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

Plasma obtained from fasted rats provoked a dose-dependent stimulation of fat cell glycerol release and was able to inhibit also generation of prostaglandins E2 and F2 alpha from arachidonate, in vitro, over a very similar range of doses. It is proposed, therefore, that a plasmatic fat-mobilizing factor may act as an endogenous inhibitor of adipose tissue prostaglandin biosynthesis, mediating in the acute (long-term not precluded) regulation of adipose tissue lipolysis. The proposed mechanism of permissive effects of the plasmatic factor in reducing the effects of endogenously-generated inhibitory prostaglandins may be implicated in the development of obesity by reduced availability of the factor and thus reduced ability to utilize fat stores.
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PMID:Permissive effects on adipose tissue lipolysis of a plasmatic factor which inhibits prostaglandin biosynthesis. 55 Jan 59

Metabolic adaptations to cyclic patterns of food intake were studied in genetically lean and obese Zucker rats. Twenty-four lean and 24 obese rats were exposed to 12 hours of light and 12 hours of dark and allowed food ad libitum. Both groups of rats ate more during the dark period of the cycle. The obese consumed nearly twice as much food as the lean during the light period of the cycle. At 4-hour intervals, rats were killed and liver and epididymal fat pads were removed for metabolic studies. Adipose tissue from lean rats demonstrated marked changes in rates of lipogenesis during the 24-hour cycle whereas adipose tissue from obese rats maintained a relatively steady rate of lipogenesis. Glucose incorporation into the glycerol moiety of triacylglycerol was nearly 3-fold higher in adipose tissue from obese rats. Liver lipogenesis in lean and obese rats followed their food intake pattern. Liver lipogenic rate (expressed per organ) was 3- to 5-fold higher in obese than lean rats during most of the 24-hour cycle. These data support the concept that the excessive fatty acids produced in the liver of obese rats are being esterified by adipose cells. Lipolytic response to glucagon was found in adipose tissue from obese rats during the dark and light periods, but only during the dark period for lean rats. These data suggest, in comparison to lean rats, that obese rats do not enter a relative catabolic state during a 24-hour cycle. A constant anabolic state in the genetically prone individual may lead to excessive lipid deposition and obesity.
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PMID:Diurnal changes in adipose and liver tissue metabolism of lean and obese Zucker rats. 57 Oct 11

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

Studies of fat mobilization and transport are reported in six patients with the Prader-Willi syndrome. Two patients had carbohydrate intolerance. One of these had a low and the other an augmented insulin response to glucose challenge. Following challenge with glucose, three of the four nondiabetics had normal insulin responses or increased responses consistent with their obesity; the other nondiabetic had insulinopenia. Measurements of the effects of norepinephrine, insulin, glucose, and 5-methylpyrazole-3-carboxylic acid on plasma levels of FFA, glycerol, and ketones provide no evidence for abnormal regulation of mobilization of fat from adipose tissue. Measurements of plasma lipids and postheparin lipolytic activity are consistent with normal uptake of fat into adipose tissue, and normal fatty acid composition of adipose tissue gives no evidence for abnormal lipogenesis.
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PMID:The Prader-Willi syndrome. Regulation of fat transport. 89 39

It is supposed that the excess of fatty tissue exerts a diabetogenic effect. In obese subjects changes in the reactivity of the enlarged adipocytes to insulin might play a significant role in the pathogenesis of diabetes. Using the method of Rodbell in our own modification the responses of isolated adipocytes obtained from 10 lean and 15 obese subjects to a) insulin, b) theophylline and c) insulin and theophylline jointly (metabolism of glucose and glycerol) were determined. The dose-effect relationship curve was plotted against the effect of glucose utilization caused by increasing concentrations of insulin in the suspensions of adipocytes of lean and obese subjects. In adipocyte donors insulin sensitivity was also determined by Himsworth's test. It was found that adipocytes of 15 subjects with hyperthrophic obesity showed a significantly decreased effect of insulin regulating glucose utilization and glycerol release. They maintained a normal pattern of response to theophylline. The curve of relationship between insulin concentration in the incubation medium and its effect on glucose utilization by the adipocytes was changed. The adipocytes of these donors were relatively refractory to insulin in vivo as determined by the test of Himsworth. The cause of these disturbances may lie in the changed function of insulin receptors in the enlarged adipocytes. The observed disturbances may play a significant role in the pathophysiology of the diabetogenic effect of obesity.
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PMID:Role of disturbed metabolism of fat tissue cells in the pathogenesis of the diabetogenic effect of obesity in humans. 99 68

The metabolic effect of ventromedial hypothalamic (VMH) lesions, which are known to cause hyperphagia and obesity, has been studied in rats kept on a controlled light and food regimen. The animals were sacrificed at 4 different times during the second postoperative day. A feeding-induced hypersecretion of insulin was found to the VMH-lesioned animals. It was accompanied by a marked hypoglycemia as compared to the control groups during the feeding period. The glycogen content of liver and diaphragm in the lesioned groups is increased as compared to the controls during the same period. The VMH-lesioned animals showed hypertriglyceridemia both in the fed and fasted state, whereas the postabsorptive plasma levels of free fatty acids and glycerol were decreased. An increased level of urea was observed in all lesioned groups. This is in accordance with the demonstrated protein catabolism which follows VMH lesions.
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PMID:The effect of ventromedial hypothalamic lesions on metabolism and insulin secretion in rats on a controlled feeding regimen. 102 15

