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

Among the numerous alterations in adipose tissue metabolism in obesity is an increased activity of lipoprotein lipase (LPL), the rate-limiting enzyme in triglyceride assimilation. The present paper summarizes a series of experiments demonstrating that the regulation of LPL activity is also impaired in obesity. In normal subjects, glucose intake leads to an increase in adipose tissue LPL activity; this phenomenon can also be demonstrated by incubation of adipose tissue in an insulin-containing buffer in vitro. In contrast, the initially high enzyme activity of adipose tissue from obese subjects is non-responsive to glucose and insulin in vivo and in vitro. However, incubation of adipose tissue from obese subjects in the absence of glucose and insulin led to a rapid decline in enzyme activity and elicited a normal response to subsequent exposure to glucose and insulin. These data indicate that the hyperinsulinemia of the obese tissue donor may be of importance for the abnormalities of LPL activity. However, experiments with VMH-lesioned rats demonstrated that insulin levels and LPL activities could be dissociated. In obese and normal-weight rats, standardized with regard to insulin levels by abolition of endogenous insulin production by streptozotocin treatment and substitution with identical doses of insulin, LPL activities and regulation differed markedly, indicating that factors other than insulin are also involved in the dysregulation of LPL activity in obesity.
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PMID:Impaired regulation of adipose tissue lipoprotein lipase in obesity. 703 53

Serum lipoproteins and the heparin-releasable lipoprotein lipase (LPL) activity of adipose tissue and skeletal muscle were measured in 36 untreated obese patients with Type 2 (insulin-independent) diabetes and the values were compared with those of non-diabetic subjects of similar age, sex and relative body weight. In diabetic men, the LPL activity of adipose tissue was significantly reduced when expressed per tissue weight or per fat cell (p less than 0.01). Diabetic females had slightly but not significantly lower LPL activity in adipose tissue than the non-diabetic females. The muscle LPL activity was similar in diabetic and non-diabetic subjects of both sexes. When the diabetic men were classified according to fasting blood glucose, the patients with high glucose levels had lower adipose tissue LPL activity than those with moderate hyperglycemia. In both diabetic and non-diabetic subjects, there was a significant positive correlation between HDL cholesterol concentrations and adipose tissue LPL activity. It is concluded that Type 2 diabetes influences adipose tissue LPL activity and plasma lipoprotein concentrations and that this effect is superimposed on the similar changes produced by obesity alone.
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PMID:Lipoprotein lipase activity and serum lipoproteins in untreated type 2 (insulin-independent) diabetes associated with obesity. 703 8

Obese and lean alloxan-diabetic rats were given daily injections of insulin for 9 days. Plasma glucose and insulin concentrations were not different between the two genotypes given comparable amounts of insulin. Carcass fat and epididymal and retroperitoneal fat pad weights increased as the dose of insulin was increased. At each of four doses, fatties had larger fat cells, bigger pads, and more body fat than lean rats. Adipose lipoprotein lipase (LPL) activity per pad or per fat cell was increased by insulin. Except for the lowest dose of insulin, LPL activity was higher in obese rats than in lean rats. LPL activity per cell and cell size were highly correlated. However, when differences in cell size were corrected for, no significant effect of genotype existed. Cardiac LPL activities were different between the two genotypes only in nondiabetic rats. These results suggested that both insulin and some other genetic factors were important in elevating adipose LPL activities and thus fat deposition in obese Zucker rats.
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PMID:Adipose lipoprotein lipase in insulin-treated diabetic lean and obese Zucker rats. 704 62

Zucker rats were early weaned onto either medium-chain (MCT) or long-chain triglycerides (LCT) to examine the effect on the development of obesity. Preobese and lean pups were weaned at 16 days to isocaloric, isonitrogenous liquid diets containing either 65% MCT or LCT (by calories) or to a "stocklike" (5.5% fat, 72.6% carbohydrate) control diet or were pair-fed stocklike diet to MCT-fed rats until day 45. MCT-feeding lowered body weight gain and fat pad weight in obese and lean rats compared to stocklike-fed controls. Additionally, fat cell size and lipoprotein lipase (LPL) activity and hepatic acetyl CoA carboxylase activity were reduced in obese MCT-fed rats compared to obese controls fed stocklike diet. Except for altered LPL activity the effects produced by MCT-feeding were attributable to its anorectic effect. However, all obese rats, including the MCT group, developed an obese body composition and were hyperinsulinemic. The development sequence leading to obesity may be derived from a fundamental cellular defect that results in metabolic alterations in different tissues at critical periods of development. Thus, effective treatment of this genetic obesity requires a better understanding of fa gene action.
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PMID:Effect of high fat weanling diets containing either medium-chain triglycerides or long-chain triglycerides on the development of obesity in the Zucker rat. 704 90

