Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The effects of 17 beta-estradiol and testosterone administration on cholesterol esterase, lipoprotein lipase activities and adrenalin-induced lipolysis were examined in rat adipose tissues with the change in serum lipid level. The administration of 17 beta-estradiol (500 micrograms/kg, 2 or 4 weeks) to male rats significantly reduced the body weight, and markedly increased serum cholesterol, triacylglycerols and phospholipids. Cholesterol esterase activity was significantly enhanced in the epididymal adipose tissue from estradiol treated rats and the effect was greater with duration of the treatment. In contrast, lipoprotein lipase activity was markedly reduced. Testosterone reduced cholesterol esterase activity in the parametrial adipose tissue through the treatment with 500 micrograms/kg for 6 weeks, but it did neither influence serum lipids nor lipoprotein lipase activity. Basal lipolysis and adrenalin-induced lipolysis were also significantly enhanced in the epididymal adipose tissue from the male rat treated either with 7 mg/kg estradiol 12 h ahead or with 500 micrograms/kg estradiol for 2 weeks. These results indicate that estradiol exerts strong effects on metabolism of the adipose and these effects seems to be mediated through cyclic-AMP. An alteration of adrenergic functions by gonadal steroids might be intervened.
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PMID:Enhancement in cholesterol-esterase activity and lipolysis due to 17 beta-estradiol treatment in rat adipose tissue. 650 Apr 87

Guinea pigs have varying plasma triglyceride concentrations ranging from 28 to 1392 mg/dl, with relatively uniform plasma cholesterol and phospholipid levels. To understand why the animals exhibit such wide variations of plasma triglyceride concentrations, we have explored the triglyceride hydrolyzing system by measuring tissue lipoprotein lipase activities and plasma activator for the enzyme. Lipoprotein lipase activities of epididymal adipose tissue of these animals were 759 +/- 117 (mean +/- SE) n moles FFA X min-1 X g wet tissue-1, markedly low compared with those of rats. There were no relationships between plasma triglyceride concentrations and tissue lipase activities. Plasma activator for lipoprotein lipase was lacking in this animal. Guinea pigs with ascorbic acid deficiency for 2 weeks also showed marked variations of plasma triglyceride concentrations, without any changes in tissue lipoprotein lipase activities. Low adipose tissue lipoprotein lipase activities with deficient plasma activator for the enzyme suggest that the lipoprotein lipase-mediated triglyceride degradation could be impaired in this animal, and this may account for the marked variation of plasma triglyceride concentrations.
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PMID:Wide variations of plasma triglyceride concentrations in guinea pigs. 652 15

The effects of 2-aminoethanesulfonic acid (taurine) and its structural analogs, 3-aminopropanesulfonic acid (homotaurine) and 4-aminobutanesulfonic acid (ABSA), on lipid metabolism were investigated in rats with dietary hyperlipidemia. The serum cholesterol levels increased approximately five-fold in rats fed a diet containing 0.5% cholesterol and 1% cholic acid for 10 d. omega-Aminosulfonic acids dissolved in water were orally administered for 10 d concurrently with the 0.5% cholesterol diet. Taurine suppressed elevation in serum cholesterol levels by 46.9 and 63.9% at doses of 250 and 500 mg/kg, respectively. Serum triglycerides levels, however, were not significantly altered by taurine. Both homotaurine and ABSA, 500 mg/kg each, inhibited the elevation in serum cholesterol levels to an extent, namely, 32.0 and 22.3% lower than that of the controls, respectively. Treatment with homotaurine in doses of 250 and 500 mg/kg significantly increased serum triglycerides levels by 37.6 and 35.9%, respectively, and ABSA (500 mg/kg) also revealed a tendency to raise these levels. All the sulfonic acids (500n mg/kg each) reduced cholesterol levels in the liver similarly, while changes in triglycerides levels in the liver were insignificant. Both taurine and homotaurine (t00 mg/kg each) inhibited intestinal absorption of cholesterol. The inhibitory effect of homotaurine was as great as 31.5% and greater than that of taurine. No influence of taurine (500 mg/kg) was observed in lipoprotein lipase activity in the epididymal fat tissue, but the activity did appear to be inhibited by homotaurine (500 mg/kg).
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PMID:Effects of omega-aminosulfonic acids on lipid metabolism in dietary hyperlipidemic rats. 663 58

Atherosclerotic lesions formed in the aorta of rats given diet containing propylthiouracil (PTU), vitamin D2 and high cholesterol diet (atherogenic) for 8 weeks. The effect of clinofibrate, which lowers the plasma lipid level, on lipid metabolism in the arterial wall of the atherosclerotic rats was studied. Clinofibrate significantly decreased the high plasma cholesterol level of atherosclerotic rats, which was 823 +/- 256 (mean +/- SD) mg/dl, or about ten times that of control rats (85 +/- 11 mg/dl). On treatment with clinofibrate, the cholesterol level was reduced most in the very low density lipoprotein (VLDL) fraction (d less than 1.006). Heparin-releasable lipoprotein lipase activity in epididymal adipose tissue, lipoprotein lipase activity in post heparin plasma, and VLDL-triolein hydrolizing activity in adipose tissue stromal vessels were higher in clinofibrate-treated rats than in atherosclerotic rats. Of the enzymes in the arterial wall concerned with cholesterol ester metabolism, acid cholesterol esterase activity was decreased in atherosclerotic rats, and clinofibrate treatment increased this activity. The ratio of acyl-CoA cholesterol acyltransferase activity (ACAT) to neutral cholesterol esterase activity was higher in atherosclerotic rats than in control rats and was lower in clinofibrate-treated rats than in atherosclerotic rats. From these results, it is concluded that clinofibrate modifies enzyme activities in such a way as to cause a reduction of cholesterol accumulation in the arterial wall and lowers the plasma VLDL and LDL cholesterol levels.
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PMID:Effect of clinofibrate on lipid metabolism of aorta in atherosclerotic rats. 668 Sep 96