Insulin-carbohydrate relationships were investigated in four groups of young rats fed low protein diets differing in carbohydrate and fat contents: (1) a diet in which the nonprotein energy was provided by fatty acids (FA); (2) a similar diet in which the fatty acids were substituted by neutral fat (NF); (3) FA diet supplemented with glycerol (FA-Glyc); and (4) a carbohydrate-rich diet (HC). Control rats were fed a stock diet. Rats fed the FA diet lost weight, were hypoglycemic and hypoinsulinemic in the fed state and normoglycemic and normoinsulinemic in the fasted state, and had an impaired glucose tolerance and hyperinsulinemia after a glucose load. Liver and muscle glycogen were low in fed rats. Fasting increased glycogen in liver and decreased glycogen in muscle. NF animals gained weight, were hypoglycemic in both fed and fasted states, and their plasma glucose level after an oral glucose load was almost normal. Plasma insulin/glucose ratio, both in fed and fasted states and after a glucose load indicated hyperinsulinism, which was accompanied by obesity. Muscle and liver glycogen were low in fed animals and did not change after a fast. Supplementation of the FA diet with glycerol (FA-Glyc) abolished weight loss and fasting hyperglycemia and normalized plasma glucose and insulin response to a glucose load. Rats fed the HC diet had an improved glucose tolerance and an increased sensitivity to insulin. Liver glycogen was high in the fed state and normal in the fasted state, whereas muscle glycogen was normal in both nutritional states.
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PMID:Effects of carbohydrate-free diets on the insulin-carbohydrate relationships in rats. 115 29

In altogether 32 test persons with normal weight and obese test persons glucose-insulin-tolerance-tests were carried out. In obese persons with normal carbohydrate tolerance -- characterized by 50 g oral glucose tolerance test -- by the decreased glucose assimilation coefficients and the significantly increased level of glycaemia after intravenous application of glucose a disturbance of the glucose-insulin-homoeostasis is already implied. Basal and glucose-stimulated concentrations of IRI in the peripheral venous blood were significantly increased in obese persons. The parameters of lipolysis glycerol and free fatty acids show after a glucose-stimulated insulin excretion and after exogenic insulin application a somewhat retarded decrease in obese persons compared with the control group. In connection with the significantly increased insulin levels in obese persons these findings might refer to a decreased antilipolytic effect of insulin. The two fundamental physiological effects of insulin in the carbohydrate and fat metabolism -- glucose utilization and inhibition of lipolysis -- seem to be distrubed in the same way in obesity.
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PMID:[Study on the effect of insulin on carbohydrate and lipid metabolism in obese subjects with normal glucose tolerance]. 118 93

1. In obese patients with normal glucose tolerance the norepinephrine-induced lipolysis in vivo was significantly higher as compared with a non-obese group. This was observed both during weight-related and constant norepinephrine infusion. 2. In the obese group a discordant release of free fatty acids and glycerol and a significantly lower quotient of FFA/Glycerol than in the controls was found. It is supposed that in obesity the re-esterification of FFA is increased.
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PMID:[Studies on lipid mobilization in obesity without glucose intolerance. 1st communication. Noradrenaline-stimulated lipolysis]. 121 97

Concentrations of immunoreactive insulin activity (IRI) and proinsulin activity (IRP), blood glucose, free fatty acids (FFA), glycerol, cholesterol, triglycerides were analyzed in 140 subjects suspect of protodiabetes and 50 healthy persons before, during and after a glucose infusion test (GIT). The protodiabetic subjects were classified into normweight, overweight, obese, hyperlipemic groups with diet or with Regadrin therapy and each of them subdivided into such with normal and such with pathological carbohydrate tolerance. Norm- and overweight subjects with asymptomatic diabetes were characterized by a significant reduction of insulin secretion during both phases. Obese patients with or without hyperlipoproteinemia demonstrated an increased IRI reaction during the late phase of secretion. Carbohydrate intolerance was associated with an enhancement of basal triglyceride levels and a reduced depression of glycerol and FFA during the GIT. There were no differences in fasting or reactive IRP concentrations between healthy and protodiabetic subjects with normal carbohydrate tolerance. In asymptomatic diabetes the IRP levels were increased during the late secretion phase, but the percentage of IRP in total IRI was normal or--in existing high response--significantly reduced in comparison to norm response. The results do not support an enhanced IRP secretion as the cause of carbohydrate intolerance.
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PMID:Effect of glucose infusion on venous blood levels of immunoreactive proinsulin activity, insulin activity and fat parameters in healthy and protodiabetic subjects. 122 47


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