To determine the relative rates of lipid metabolism in muscle and adipose tissues in obesity, we measured uptake and oxidation of free palmitate or tripalmitin into tissue slices in vitro. We also measured lipoprotein lipase (LPL) activity of soleus muscle and perirenal adipose tissues. Muscle took up more liquid from tripalmitin than from free palmitate (FFA) at 6 and 12 wk of age, whereas adipose took up more from FFA. The relative uptake of tripalmitin in adipose decreased from twofold that of muscle at 6 wk to 60% of muscle at 12 wk. Uptake from FFA in adipose was faster than in soleus at both ages. LPL/g of soleus muscle at 12 wk was higher than that of adipose. LPL/g protein was higher in adipose tissue than in muscle at 12 wk. Muscle oxidized 15-32% of FFA, obese muscles more than lean at 12 wk. AT 15-h fast decreased lean adipose tripalmitin uptake 50%, did not affect obese adipose lipid uptake, and decreased obese soleus palmitate uptake. In soleus muscle, triglyceride uptake is as active as in adipose. Obese muscles at 12 wk oxidized more FFA than lean and respond to a short fast by increasing the percent lipid oxidized.
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PMID:Lipoprotein lipase and lipid metabolism in muscle and adipose tissues of Zucker rats. 711 87

The spiny mouse Acomys cahirinus, which exhibits beta-cell hyperplasia but low insulin secretion in captivity responded with hyperlipidemia without obesity or diabetes on a sucrose diet and became obese, and glucose-intolerant on a diet of fat-rich seeds. A three-month sucrose diet induced a marked rise in the activity of regulatory enzymes of glycolysis and lipogenesis in the liver but not in adipose tissue. There was also increased energy waste on this diet evident from a three-fold rise in the activity of hepatic mitochondrial FAD-glycerophosphate oxidase associated with an elevation in circulating triodothyronine. The obesity in mice maintained for three months on fat rich seeds was associated with moderate hyperglycemia, mild hyperinsulinemia and little change in circulating lipids. There was a decrease in the activity of glycolytic and lipogenic enzymes both in the liver and adipose tissue. Adipose tissue lipoprotein lipase activity rose, suggesting that the chylomicrons carrying the exogenous fat were better assimilated than the very-low-density lipoproteins synthesized from the dietary carbohydrate. Along with adipose tissue gain, triglyceride deposition was apparent in several muscles, accompanied by increased tissue free fatty acid, citrate and glycogen content. This suggested relation of increased muscle fat utilization with decreased glucose metabolism and insulin sensitiveness. Diverse responses to diets were thus elicited, which were particularly discernible in desert animals surviving on a limited caloric intake. Detailed follow up of these enzymatic and endocrine adaptation patterns to selective nutritional affluence may promote the understanding of the mechanisms leading to hyperlipidemia with leanness and normal glucose homeostasis versus obesity with diabetes but without hyperlipidemia.
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PMID:Intermediary metabolism during the development of obesity and diabetes in the desert rodent Acomys cahirinus. 711 67

Adipose tissue and muscle lipoprotein lipase and postheparin hepatic and lipoprotein lipase activities have been measured in a group of 21 Pima Indian males over a wide range of body weight to determine the relationship between obesity and these lipase activities. There was a significant positive correlation between adipose tissue lipoprotein lipase and obesity; muscle and postheparin lipoprotein lipase and hepatic lipase were not related to degree of obesity. Fasting insulin levels were not related to any of the measurements of lipase activity. There were racial differences in adipose and postheparin lipoprotein lipase activities; both were significantly lower in the Pimas as compared with a group of weight-matched Caucasian males. Lipase activities were remeasured in eight subjects after a period of weight reduction including several weeks of stabilization at the reduced weights. After the period of weight reduction adipose tissue lipoprotein lipase declined in all subjects. Hepatic lipase also declined in all but two patients. Muscle and postheparin lipolytic activities were not affected by weight loss. The data indicate that (a) there are racial differences in adipose tissue lipoprotein lipase; and (b) the elevated adipose lipoprotein lipase associated with obesity, like many other biochemical variables in the obese state, returns toward normal after weight reduction.
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PMID:Characterization of lipase activities in obese Pima indians. Decreases with weight reduction. 711 15

