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

Obese and lean Zucker rats, 7 wk old, were swim trained or kept sedentary. Another group of obese rats was food restricted and exercised. Half the rats were killed after training for 8 wk, the remainder were retired and killed after an additional 8 wk. Neither treatment decreased adipocyte size in obese rats. Although basal lipolysis per cell was elevated in obese rats, their adipocytes were insensitive to epinephrine at 15 and 23 wk of age. Exercise training did not affect lipolysis. At all ages, adipose lipoprotein lipase (LPL) capacity was higher in obese relative to lean rats. In obese rats, swim training and exercise plus food restriction increased adipose and gastrocnemius LPL activity and depressed plasma insulin and triglyceride levels. All effects of exercise were transient. Thus, exercise training improved some of the metabolic disturbances in the Zucker obese rat but did not normalize adipocyte size, LPL activity, or lipolysis.
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PMID:Lipoprotein lipase activity and lipolysis after swim training in obese Zucker rats. 663 16

Five-week-old male, Osborne-Mendel rats were fed a control (CON) or high fat diet (HF) (18 and 68% calories as fat, respectively). At 15 weeks of age HF rats weighed more and had a greater percent body fat than CON rats. Half the rats in each diet group were then exercised for 6 weeks on a treadmill. During exercise, food intake was unaffected in both diet groups, while body weight gain was reduced only in HF rats compared to sedentary rats. Exercise lowered fat gain and decreased lipoprotein lipase (LPL) activity in all rats, reduced in vivo lipogenesis in CON rats, and attenuated the development of obesity in HF rats. Following exercise, rats were kept inactive (i.e., detrained) for 2 weeks. Detraining increased food intake, weight gain, fat deposition and LPL activity in comparison to sedentary rats. In CON detrained rats lipogenesis returned to sedentary levels; in all detrained rats retroperitoneal fat cell number increased over that found in exercised rats. Thus, HF feeding induced obesity while exercise attenuated its development. Exercise-induced effects were not long lasting as they were reversed within 2 weeks of exercise termination as evidenced by a rapid increase in food intake, weight gain and lipogenesis.
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PMID:Exercise and detraining: effect on food intake, adiposity and lipogenesis in Osborne-Mendel rats made obese by a high fat diet. 669 4

The genetically obese adult Zucker rat (fafa) exhibits reduced thermogenesis when stimulated by physiological agents (cold, catecholamines). Recent evidence suggests that this thermogenic defect may be important in the manifestation of the animal's obesity and that it reflects a reduced thermogenic contribution from brown adipose tissue, the major nonshivering thermogenic site in many mammals. The present study describes the effects of the obese genotype on brown (and white) adipocyte size, number, and lipid content and tissue lipoprotein lipase (LPL) activity. In the obese rats, brown fat depots were increased in mass. This increase could be accounted for by brown fat hypertrophy (due primarily to an increase in the amount of triglyceride present in each cell) rather than hyperplasia (there being no increase in the number of brown fat cells). In addition, unlike the situation in white fat, the brown fat from the obese rats did not exhibit higher LPL activity than did the brown fat from their lean littermates. This absence of an increased capacity for triglyceride uptake, coupled with the greater amount of triglyceride per brown adipocyte, is consistent with a reduction of triglyceride oxidation (and, thus, heat production) in the cells from the obese (v the lean) rats.
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PMID:Lipoprotein lipase activity and cellularity in brown and white adipose tissue in Zucker obese rats. 670 19

To define the effects of moderate alcohol intake on cholesterol and triglyceride metabolism in man, twelve patients were hospitalized on a metabolic ward and were fed defined diets for 10 weeks. Each patient underwent testing of plasma lipid and lipoprotein levels, of cholesterol metabolism (absorption, fecal excretion, bile saturation), and of triglyceride metabolism [turnover of triglycerides in chylomicrons and very low density lipoproteins (VLDL)]. This testing was done twice, first during a 4-week control period and then during a 4-week period in which 630 calories of alcohol were either added to or substituted for baseline calories. This increased the average baseline caloric intake by only 24% (range 20% to 30% depending on the initial caloric intake). Addition of alcohol to the baseline diet did not cause weight gain in lean individuals. Obese individuals' responses were more variable, and 3/6 definitely gained weight when the diet was supplemented with alcohol. In addition, obese subjects appeared to be more susceptible to the hyperlipidemic effects of alcohol; whereas 4/6 obese patients developed increased total triglyceride and VLDL-triglyceride concentrations when alcohol was administered, concentrations increased with alcohol administration in only 1/6 lean individuals. High density lipoprotein (HDL) cholesterol increased in all volunteers. Low density lipoprotein (LDL) levels did not change. Metabolic studies showed increased transport of VLDL-triglycerides in overweight patients but not in normal weight individuals; increased transport of VLDL-triglycerides in the former was associated with delayed clearance of chylomicron triglycerides. Alcohol consumption did not affect lipoprotein lipase or hepatic triglyceride lipase in six patients in whom these enzyme activities were measured. In the amounts of alcohol taken in this study, no changes were observed in absorption, synthesis, or excretion of bile acids, or percent saturation of gallbladder bile with cholesterol.
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PMID:Effects of alcohol on plasma lipoproteins and cholesterol and triglyceride metabolism in man. 673 83

