Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.34 (lipoprotein lipase)
 7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several mammary and adipose enzymes were measured in normal, adrenal-ectomized, adrenalectomized cortisol-treated, and intake-restricted lactating rats. Acetyl-CoA carboxylase, lipoprotein lipase, and triglyceride synthetase complex activities in mammary tissue were unchanged by intake restriction, decreased by adrenalectomy, and increased by glucocorticoid-replacement therapy. Malic dehydrogenase, glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, and lipoprotein lipase activities in adipose were unchanged after adrenalectomy.
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PMID:Effects of adrenalectomy and glucocorticoid therapy on enzyme activities in mammary and adipose tissues from lactating rats. 0 27

5 French Alpine Goats were studied after normal or premature parturition. Mammary tissue acetyl-C oA carboxylase, glucose-6-phosphate dehydrogenase, malic enzyme and lipoprotein lipase (LPL) activities varied in parallel with milk fat secretion from the 3rd to the 9th week of lactation. Variations of mammary LPL activity and of long chain fatty acid secretion were positively highly correlated during that period. In goats with normal parturition, lipogenic activities seemed to reach a maximum level shortly after parturition. There was a positive correlation between mammary Ll activities and plasma non esterified fatty acid contents, possibly reflecting a relationship between adipose tissue mobilisation and mammary metabolism.
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PMID:[Changes in mammary tissue lipid metabolism in the goats during the first 2 months of lactation]. 3 69

The lipogenic capacity of omental adipose tissue and liver was measured in vitro from samples obtained at slaughter from 33 young male goats. The animals were slaughtered either on the day of weaning (d 0) or 2, 14, or 56 d after weaning. Ages at weaning were 4 wk (early weaning) or 6 or 8 wk (late weaning). Blood samples from the jugular vein were taken before slaughter to measure the concentrations of plasma glucose and nonesterified fatty acids. There was a 30% decrease in glucose concentration after weaning. Nonesterified fatty acid concentration increased fourfold between d 0 and 2 after weaning. By d 14 after weaning, nonesterified fatty acids returned to basal concentration. The lipoprotein lipase (LPL) activity of adipose tissue declined markedly (90%) on d 2 after weaning. Lipoprotein lipase activity returned to preweaning values by d 56 after weaning in those goats that had ad libitum access to feed. In adipose tissue, nicotinamide adenine dinucleotide phosphate (NADP)-malate dehydrogenase activity fell by only 17% by d 2 after weaning and to 63% by d 14 after weaning. Lipoprotein lipase activity was closely related to metabolizable energy intake the day before slaughter. Acetyl-coenzyme A carboxylase activity was low in adipose tissue and it increased only slightly by d 56 after weaning. The data indicated that LPL played a preponderant role in the restoration of lipid stores after weaning. High NADP-malate dehydrogenase activity together with a high concentration of plasma glucose by d 56 after weaning suggested that this enzyme activity could be enhanced by high glucose availability in goat kids. Activities of lipase, acetyl-coenzyme A carboxylase, NADP-malate dehydrogenase, and glucose-6-phosphate dehydrogenase in liver were essentially unaffected by weaning. The extent and rapidity of change of lipogenic enzymes of goat kids was much more pronounced in adipose tissue than in liver.
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PMID:Changes in activities of lipogenic enzymes in adipose tissue and liver of growing goats. 136 29

The thiazolidinediones are a class of novel antidiabetic compounds that enhance the response of target tissues to insulin. Pioglitazone, a thiazolidinedione analog, lowers blood glucose and insulin levels in rodent models of non-insulin-dependent diabetes mellitus. We have studied the effect of pioglitazone on 3T3-L1 cells, a cell line that undergoes differentiation from a preadipocyte fibroblastic morphology to that of an adipocyte. Pioglitazone treatment of preadipocytes enhanced the insulin- or insulin-like growth factor-1 (IGF-I)-regulated differentiation (monitored by the rate of lipogenesis or triglyceride accumulation), whereas treatment of the cells in the absence of insulin or IGF-I resulted in no apparent change in the cellular phenotype. Pioglitazone caused both a leftward shift and enhanced maximum response for the IGF-I-regulated differentiation of the cells, consistent with the idea that the drug enhances the sensitivity of cells to polypeptide hormones. A series of pioglitazone analogs were tested in this system, and variations in activity relative to that of the parent compound were observed. A study of the time required for the drug to exert an effect on differentiation revealed that an increased rate of lipogenesis occurred 16-24 hr after drug treatment in appropriately staged cells. An increased rate of glucose transport and increased activity of lipogenic enzymes were noted in a time frame that correlated with the change in lipogenesis. Analysis of mRNA abundance for Glut-4, lipoprotein lipase, and glucose-6-phosphate dehydrogenase showed that pioglitazone enhanced the insulin induction of these mRNA species. Thus, pioglitazone, in combination with insulin or IGF-I, appears to be exerting effects on the cellular phenotype by eliciting changes in the expression of genes that regulate metabolic pathways leading to the acquisition of the differentiated phenotype.
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PMID:Enhancement of adipocyte differentiation by an insulin-sensitizing agent. 153 16

