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

Effects of a 24 hour fast were studied in 21 obese children aged 7 to 14 and in 8 controls. Mean blood glucose (BG) during fast dropped more in controls (0.88 to 0.54 g/l) than in obese (0.90 to 0.63 g/l) Plasma cortisol changes were similar in the 2 groups, FFA increased (p less than 0.01) in the 2 groups, but the 24 hour mean level was higher in controls (4.0 mEq/l) than in obese (2.06 mEq/l). At the end of the fast, a ketonuria was present in all obese children except 2. Serum alanine dropped similarly in obese (28 to 24 muM p. cent ml) and in controls (30 to 22 muM p. cent ml). All obese exhibited at the end of the fast a significant rise (p less than 0.01) of branched chain aminoacids, not observed in controls. Responses to glucagon (0.03 mg/kg I.M.) were studied before and after fast. At time 0, BG response was higher and more prolonged in obese in spite of hyperinsulinism. At time 24 hours, BG raised from 0.50 to 0.74 g/1 and insulin from 8 to 35 muU/ml in controls, while in obese BG raised from 0.63 to 1.06 g/l and insulin from 25 to 88 muU/ml. Concomitant hyperinsulinsim and biological criteria of hypoinsulinism demonstrated in obese children the peripheral resistance to insulin. The contrast between a normal degree of protein gluconeogenesis and a reduced rate of fat mobilization during fast may be a major biological feature of obesity in childhood.
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PMID:Effect of 24 hour fast in obese children. 100 33

Weanling Sprague-Dawley rats received bilateral anodic electrolytic lesions with platinum-iridium (PtIr) electrodes in the ventromedial (VMN) and dorsomedial (DMN) hypothalamic areas. Sham-operated rats served as controls. The rats were maintained for 48 days (experiment 1) and 33 days (experiment 2) and food intake, body weight (b.w.), nose-tail length and obesity index were recorded. The data of both experiments indicate that all parameters change in the same direction, as they do when lesions are produced with anodic stainless steel electrodes: in the VMN-P-lesioned animals, b.w. gains and overall mean food intake were normal, carcass fat increased and linear growth was reduced. In experiment 2, however, there was a temporary hyperphagia during the 1st 2 weeks of the study. In the DMN-lesioned rats, both ponderal and linear growth and food intake were decreased but body composition was normal. Plasma obtained at sacrifice in experiment 2 showed slight but significant hyperinsulinemia in the VMN rats (p less than 0.02 vs control and p less than 0.05 vs DMN rats). Prolactin (PRL) levels, on the other hand, were higher in the DMN-lesioned rats (p less than 0.05 vs control and p less than 0.02 vs VMN rats). The data indicate that the changes characteristic of the weanling rat VMN and DMN syndrmes are due to 'true' tissue destruction rather than to artifactitious side effects of the lesions. They also suggest, therefore, than an 'irritative focus' hypothesis is not required to account for the observed alterations. They further suggest that the DMN may play role in the control of PRL release.
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PMID:Production of weanling rat ventromedial and dorsomedial hypothalamic syndromes by electrolytic lesions with platinum-iridium electrodes. 102 49

The pathophysiologic considerations support the causal relationship between the secular trend of sugar consumption in industrialized society and the development of prenatal acceleration, which is evident on the basis of epidemiological data. The excessive consumption of sugar and the other quickly absorbed "refined" carbohydrates enhances the hormonogenic effect of food which is also potentiated by the proteins. Together with the caloric overloading, provoked also by the excess in fat, characteristic for the affluent society, the excessive sugar consumption enhances in the pregnant women obesity and "protodiabetes" (PFEIFFER), in the predisposed child the tendency to hyperinsulinism with its consequences. In a prediabetic mother with normal glucose-tolerance the regularly repeated postprandial overfloating of the fetus with maternal glucose changes the feto-maternal hormonal regulation and enhances together with the overloading of substrate, i.e. energy and elements of biosyntheses, the accelerated fetal growth and especially the obesity of the large baby.
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PMID:[Sugar consumption and prenatal acceleration. II. Studies on the etiology and pathophysiology of secular prenatal acceleration]. 103 12