Postheparin plasma-lipoprotein lipase (LPL) and hepatic triglyceride lipase (H-TGL) were investigated in rats 1 week after ventromedial-hypothalamic lesions. The enzyme activities were measured using radio-labelled triolein as a substrate. Two lipases were measured separately using specific antiserum prepared against H-TGL. VMH-lesioned rats fed ad lib. showed an increase in plasma LPL with normal H-TGL activity and an elevation of plasma insulin. There was a positive correlation between plasma-LPL activity and insulin levels in VMH-lesioned rats. When rats were examined after overnight fast, VMH-lesioned rats again showed an increase in plasma LPL with normal H-TGL activity and an elevation of plasma insulin. There was also a positive correlation between plasma LPL activity and insulin levels. In order to examine the effect of insulin, rats were treated with daily doses of 3 units of insulin for 1 week. Rats fed ad lib. were insulin treatment showed an increase in plasma LPL with normal H-TGL activity. These results indicate that hyperinsulinemia which was produced by VMH lesions may increase postheparin plasma-LPL activity. We speculate that this increase in plasma-LPL activity mainly reflects that of adipose tissue. The increase of LPL activity can accelerate fat deposition into adipose tissue, contributing to one of the factors causing hypothalamic obesity.
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PMID:Increase of postheparin plasma-lipoprotein-lipase activity in ventromedial-hypothalamic obesity in rats. 674 14

Hyperlipidemia is common in diabetic patients. While our understanding of lipid and lipoprotein metabolism in diabetes is incomplete, a pathophysiologic approach to this problem is presented. It is based on the recognition that diabetes is metabolically heterogeneous. Thus the roles of insulin deficiency, insulin resistance, obesity, and genetic factors are discussed in relation to their effects on lipoprotein production and catabolism. The most important defect in insulin-deficient subjects appears to be a deficiency of lipoprotein lipase, which is responsible for the removal of the triglyceride-rich lipoproteins. In non-insulin-dependent subjects there is evidence for a removal defect as well as, in some patients, for overproduction of VLDL-triglyceride. Cholesterol levels may be elevated and it is important to distinguish between VLDL, LDL, and HDL as the causes for these increases. HDL-cholesterol levels may be increased in insulin-dependent subjects, whereas they may be decreased in obese non-insulin-dependent patients. Mild elevations of LDL-cholesterol may occur in inadequately controlled type I and II diabetic patients, while elevated VLDL may raise the serum cholesterol in addition to the triglyceride levels. The rationale for therapy is based on the complications of severe hypertriglyceridemia and the risk of occlusive atherosclerosis. Management is directed at improving glycemic control, altering dietary composition, and reducing calories in obese patients. Improved glycemic control is effective in reducing triglyceride and cholesterol levels in insulin-deficient subjects. The response of the non-insulin-dependent diabetic patient to improved control may be complicated by associated obesity or familial hyperlipidemia. The advantages and disadvantages of fat versus carbohydrate restriction in the diet are discussed. Finally, resistant hyperlipidemia may require drug therapy. Diabetic hyperlipidemia should be viewed as resulting from an interaction between the diabetic syndrome, the genetic background of the patient, and the environment.
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PMID:Lipid disorders in diabetes. 675 32

In order to evaluate the long-term effects of intestinal bypass surgery in an animal model of early onset hypercellular-hypertrophic obesity, adult female obese and lean Zucker rats were given jejunoileal bypass surgery or sham operations. At sacrifice ten months post-surgery, body weights of obese bypass rats were nearly reduced to lean bypass levels. This reduction in body weight was not accompanied by normalization of body composition or of the hyperinsulinemia and hypertriglyceridemia characteristic of this obese syndrome. Obese bypass rats maintained 44 percent of their weight as lipid compared to 12 percent in lean bypass rats and 15 percent in sham-operated lean rats. In addition, obese bypass rats maintained elevated adipose tissue lipoprotein lipase activity and increased fat cell size and were hyperinsulinemic and hypertriglyceridemic. Furthermore, obese bypass rats had reduced carcass protein and reduced weight and DNA and/or protein contents in heart, liver, muscle and kidney. Therefore, although bypass surgery resulted in significant weight loss, it did not normalize the obese syndrome and may result in serious reductions in the weight and cellularity of vital organs.
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PMID:Zucker fafa rats maintain their obese body composition ten months after jejunoileal bypass surgery. 676 Dec 86