Endothelial cells from rat epididymal fat pad capillaries were isolated from rats immediately after weaning. The cells were obtained after an initial brief incubation with collagenase under conditions of minimal breakage of cells. Adipocytes were removed by flotation and endothelial cells were then obtained as cell aggregates by fractional filtration procedures whereby intact tissue as well as free cells were removed. These aggregates were then dispersed and cultured in supplemented medium 199 whereby a monolayer of cells with a growth pattern, numerous pinocytotic vesicles, and intercellular junctions typical of endothelial cells were obtained. Minor contaminations of precursor cells to adipocytes were absent after one subculture. Here greater than 95% of the cells showed the presence of Factor VIII. Further subcultures produced nonhomogenous cells and decreasing rates of replication. The endothelial cells showed a very low rate of triglyceride synthesis and release, and collected no visible lipid upon prolonged cultures in the presence of an abundance of triglyceride substrate. They bound lipoprotein lipase from rat adipocytes, whereby the lipase was stabilized. This binding was released by heparin, and the cells did not synthesize the enzyme.
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PMID:Isolation and characterization of endothelial cells from the epididymal fat pad of the rat. 683 87

Adipocyte precursor cultures prepared from the epididymal fat pads of genetically obese (fa/fa) and lean (Fa/Fa) Zucker rats grow similarly in culture. Addition of enriched medium (EM) containing human serum, insulin, and glucose stimulated lipid filling of the adipocyte precursors in both cultures. However, [3H] H2O incorporation into total lipids, fatty acid synthetase and lipoprotein lipase activities, and cytosolic protein contents are all decreased in the fa/fa compared with the Fa/Fa cultures. Substitution of lean or obese rat serum for human serum in the enriched medium does not alter the decreased lipogenic capacity of the fa/fa adipocyte precursor cultures.
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PMID:Lipogenesis in primary cultures of adipoblasts derived from genetically obese Zucker rats. 686 57

The effects of tumor growth on lipid metabolism were investigated by evaluating serum lipids, lipoprotein lipase activity (LPLA), the lipogenic enzymes, urinary catecholamines along with serum insulin and glucagon levels. We injected 1.5 X 10(6) cells of rat mammary tumor, AC33, and killed the rats on the 18th day. Serum triglycerides and free fatty acids of the tumor-bearing (TB) rats increased 4 and 5 times, respectively, more than the control (C) rats. Total liver lipids were not significantly different between the two groups. Tumor growth produced a 70% decrease in total epididymal fat pad LPLA; there were no changes in soleus muscle LPLA. Serum insulin levels of the TB rats were 49% less than the C rats. The TB rats had significantly lighter epididymal fat pads and lower activities of adipose fatty acid synthetase and citrate cleavage enzyme. Urinary catecholamines of the TB rats were reduced over 30% compared with the C rats. These results show that the hypertriglyceridemia of the TB rats may be due, in part, to a deficiency of adipose tissue LPLA. The data also suggest that the effects of the tumor on lipid metabolism may be mediated through insulin.
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PMID:Changes in the activities of lipoprotein lipase and the lipogenic enzymes in tumor-bearing rats. 698 80

The lipoprotein lipase activity of epididymal fat-bodies from starved rats was measured during incubations at 37 degrees C in vitro. Protein synthesis independent activation of the enzyme, previously observed during incubations at 25 decrease C, also occurs at 37 degrees C. Protein-synthesis-dependent increases in the activity of the enzyme occur in the presence of insulin and are markedly potentiated by glucocorticoids. The effects on the activity of the enzyme of insulin alone, or in the presence of glucocorticoids, are correlated with its effects on total protein synthesis in the tissue. Adrenaline antagonizes the increase in activity of the enzyme brought about by insulin and abolishes the potentiation of insulin action by glucocorticoids. These changes may be due, at least in part, to its stimulation of inactivation of the enzyme in the tissue. It is suggested that changes in adipose-tissue lipoprotein lipase activity that occur with changes in nutritional status in vivo result from the combined effects of changes in plasma insulin and glucocorticoid concentrations.
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PMID:Effects of insulin, glucocorticoids and adrenaline on the activity of rat adipose-tissue lipoprotein lipids. 699 75

Glucose, and certain sugars that can readily be converted to glucose 6-phosphate, bring about an activation of adipose-tissue lipoprotein lipase when epididymal fat-bodies from starved rats are incubated in the presence of cycloheximide. Other substrates do not support the activation. If the tissue is preincubated in the presence of cycloheximide for longer than 2h, the ability of added glucose to activate the enzyme is lost. On the other hand, the addition of glucose still brings about an increase in lipoprotein lipase activity after preincubation in the absence of cycloheximide for as long as 4h. The magnitude of the increase in enzyme activity brought about by the addition of glucose is increased when protein synthesis is stimulated during the preincubation period by insulin. The results are interpreted in terms of the existence in adipose tissue of a proenzyme pool of lipoprotein lipase that is normally maintained by protein synthesis and that is converted to complete enzyme of higher specific activity by a process that specifically requires glucose.
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PMID:Effects of glucose and insulin on the activation of lipoprotin lipase and on protein-synthesis in rat adipose tissue. 699 76

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


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