Inhibitors of 3-hydroxy-3-methyl glutaryl coenzyme A (HMG-CoA) reductase have been approved for treatment of hypercholesterolemia in humans. This class of therapeutic agents, in addition to lowering plasma cholesterol, reduces plasma triglyceride levels. We have investigated the mechanism of triglyceride-lowering effect of lovastatin in the hypertriglyceridemic state by using a rodent model of hypertriglyceridemia and obesity, the Zucker obese (fa/fa) rat. Lovastatin treatment (4 mg/kg), as compared to placebo, caused a 338% reduction in plasma triglyceride (146 +/- 5 vs. 494 +/- 76 mg/dl), a 58% decrease in total cholesterol (99 +/- 13 vs. 156 +/- 18 mg/dl), and a 67% reduction in high density lipoprotein (HDL)-cholesterol (69 +/- 8 vs. 115 +/- 15 mg/dl). The fall seen in plasma triglyceride was due to a decrease in hepatic secretion of very low density lipoproteins (VLDL), determined after blocking the clearance of triglyceride-rich lipoproteins with Triton WR-1339. Lovastatin treatment did not affect either the activities of hepatic lipogenic enzymes, glucose-6-phosphate dehydrogenase, or malic enzyme, or the activities of the lipolytic enzymes of adipose tissue, lipoprotein lipase, or liver, hepatic triglyceride lipase. Supplementation of mevalonolactone in the diet partially reversed the changes in plasma triglyceride (265 +/- 37 vs. 146 +/- 5 mg/dl), but not in total or HDL-cholesterol. These data demonstrate that, in the hypertriglyceridemic Zucker rat model, HMG-CoA reductase inhibitors reduce the rate of secretion of VLDL and this effect can be partially reversed by administration of mevalonolactone.
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PMID:Mechanisms of triglyceride-lowering effect of an HMG-CoA reductase inhibitor in a hypertriglyceridemic animal model, the Zucker obese rat. 155 26

Lipogenic activities of perirenal adipose tissue were investigated in early (wk 3) and midlactation (wk 19 to 26) cows that received a duodenal rapeseed oil infusion (1.0 to 1.1 kg/d). In midlactation, oil infusion resulted in a decreased rate of fatty acid synthesis from acetate and a decreased rate of the activities of fatty acid synthetase and glucose-6-phosphate dehydrogenase, whereas lipoprotein lipase activity tended to increase. The rate of glucose incorporation into glyceride-glycerol and the activities of glycerol-3-phosphate dehydrogenase and malic enzyme were not significantly affected. Fatty acid C14:0 content of perirenal adipose tissue was decreased, and fatty acid C18:2 and C18:3 contents were increased in oil-infused cows. In early lactation, rates of acetate incorporation into fatty acids and activities of fatty acid synthetase and lipoprotein lipase were very low. Activities of glucose-6-phosphate dehydrogenase and glycerol-3-phosphate dehydrogenase were lower in the early than in the midlactation trial. Oil infusion did not change the measured parameters. In both trials, percentages and yields of milk fatty acids C18:1, C18:2, and C18:3 were increased, whereas those of C14:0 and C16:0 were decreased by oil. Calculated transfer rates of absorbed fatty acid C18:2 from oil to milk fat were 16 to 26%. Results suggested that oil fatty acids affected adipose and mammary de novo lipogenesis in a direct way without affecting fatty acid esterification in adipose tissue or total fat secretion in mammary tissue.
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PMID:Duodenal rapeseed oil infusion in early and midlactation cows. 5. Milk fatty acids and adipose tissue lipogenic activities. 189 93