Muscles of genetically-obese animals exhibit decreased binding of and metabolic responses to insulin. Muscle protein catabolism was investigated by measuring the activity of alkaline, myofibril-bound protease in male (ob/ob) mice, fed ad libitum, or fasted for 5 d. Enzyme activity in the isolated myobrillar fraction was determined by the degradation of 14C-globin. Compared to the lean siblings, protease activity in the obese mice was 2.0, 1.5 and 1.3-fold higher in gastrocnemius, diaphragm and soleus muscle respectively, but without change in heart. The higher protease activity in gastrocnemius, diaphragm and soleus was associated with a parallel decrease in the weight and protein mass of the muscles. The muscles of obese mice also showed a 3 to 4-fold increase in triglyceride and a 2-fold increase in glycogen content. After 5-d starvation, the activity of protease rose in the gastrocnemius of obese mice only 1.5 fold, while it increased as much as 4 and 2 fold in gastrocnemius and diaphragm, respectively, in the lean mice. There was no significant change in heart enzyme activity. After 5-d starvation, serum insulin in obese mice fell markedly but remained still higher than that in ad libitum fed lean mice. Insulin-dependent serum metabolites, as well as adipose tissue lipoprotein lipase and hepatic enzymes related to lipogenesis and gluconeogenesis were consequently much less affected in obese mice and the prevalence of adequate insulin supply appeared to be the cause for lack of significant effect on muscle protease activity in fasting obese mice. It is suggested, therefore, that the induction of myofibrillar protease in obesity is linked to the decrease in cellular responsiveness to insulin and may also be interrelated with the intracellular metabolic adjustments to the enhanced muscle lipid availability.
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PMID:Increased protease activity in muscles of obese- (ob/ob) mice. 676 Dec 89

The relationship between obesity and alterations in adipose tissue metabolism and lipid transport was studied in fourteen obese subjects before and after a weight reduction of 4-22 kg. Blood glucose and plasma insulin patterns after peroral glucose intake improved significantly, and plasma glucagon levels decreased markedly after treatment. Plasma triglyceride and total cholesterol levels were not altered, but there was a 20% (P less than 0.05) increase in HDL concentrations. Plasma free fatty acid and glycerol concentrations decreased, in parallel to a decrease in lipolysis rate in vitro. Lipoprotein lipase and hepatic lipase activities in postheparin plasma, as well as the intravenous fat tolerance test, were normal and did not change significantly after weight loss. Lipoprotein lipase activity in adipose tissue, expressed per cell, was elevated and did not change after weight reduction. Also, the enzyme activity did not increase after glucose intake before or after treatment. The lack of effect on lipoprotein lipase activity and regulation in combination with significant improvements of other aspects of lipid and glucose transport is consistent with the view that alterations in LPL activity and regulation may represent an early and possibly primary defect in the development of obesity.
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PMID:Effects of weight reduction on plasma lipoproteins and adipose tissue metabolism in obese subjects. 680 Aug 25

During cold-induced nonshivering thermogenesis, interscapular brown adipose tissue (BAT) lipoprotein lipase (LPL) activity and lipogenesis are elevated. Because of the many similarities between cold- and diet-induced thermogenesis, we examined the effect of ad libitum access to a 32% sucrose solution on caloric intake, adiposity, and BAT enzyme activities in male rats. Daily caloric intakes of sucrose-fed animals were elevated by 20%-25%, and 8 wk of sucrose feeding doubled carcass fat content. This sucrose-feeding induced obesity was associated with increases in circulating triglyceride and insulin levels as well as increased retroperitoneal white adipose tissue LPL activity. However, the increased carcass lipid content accounted for less than half of the excess calories ingested by the sucrose-fed rats. Sucrose feeding stimulated in vivo lipogenesis in BAT and elevated BAT fatty acid synthetase and acetyl-CoA carboxylase activities but not LPL activity. These findings suggest that overeating enhances endogenous lipogenesis but not uptake of circulating triglyceride in BAT. Thus, both cold- and diet-induced thermogenesis increase BAT lipogenesis, while only cold-induced thermogenesis is associated with elevated LPL activity in BAT.
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PMID:Effect of sucrose overfeeding on brown adipose tissue lipogenesis and lipoprotein lipase activity in rats. 682 91


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