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

Peripheral serum insulin and C-peptide concentrations during oral glucose tolerance tests were measured in 10 nondiabetic Pima Indians and 10 nondiabetic Caucasians with varying degrees of obesity. Although both insulin and C-peptide levels were elevated in the Indians compared to the Caucasians (p less than 0.05), hepatic insulin extraction, measured by comparing the C-peptide to insulin ratios, was similar over a wide range of insulin concentrations in both groups. The ratios of C-peptide to insulin were independent of the degree of obesity. These studies indicate that the peripheral hyperinsulinemia in Pima Indians and obese subjects is due in general to pancreatic hypersecretion rather than to diminished hepatic extraction of insulin.
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PMID:C-Peptide and insulin secretion in Pima Indians and Caucasians: constant fractional hepatic extraction over a wide range of insulin concentrations and in obesity. 42 4

The acute effect of bilateral electrolytic ventromedial hypothalamic lesions (20-25-m Coulomb stainless steel electrodes) on plasma levels of insulin and glucose was studied in anesthetized rats to determine early effects that would occur before hyperphagia and obesity. In rats fed ad libitum, lesions in the ventromedial hypothalamus (VMH) but not in the cortex produced a marked increase in circulating insulin levels (starting at 20 min postlesion) and a small increase in glycemia which, however, was not significant and could therefore not be the cause of increased insulin secretion. Hyperinsulinemia after VMH lesions was more pronounced when glucose was infused iv at a rate of 7-8 mg/kg . min. Bilateral subdiaphragmatic vagotomy, performed 50 min after VMH lesions, immediately and completely reversed the observed hyperinsulinemia. With the exception of a tendency of lesions producing the highest degree of hyperinsulinemia to be slightly larger than the lesions not producing any hyperinsulinemia, no statement about the critical involvement of a specific hypothalamic locus can be made. It is concluded that electrolytic VMH destruction causes immediate hypersecretion of the pancreatic B cell, an effect that requires the integrity of the vagus nerves. Further localization of the central circuitry responsible for this mechanism, however, will require more specific methods than electrolytic lesions.
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PMID:Acute hyperinsulinemia and its reversal by vagotomy after lesions of the ventromedial hypothalamus in anesthetized rats. 44 4

1) Protein restricted diets decrease basal plasma insulin levels in obesity. 2) This effect occurs even in the presence of sufficient calories to maintain body weight and while the diet is high in carbohydrate. 3) The decrease in insulin is accompanied by a fall in plasma glucose and in the I/G ratio, suggesting an increase in insulin sensitivity. 4) Excessive protein intake, in addition to carbohydrate, may play a role in the pathogenesis of the hyperinsulinemia and insulin resistance found in obesity.
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PMID:Suppression of insulin secretion by protein deprivation in obesity. 49 74

The effect of intravenous injection of 0.1 I.U./kg insulin on blood glucose response and on lipolysis, induced by intravenous infusion of 0.2 microgram/kg - min norepinephrine, were studied in 12 normal subjects and 17 obese patients with normal 50 g oral glucose tolerance test and normal thyroid function. In the obese group the insulin-induced hypoglycemia during norepinephrine-infusion was significantly less than in normal subjects. Moreover, the inhibition of norepinephrine-stimulated FFA and glycerol-release by insulin was significantly less in obesity as compared with the non-obese group. It is concluded that in obesity the action of insulin is decreased both in carbohydrate metabolism and in lipolysis. These results provide arguments for the role of an impaired antilipolytic insulin effect in the pathogenesis of hyperinsulinism in obesity.
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PMID:[Effect of insulin on stimulated lipolysis in obesity with normal carbohydrate tolerance and unimpaired thyroid function]. 59 Feb 7

The methods utilized in our laboratory for a biochemical approach of obesity include dietary manipulations, fatty acid analysis of tissue lipids, in vivo lipogenesis from [3H H2O and [1-14C] acetate, in vitro utilization of [3H] H2O, [U-14C] glucose, [U-14C] fructose, [U-14C] alanine and [1-14C] acetate by adipose tissue fragments, hormone sensitivity (to insulin and catecholamines), and the activity of enzymes such as fatty acid synthetase and adenylate cyclase in adipose tissue extracts. With these methods at hand, it is possible to estimate the major biochemical factors responsible for fat accumulation in adipose tissue. As an example, the case of obese (ob/ob) homozygotic animals of the C57BL/6J strain of Bar Harbor, which suffer from an autosomal recessive obese-hyperglycemic (O-H) syndrome, is compared to that of control nonobese (ob+/ob+) mice from the same strain. The hereditary O-H syndrome in ob/ob mice is characterized by obesity, resistance to the action of insulin, and hyperinsulinism. The development of obesity depends on high lipogenesis in fat depots. Contribute also to obesity a large influx of fatty acids of hepatic and dietary origin, and reduced lipolysis. In these mice, a high fat diet is more propitious to fat accretion than a high-carbohydrate diet.
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PMID:Experimental basis of obesity. 62 36

