be due to increased NPY-ergic activity in the hypothalamus.
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PMID:Altered neuropeptide Y concentrations in specific hypothalamic regions of obese (fa/fa) Zucker rats. Possible relationship to obesity and neuroendocrine disturbances. 165 67

The beta 3-adrenoceptor agonist, BRL 26830A, which is not inhibited by either beta 1 or beta 2-selective antagonists, has been shown to possess anti-obesity and anti-diabetic actions. However, the effects of this agent on insulin and glucagon release have not yet been substantiated. Therefore, we tested the hypothesis that BRL 26830A promotes insulin and glucagon secretion via beta 3 receptors on pancreatic islet B and A cells. In ICR mice fasted for 48 h, BRL 26830A significantly stimulated insulin secretion from 5 min after administration, markedly decreased blood glucose levels from 30 min after administration, and significantly increased glucagon secretion from 30 min after administration. The administration of a non-selective beta-receptor antagonist, at a dose of 50 mg/kg, 30 min prior to BRL 26830A injection completely abolished the effects induced by BRL 26830A. However, the administration of a beta 1-selective antagonist at doses of 50 or 100 mg/kg did not produce any significant effects. On the action of BRL 26830A, whereas the administration of a beta 2-selective antagonist at 50 mg/kg, a near maximal effective dose, partially abolished the effects of BRL 26830A. BRL 26830A had no effect on insulin, glucagon, or glucose levels in streptozocin (STZ) diabetic mice fasted for 48 h. These results suggest that, in mice, BRL 26830A may promote insulin secretion mainly via beta 3 receptors and partially via beta 2 receptors on pancreatic-islet B cells, and that glucagon may be secreted as the result of hypoglycemia induced by this agent.
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PMID:Effects of a beta 3-adrenoceptor agonist, BRL 26830A, on insulin and glucagon release in mice. 168 48

To determine whether hyperinsulinaemia of human obesity is dependent on the activity of the parasympathetic nervous system, and whether activation of the parasympathetic nervous system plays a role in glucose-induced thermogenesis, the metabolic effect of a continuous intravenous glucose infusion [44.4 mumol kg-1 body weight (bw) min-1] with or without atropine infusion was assessed in 11 obese patients and 10 lean controls. Compared with lean controls, obese patients had increased basal and glucose-stimulated plasma insulin and C-peptide concentrations and increased plasma glucose concentrations during glucose infusion. Glucose oxidation during i.v. glucose was lower in obese patients than in lean controls. Glucose-induced thermogenesis was similar in obese patients and in lean controls. Atropine infusion did not affect basal plasma glucose, insulin or free fatty acid concentrations nor glucose-stimulated plasma glucose, insulin, C-peptide, glucagon or free fatty acid concentrations in both groups of subjects. Glucose and lipid oxidation rates and glucose-induced thermogenesis were also unaffected by atropine administration. It is concluded that (1) glucose-stimulated hyperinsulinaemia in human obesity is not dependent on a hyperactivity of the parasympathetic nervous system, which indicates that human obesity is different from most animal models of obesity; (2) glucose-induced thermogenesis is similar in obese and lean subjects when a similar load of glucose is administered; (3) inhibition of the parasympathetic nervous system does not affect the thermic effect of i.v. glucose.
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PMID:Effects of muscarinic blockade on insulin secretion and on glucose-induced thermogenesis in lean and obese human subjects. 177 22

The present study was performed using indirect calorimetry to test the hypothesis of a reduction of the basal energy expenditure in obese prepubertal children. The obese and control children studied were comparable regarding age, height and fat-free mass (FFM). Total weight and body fat percentage were significantly greater in the obese children. Plasma insulin and glucagon concentrations were significantly higher in obese than in control children. In the two groups of children the basal metabolic rates (BMRs) were comparable in both absolute values and values adjusted for FFM, age and gender utilizing the multiple regression analysis. The most important variable to predict BMR was FFM, followed by age. BMR was significantly correlated with FFM, both for obese and control children, and also when the two groups were combined. In conclusion, our data do not support the idea that a child's obesity is maintained by increased metabolic efficiency at least in basal conditions.
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PMID:Basal energy expenditure in obese and normal weight schoolchildren. 178 86

The long-term results of dietary treatment for obesity are often very poor. To predict the effect of a hypocaloric diet, it may be important to consider factors that could influence energy expenditure, especially those altered in obesity. Elevated plasma levels of glucagon are associated with obesity. In this study, the relationship of glucagon to resting metabolic rate (RMR) and glucose-induced thermogenesis (GIT) has been investigated. RMR and GIT, after ingesting 100 g glucose, were measured by indirect calorimetry in 25 obese premenopausal women (body mass index [BMI], 37.2 +/- 4.7 kg.m-2). RMR was significantly related to fat-free mass (FFM) (r = .50, P less than .005). A significant relation could be found between RMR and fasting glucagon levels (r = .36, P less than .05). Plasma glucose and insulin levels were not predictive for RMR. Mean GIT increased with increasing waist-hip circumference ratio (WHR) (r = .71, P less than 0.0001), confirming previous findings of our group. No relation was found between GIT and glucagon levels, neither in the basal state nor after glucose. The only important metabolic determinant was area under the curve (AUC) for glucose (r = .45, P less than .01), suggesting a higher GIT in obese women with impaired glucose intolerance. This suggests that the control of energy metabolism by the concentration of glucagon may be more important in the fasting state than after a meal. Plasma glucagon concentration should be considered in the evaluation of RMR.
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PMID:Importance of glucagon as a determinant of resting metabolic rate and glucose-induced thermogenesis in obese women. 187 Apr 20


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