An effort was made to determine to what degree the hyperinsulinemia found in the genetically obese Zucker rat is the result of the carbohydrate content of the diet. When Zucker obese rats are fed precisely the same amount of carbohydrate as lean controls and allowed to become obese by drinking vegetable oil, their pancreatic islets still release 59% more insulin than do those from lean controls. When their diet contains even more carbohydrate, fed from weaning, and they become equivalently obese, their islet insulin release is increased by an additional 46%. An obese Zucker rat fed a high-carbohydrate diet possesses muscle sensitivity to insulin and enlarged adipocytes undergoing active lipogenesis. A rat becoming equivalently obese on a high-fat diet has an absence of insulin sensitivity in muscle and diminished lipogenesis in adipocytes. Clearly, the composition of the diet plays an important role in the metabolic consequences of obesity, but neither diet nor changes in peripheral glucose metabolism can completely explain the hyperinsulinemia.
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PMID:Pancreatic insulin release and peripheral tissue resistance in Zucker obese rats fed high- and low-carbohydrate diets. 109 Nov 58

The hormone-substrate milieu has been investigated in male fasted lean (C57BL/6-+/+) mice and mutant obese mice of the same strain (C57BL/6-obob). The lean mouse, in winter, mobilized insufficient fat (due to inadequate stores) to permit survival beyong 3 days and was unable to achieve any degree of conservation of vital protein stores. By contrast, in summer, the same animals survived 7 days and showed evidence of greater and more sustained fat mobilization and ketosis and the ability to conserve protein. The insulin, glucagon, and insulin/glucagon molar ratios changed in both groups in a direction consistent with conversion to a catabolic state, and hence were probably largely responsible for the mobilization of substrates and stimulation of gluconeogenesis and ketogenesis. The seasonal difference in response is unexplained. The obob mice, generally employed as a model for obesity, hyperglycemia, and hyperinsulinemia showed these features but also adapted to fasting in a fashion permitting prolonged survival during this state. In a fashion analogous to that known to occur in man, these animals developed fall in glycemia, rise in circulating fat-derived substrates, and marked protein conservation. Profound fall in insulinemia was associated with a fall in glucagonemia, the latter from normal levels. Thus the initial markedly "anabolic" insulin/glucagon molar ratio diminished, but nevertheless remained higher than at any time in the lean mice. Pancreatic contents of insulin showed markedly different changes with fasting in obob compared with lean mice. The ability of the obese mouse to adapt to prolonged fasting in a fashion largely analogous to that of man renders it a useful model for the study of metabolism in this state, with the potential of applicability of findings to man.
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PMID:Hormone-substrate responses to total fasting in lean and obese mice. 109 42

The dynamics of insulin secretion from pancreatic islets of the Zucker-obese rat were studied by in vitro perfusion of individual islets. Glucose and L-leucine were used as insulinogenic stimuli. Control pancreatic islets were obtained from both normal weight Zucker-thin littermates and equivalent weight Sprague-Dawley rats. Our results demonstrate that pancreatic islets from 13-wk-old Zucker-obese rats hypersecrete insulin in the basal state and in response to both glucose and amino acid (L-leucine) stimuli. Neither pancreatic islets from control Zucker-thin littermate animals (matched with the Zucker-obese animals for age or for total body weight), nor islets from Sprague-Dawley rats of comparable age and weight demonstrate comparable hypersecretion of insulin. These findings; i.e., hypersecretion of insulin from obese pancreatic islets, suggest that the plasma hyperinsulinism characteristic of the obese state is maintained, at least in part, by an inherent abnormality of beta cell secretion. Whether this abnormality in beta cell secretion results from a genetic trait in the Zucker-obese strain or is induced by the insulin resistance of the obese animal is not resolved by this study. In any case, the observed in vitro hyperinsulin secretion from these islets supports the postulation that in vivo peripheral insulin resistance characteristic of obesity may be a physiological response that protects the animal from insulin-induced hypoglycemia.
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PMID:Insulin secretion by perfused islets from the obese Zucker rat. 109 49