The influence of training on fatty acid and glyceride synthesis by liver and adipose tissue homogenates of young and old Fischer-344 rats was examined. Four groups of rats (10 animals/group) were studied: young untrained, young trained, old untrained, and old trained. Training of each group was for 10 wk at 75% maximal O2 uptake. Young rats were killed at 6 mo of age and old rats were killed at 27 mo of age. Fatty acid synthesis was assessed by measuring the activities of acetyl-CoA carboxylase, fatty acid synthase, ATP citrate-lyase, "malic" enzyme, and glucose-6-phosphate dehydrogenase. Glyceride synthesis was evaluated by determining the rate of incorporation of [14C]glycerol 3-phosphate into lipids. In addition, lipoprotein lipase activity was measured in acetone-ether powders of adipose tissue from the four groups of rats. In liver, training had no effect on fatty acid or glyceride synthesis in either group. However, aging caused a significant decrease in the activities of four of the lipogenic enzymes but had no effect on glyceride synthesis. Training caused an increase in fatty acid synthase and glyceride synthesis in adipose tissue, and aging decreased lipoprotein lipase activity. It was concluded that training enhances the synthetic capacity of lipids by adipose tissue but that aging had a more profound effect in that the activities of the enzymes involved in these processes were lower in the old rats. Furthermore, the decreased activity of lipoprotein lipase in the older rats may explain the higher plasma triglyceride levels that were observed in these animals.
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PMID:Influence of age and exercise training on lipid metabolism in Fischer-344 rats. 257 7

Effects of capsaicin, a pungent principle of hot red pepper, were studied in experiments using male rats fed a diet containing 30% lard. Capsaicin was supplemented at 0.014% of the diet. The level of serum triglyceride was lower when capsaicin was present in the diet than when it was not. Levels of serum cholesterol and pre-beta-lipoprotein were not affected by the supplementation of capsaicin. The perirenal adipose tissue weight was lower when capsaicin was present in the diet than when it was not. Hepatic enzyme activities of glucose-6-phosphate dehydrogenase and adipose lipoprotein lipase were lower in rats fed the 30% lard diet than in those fed a nonpurified diet. Activities of these two enzymes were higher when capsaicin was added to the diet than when it was not. Hepatic acetyl-CoA carboxylase, beta-hydroxyacyl-CoA dehydrogenase, and adipose hormone-sensitive lipase activities were not affected by capsaicin feeding. Lipid absorption was not affected by the supplementation of capsaicin. The perirenal adipose tissue weight and serum triglyceride were decreased as the level of capsaicin in the diet increased up to 0.021%. These results suggest that capsaicin stimulates lipid mobilization from adipose tissue and lowers the perirenal adipose tissue weight and serum triglyceride concentration in lard-fed rats.
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PMID:Effects of capsaicin on lipid metabolism in rats fed a high fat diet. 287 41

Prolonged exposure of rats to cigarette smoke resulted in significant alterations in the metabolism of lipids. There was a significant increase in the concentration of cholesterol, triglycerides and phospholipids in most of the tissues, particularly the heart, aorta and lungs. Cholesterol, triglycerides and phospholipids decreased in the serum HDL and increased in LDL + VLDL. There was increased cholesterogenesis in the heart, lungs and liver, as evidenced by increased activity of HMG-CoA reductase and increased incorporation of labelled acetate into cholesterol. Incorporation of label into the triglycerides also increased in these tissues. Activity of lipoprotein lipase in the extrahepatic tissues was decreased. Activity of glucose-6-phosphate dehydrogenase and malic enzyme increased in the heart and lungs. There was decreased concentration of bile acids in the liver.
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PMID:Effect of exposure of rats to cigarette smoke on the metabolism of lipids. 336 90

The differentiation of perirenal adipose tissue was ascertained in fetuses from Ossabaw (wild and obese) and cross-bred lean dams at 70, 90 and 110 days gestation and from domestic lean and obese dams (USDA) at 110 days gestation. Condensation of presumptive adipocyte clusters was more apparent in Ossabaw sections than in cross-bred (lean) sections at 90 and 110 days gestation. Enzyme and lipid histochemistry showed fat cell cluster development to be largely independent of fetal strain (Ossabaw vs crossbred). However, adipocytes in Ossabaw fetuses were larger (110 days) and more reactive for esterase activity (all three ages) than were adipocytes from crossbred fetuses. Fetuses from USDA-obese dams had larger fat cell diameters (P less than 0.01), a higher percentage of lipoprotein lipase (LPL) positive cells than did fetuses from USDA-lean dams. Perirenal fat pad weights, percent depot lipid, percentages of glucose-6-phosphate dehydrogenase (G6PDH) and succinate dehydrogenase (SDH) positive cells were independent of fetal strain (USDA, lean vs obese). Fat cell cluster development was independent of fetal strain but large cellular condensations of presumptive cells were only present in sections from lean fetuses. Immature capillary beds (devoid of adipocytes) were demonstrable in lean sections but were not observed in obese sections. Morphological and histochemical results from both studies provide no evidence for brown adipocyte-like cells in fetal perirenal tissues.
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PMID:The development of perirenal fat depots in obese and lean pig fetuses. 342 14


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