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)

Pharmacological intervention for altering plasma levels of lipoproteins is usually aimed at reducing atherogenesis and preventing coronary heart disease (CHD). Drug therapy should be attempted only after other nonpharmacological methods (such as elimination of smoking, weight reduction and exercise) have been tried. An overview of the metabolism of low density lipoprotein (LDL) and high density lipoprotein (HDL) particles is the basis of this paper. Various sites suitable for pharmacological intervention are identified. LDL metabolism can be altered at 2 potential sites, with a consequent reduction in the plasma level of this atherogenic lipoprotein. Hydroxymethylglutaryl coenzyme A (HMG CoA) reductase inhibitors (such as lovastatin) and cation-exchange resins (e.g. cholestyramine) reduce LDL levels by stimulating the hepatic synthesis of apolipoprotein (apo) B,E receptors. Very low density lipoprotein (VLDL) secretion is inhibited by nicotinic acid (niacin) and gemfibrozil, leading to a secondary decrease in LDL production from VLDL. Probucol also reduces the LDL concentration and inhibits the oxidative modification of LDL. Gemfibrozil and other fibrates stimulate lipoprotein lipase activity, thereby decreasing VLDL concentration. Reduction of the LDL concentration is effective in reducing CHD incidence, whether this is achieved by stimulation of catabolism or inhibition of production of the lipoprotein. In contrast, the mechanism of raising plasma HDL-cholesterol levels is probably relevant to the potential clinical benefits associated with drug therapy. Gemfibrozil and cholestyramine stimulate synthesis of apoprotein A1, the major protein constituent of HDL particles. Both drugs have been shown to reduce the incidence of CHD in clinical trials, via mechanisms that are related in part to their HDL-raising activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacological intervention for altering lipid metabolism. 228 8

Experiments were conducted to study the effects of high density lipoprotein (HDL) and apolipoproteins C, E, and A on lipoprotein lipase activity in rhesus monkeys. The lipoprotein lipase activity was inhibited up to 32 +/- 6 per cent by monkey HDL. This inhibition was considerably decreased (2 +/- 0.02%) by using apolipoprotein-poor HDL. Apolipoproteins C and E inhibited the hydrolysis of activated intralipid by monkey lipoprotein lipase to a maximum of 83 +/- 7 and 57 +/- 5 per cent respectively. Apolipoprotein A produced little inhibition of lipoprotein lipase activity. The results of these studies demonstrate that HDL and apolipoproteins compete with the substrate for the binding to lipoprotein lipase in rhesus monkeys.
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PMID:Inhibition of lipoprotein lipase activity by high density lipoprotein & apolipoproteins C, E & A in rhesus monkeys. 237 91

Estrogen administration (25 mg/kg body weight) in chicks resulted in a marked elevation of plasma very-low-density lipoprotein (VLDL) triacylglycerol (TG). To determine whether the VLDL produced from estrogen (E)-treated birds is catabolized differently from VLDL of control birds, VLDL-TG kinetic studies were conducted. The [14C]TG-labeled VLDL was prepared by intravenous injection of [14C]palmitate into control and E-treated chicks. The [14C]TG-labeled VLDL prepared from the control (C-VLDL-TG) and E-treated chicks (E-VLDL-TG) were then reinjected into fed and fasted chicks with or without E-treatment. The metabolism of VLDL-TG was found to be different, depending upon whether its donor was the control of E-treated chick. The fractional catabolic rate (FCR) of E-VLDL-TG was significantly (P less than 0.05) lower than that of C-VLDL-TG in both fed and fasted chicks. Compared to the fed state, fasting resulted in significantly (P less than 0.05) increased FCRs of both C-VLDL-TG and E-VLDL-TG. The turnover rate of VLDL-TG was significantly higher in E-treated chicks than in their respective controls. In addition, the endogenously produced VLDL-TG differed in their affinity for lipoprotein lipase in which E-VLDL-TG had a higher Km value for the enzyme than C-VLDL-TG. On agarose gel electrophoresis, the VLDL of E-treated chicks showed beta-mobility and it eluted into two peaks on agarose gel filtration, whereas VLDL of control chicks had a pre-beta-mobility on the former and it eluted into a single peak on the latter. SDS-gel electrophoresis also revealed that the apolipoprotein composition of VLDL from control and E-treated chicks was notably different from each other. Present findings suggest that estrogen treatment results not only in an increased secretion of VLDL but also in the production of different VLDL particles, thereby affecting their clearance from the plasma.
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PMID:Effects of estrogen on very-low-density lipoprotein triacylglycerol metabolism in chicks. 237 10