The fat cells of rat epididymal adipose tissue contain an average of 0.5 mg of cholesterol per gram of triglyceride. Of this cholesterol, 90% is nonesterified and 80% is located in the lipid storage compartment. The fat cell cholesterol content correlated positively with cell size. During fasting the free cholesterol of the adipocyte decreased in parallel with triglyceride, whereas the amount of esterified cholesterol did not change. The fat cell cholesterol content is independent of the amount of dietary cholesterol. On in vitro incubation of rat fat cells with radiolabeled acetate, mevalonate, glucose, leucine, or water, labeled cholesterol was synthesized. The rate of cholesterol synthesis increased with fat cell size. Fasting suppressed cholesterol synthesis by 90%, whereas refeeding stimulated the synthesis above values found in normally fed rats. Stimulation of lipolysis with theophylline or with dibutyryl cyclic AMP markedly inhibited cholesterol synthesis in fat cells. Insulin increased the incorporation of glucose and leucine into fat cell cholesterol. The cholesterol synthesis in fat cells was not suppressed by a high cholesterol diet. Addition of very low or low density lipoprotein into the incubation medium suppressed fat cell cholesterol synthesis whereas high density lipoprotein did not. The lipoprotein-free serum stimulated cholesterol synthesis compared with serum-free medium. The rate of cholesterol synthesis in total adipose tissue of rat was estimated to be 4% of that in the liver. It seems unlikely that the increased body cholesterol turnover present in obesity is accounted for by the enhanced cholesterol formation in the enlarged adipose tissue.
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PMID:Regulation of cholesterol synthesis and storage in fat cells. 112 58

By mating mice heterozygous for the recessive gene, obese (ob/+) (+/+), with mice homozygous for the recessive gene, dwarf (+/+)(dw/dw), and subsequent mating of the offspring, mice homozygous for both the obese and dwarf gene were obtained. It was established that the genes for obese and dwarf mice belong to different linkage groups. The homozygous obese dwarf mice develop obesity and hyperinsulinemia. The degree of hyperglycemia developed by these homozygotes is not significantly different from that of nonobese dwarf mice. Because homozygous dwarf mice are deficient in growth hormone production, it was concluded that obesity and hyperinsulinemia can develop under conditions of extreme growth hormone deficiency.
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PMID:Development of the obese-hyperglycemic syndrome in mice with a growth hormone deficiency. 112 28

Aspects of carbohydrate and lipid metabolism were studied in 50 nondiabetic African subjects living in Johannesburg. Twenty-six of them were overweight, invariably associated with a high-carbohydrate intake. In general, the obese group demonstrated significantly raised serum insulin levels, normal glucose tolerance, normal fasting serum triglycerides, and significantly elevated serum cholesterol concentrations. However, the degree of obesity was not significantly correlated with any of these metabolic variables--notably basal or stimulated insulin levels. This suggests that the obese state, per se, was not the major cause of the hyperinsulinemia, and that other factors influenced individual insulin responses or sensitivity. Inconsistently excessive dietary carbohydrate ingestion and an unusual degree of physical activity may have been important. A striking correlation emerged between fasting serum triglycerides and insulin concentrations (both basal and stimulated); the possibility that this reflects acceleration of hepatic triglyceride synthesis by insulin is discussed. The concept of obesity invariably producing insulin resistance and progressive compensatory hyperinsulinism may not apply in all environmental conditions.
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PMID:Insulin, glucose and triglyceride relationships in obese African subjects. 113 Mar 21

In 13 obese children plasma triglyceride concentrations were found to be significantly elevated, while plasma cholesterol concentrations were normal. In the hypertriglyceridemic obese children, the plasma fractional triglyceride removal, measured by the intravenous fat tolerance test, was significantly reduced. These abnormalities reverted to normal in 8 patients retested after weight loss. Plasma postheparin lipoprotein lipase activity was found to be increased and significantly related to the degree of obesity. As to carbohydrate metabolism, a decreased glucose tolerance and hyperinsulinemia were found. Hyperinsulinemia reverted to normal during dietary restriction, glucose intolerance did not.
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PMID:Plasma triglyceride clearing in obese children. 114 45


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