Metabolic parameters were studied in 6 patients before and for 18 months after jejunoileal bypass for obesity. The postoperative changes in plasma concentration of amino acids were characterized by a decrease in essential amino acids, while the non-essential amino acids were unchanged or elevated, indicating a state of protein-caloric malnutrition. The pattern of fatty acids in serum the first year after operation: an unchanged sum of unsaturated and saturated fatty acids accompanied by a significant fall in linoleic acid and a corresponding increase in oleic acid, showed that even during this period the patients were in a state of essential fatty acid deficiency. The oral glucose tolerance test and the levels of serum immunoreactive insulin activity indicated a general improvement in glucose tolerance and a normalization of preoperative hyperinsulinism. A 40-50% reduction was found both in serum triglycerides and cholesterol levels. Serum iron was reduced by approximately 30%, whereas TIBC levels remained unchanged. The Schilling test showed a significant fall in vitamin B12 absorption postoperatively with subnormal values at 6 and 12 months. Vitamin B12 in serum dropped, but remained within the normal range, suggesting that the preservation of 25 cm of distal ileum is sufficient to secure adequate absorption of vitamin B12. Folic acid levels in serum fell after the bypass, demanding supplementation in 5 of the 6 patients at 6 months postoperatively.
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PMID:Metabolic changes after jejuno-ileal bypass for obesity. 63 57

1. The syndrome of obesity induced by neonatal injection of monosodium glutamate (MSG) has been further studied in mice. In confirmation of previous studies stunting and decreased pituitary and gonadal weights were observed. 2. After weaning food intake was consistently less in MSG-treated than control mice. Body lipid stores were significantly elevated in MSG-treated mice by 2 weeks of age and increased progressively up to 4 months. 3. Plasma glucose was comparable between MSG-treated and control mice in the fed state whereas after an overnight fast MSG-treated mice exhibited relative hypoglycaemia. 4. Obese MSG-treated mice did not exhibit resistance to exogenous insulin and disposed of an intravenous glucose load more rapidly than control mice. 5. Hyperinsulinaemia was present inconsistently in both fed and fasted mice and in response to administered glucose. 6. Neonatal administration of MSG provides a useful additional model for studying the role of the hypothalamus in obesity.
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PMID:Effects of monosodium glutamate-induced obesity in mice on carbohydrate metabolism in insulin secretion. 63 58

Fasting insulinemie levels and after overload with oral glucose are studied in a group of 30 overweight children aged between 2--12 years. The results are: An increase in insulin secretion according to the age only in the overload test. The insulin and glucose areas in the overweight child is statistically bigger than in the healthy child. We conclude that hyperinsulinism in obesity, may be related with a insuline-resistance and with some kind of glucose intolerance.
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PMID:[Fasting insulinemie levels and after overload with oral glucose in overweight children (author's transl)]. 65 11

Plasma lipids and lipoproteins, glucose tolerance, plasma insulin response to glucose load, and liver function were examined in 81 relatives of 12 index cases with primary endogenous hypertriglyceridemia, hyperinsulinemia, and hepatic steatosis, as well as in 90 nonrelatives, including the spouses, as controls. Insulin hypersecretion (with or without glucose intolerance), endogenous hypertriglyceridemia, and abnormal liver function suggesting hepatic steatosis were shown to exist in the relatives mostly in combined fashion. Correlation analysis and stepwise multiple regression analysis revealed that the combined disorder developed on the basis of obesity. The incidence of diabetes mellitus was significantly high in the relatives (14.8 per cent) as compared with the normal Japanese population (3.5 per cent). Although the vertical transmission of the combined disorder was noted in almost all pedigrees, the frequency distribution analysis of insulin response, glucose tolerance, and plasma triglyceride showed the histograms of these variables similarly skewed to the right as compared with those of the controls, with no apparent bimodality. In view of the hitherto suggested role of insulin in triglyceride metabolism, it is concluded that hyperinsulinemia coupled with obesity seems to be the basic trait of this form of familial hypertriglyceridemia and hepatic steatosis, though the mode of transmission remains to be elucidated.
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PMID:Interactions of obesity and glucose-stimulated insulin secretion in familial hypertriglyceridemia. 65 14

Coronary heart disease (CHD) remains an uncommon disorder in the South African Black population. It has been suggested that herein lies an enigma, since it is believed that these people are considerably exposed to the conventional risk factors for CHD. To test this belief I have assessed the exposure of Black people, in time and degree, to the following CHD risk factors: affluence, age, hypertension, hyperlipidaemia, dietary excess, smoking, physical inactivity, diabetes, obesity, hyperuricaemia and hyperinsulinism. Among males only hypertension, and among females only hypertension and obesity, emerged as prominent factors. However, neither of these is significantly atherogenic in the social, nutritional and metabolic milieu in which Blacks generally live, and obesity is a doubtful atherogenic factor, even in westernized populations. It is therefore concluded that the rarity of CHD in Blacks is not enigmatic, but is appropriate to their environmental circumstances.
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PMID:The rarity of coronary heart disease in South African blacks. 69 6


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