To investigate the relationship between elevated adipose tissue lipoprotein lipase (LPL) activity and triglyceride uptake in Zucker obese rats, fed and 12 hour fasted female obese and lean Zucker rats were given intrajugular infusion of radio-labelled triglyceride and label clearance and uptake were examined over 35 minutes. In the fed state, obese rats showed more rapid clearance of the label from the bloodstream and, in both fed and fasted states, greater uptake into retroperitoneal and parametrical fat pads than lean rats. Obese rats showed proportionally less uptake into heart and liver. Regardless of feeding condition, obese rats exhibited elevations in adipose tissue LPL, which was significantly correlated with label uptake in adipose tissue. These results show that, in Zucker obese rats, elevated adipose tissue LPL is associated with increased adipose tissue triglyceride uptake. A preferential "shunting of calories" into adipose tissue, which is presumably mediated by LPL, could underlie the intractability of the Zucker obesity syndrome as well as the altered feeding behavior of Zucker obese rats.
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PMID:Adipose tissue lipoprotein lipase (LPL) and triglyceride uptake in zucker rats. 716 95

The effect of genetic selection for backfat accumulation on adipose tissue and muscle lipoprotein lipase (LPL) in fetal and neonatal pigs was investigated. Fetal pigs at 110 d of gestation were taken surgically from sows of either a high backfat (High) or low backfat (Low) line of Yorkshire pigs selected over 18 generations on the basis of backfat thickness at 80 kg live weight. Fetuses of Yorkshire (Control) and Ossabaw (Obese) sows were used for comparison. Activities of LPL/mg cytoplasm protein in subcutaneous adipose tissue were 2.23 +/- .19, 3.98 +/- 1.06, 6.37 +/- .83 and 7.57 +/- .66 nmol FFA released/min and LPL/g tissue was 34.80 +/- 4.06, 58.36 +/- 14.23, 99.55 +/- 15.15 and 159.94 +/- 9.7, for Low, Control, High and Obese 110-d fetuses, respectively. Muscle (semimembranous) LPL/mg protein was 1.06 +/- 1.17 and 1.39 +/- .20 and LPL/g tissue was 50.11 +/- 6.9 and 59.07 +/- 9.12 for High and Low line fetuses, respectively. Fetal body composition was not different for High and Low lines. In 14 d-old suckling pigs, adipose tissue LPL/mg protein had increased to 18.09 +/- 3.48 and 17.76 +/- 3.98 and LPL/g tissue was 291.12 +/- 56.60 and 308.45 +/- 64.43 in High and Low line pigs, respectively. Muscle LPL/mg protein had decreased to .83 +/- .08 in High and 1.25 +/- .13 in Low line pigs, while LPL/g muscle was similar between these lines. These effects of genetic selection on muscle and adipose tissue suggest that early in development, the partitioning of nutrients to lean of fat tissues may be altered, eventually leading to a marked difference in body composition.
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PMID:Muscle and adipose tissue lipoprotein lipase in fetal and neonatal swine as affected by genetic selection for high or low backfat. 717 50

Obese subjects have elevated adipose tissue lipoprotein lipase activity per fat cell when compared with lean control subjects. This enzyme, which is rate limiting for the uptake and storage of lipoprotein triglyceride in adipose tissue, has been shown to be further elevated in a group of previously obese subjects who had been weight stable at a reduced weight for 4-28 mo. In the present prospective study of eight obese subjects, adipose tissue lipoprotein lipase activity was demonstrated to increase after weight stabilization at a reduced weight (0.33 mU/10(6) cells). In three subjects who lost weight and subsequently regained their lost weight, the enzyme activity increased after weight loss and then returned toward the original basal level with weight gain. One subject who maintained his weight loss for 10 mo. continued to have an elevated level of enzyme activity. Because adipose tissue lipoprotein lipase activity does not "normalize" after weight loss, we hypothesize that this enzyme may play a counterregulatory role in resisting deviation from a "set point" for fat mass or fat cell size and thereby predispose to reattainment of the original obese state.
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PMID:Increase of adipose tissue lipoprotein lipase activity with weight loss. 722 33


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