Hypothyroidism is a major cause of secondary hypercholesterolemia. Amiodarone treatment alters both the levels of serum lipids and thyroid hormones. We investigated whether the amiodarone-induced changes in lipid metabolism are related to the changes in thyroid hormone levels. Eighteen patients received amiodarone (31 +/- 3 g cumulative dose) for six weeks. Serum triglyceride, total-cholesterol, high density lipoprotein-cholesterol and its subfractions, apolipoproteins B and AI, and plasma post-heparin lipoprotein lipase and hepatic triglyceride lipase activities were determined. Amiodarone treatment caused significant increases in serum total-cholesterol (baseline 4.4 +/- 0.21 (SE), 6 weeks 5.12 +/- 0.26 mmol/l, P less than 0.01), in low density lipoprotein cholesterol (baseline 2.61 +/- 0.26, 6 weeks 3.36 +/- 0.21 mmol/l, P less than 0.05) and in apolipoprotein B (baseline 1.95 +/- 0.15, 6 weeks 2.26 +/- 0.13 mmol/l, P less than 0.01) concentrations. Serum high density lipoprotein and its subfractions, or apolipoprotein AI levels did not change. Plasma post-heparin lipoprotein lipase activity increased (baseline 137 +/- 21, 6 weeks 168 +/- 21 U/ml, P less than 0.01) while hepatic triglyceride lipase did not change. Amiodarone also caused an increase in serum thyroxine (baseline 110 +/- 8, 6 weeks 136 +/- 6 mmol/l, P less than 0.05), although values remained in euthyroid range. In summary, amiodarone therapy increased the concentrations of atherogenic lipoproteins in the serum similar to that seen in hypothyroidism. On the other hand the effect of amiodarone on lipoprotein lipase was opposite to that seen in hypothyroidism. Therefore, amiodarone-induced changes in lipid metabolism cannot be explained solely on the basis of the changes in circulating thyroid hormone levels.
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PMID:Amiodarone-induced changes in lipid metabolism. 240 48

Twenty-five CAPD patients were given gemfibrozil in increasing doses for a total of 14 weeks. Parameters of lipid metabolism including serum total cholesterol, LDL cholesterol, HDL cholesterol, HDL2 cholesterol, HDL3 cholesterol triglyceride, apolipoprotein A-1, apolipoprotein B, postheparin lipoprotein lipase, and hepatic lipase activities were measured before the commencement, at every increment in the dose of gemfibrozil and 4 weeks after discontinuation of therapy. Gemfibrozil normalized the deranged parameters of lipid metabolism. Thus, with treatment, serum triglyceride, and total cholesterol, LDL cholesterol and apo B decreased, whereas serum HDL cholesterol, HDL2, and HDL3 (predominantly the latter subfraction), hepatic lipoprotein lipase activities increased. Apo A-1 did not change significantly. Even in normotriglyceridemic patients serum HDL cholesterol increased. The side effects consisted of muscle aches and a significant rise in serum CPK. Gemfibrozil produced a significant decrease in gamma-GT activities. A possible mechanism for the interconversion between HDL2 and HDL3 that resulted in a preferential increase in the latter was discussed. It was concluded that gemfibrozil, in a dose not exceeding 300 mg twice a day favorably improved the risk factor for ischemic heart disease in CAPD patients.
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PMID:Gemfibrozil improves abnormalities of lipid metabolism in patients on continuous ambulatory peritoneal dialysis: the role of postheparin lipases in the metabolism of high-density lipoprotein subfractions. 250 77

Treatment with etretinate is known to be effective for patients with psoriasis. However, it has been reported that the administration of etretinate often generates side effects which disturb lipoprotein metabolism. In this study, 5 patients with psoriasis vulgaris were treated with etretinate (1 mg/kg/day), and the changes in serum lipids, apolipoprotein levels, and lipoprotein lipase (LPL) activity were observed. In 4 out of the 5 cases, the above determinations were within the normal range throughout the course. However, in the case of one 35-year old man, LPL activity markedly decreased on day 28 after the administration of etretinate and was restored when the administration was suspended. Furthermore, LPL activity decreased again when the administration was resumed. Therefore, it appeared that the decrease of LPL activity in this case was mainly due to the administration of etretinate.
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PMID:[A case of psoriasis vulgaris whose lipoprotein lipase activity decreased during treatment with etretinate]. 258 75

The effects of simvastatin (MK-733), a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on serum lipids, lipoproteins, and apolipoproteins were investigated in 29 patients (12 men, 17 women, aged 37 to 73) with moderate to severe hypercholesterolemia. It was given in doses of 2.5 mg/day for four months and 5 mg/day for the succeeding four months. Total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and apolipoprotein (apo) B decreased by 18% (263 +/- 7 mg/dl to 216 +/- 7 mg/dl, P less than 0.01), 24% (180 +/- 7 mg/dl to 136 +/- 7 mg/dl, P less than 0.01), and 21% (133 +/- 4 mg/dl to 104 +/- 3 mg/dl, P less than 0.01), respectively, four months after treatment. Similar reductions (17%, 24%, and 23%, respectively, P less than 0.01) were observed at eight months. A significant reduction in triglyceride (TG) was observed (173 +/- 15 mg/dl to 136 +/- 11 mg/dl at eight months, P less than 0.01), as was a significant increase in serum high-density lipoprotein cholesterol (HDL-C) (48 +/- 2 mg/dl to 52 +/- 2 mg/dl at eight months, P less than 0.01). However, apo AI and apo AII remained unchanged. Atherogenic indices of (TC--HDL-C)/ HDL-C, LDL-C/HDL-C, and apo B/Apo AI ratios were significantly (P less than 0.01) reduced after treatment. No significant changes were observed in lipoprotein lipase, hepatic TG lipase, and lecithin: cholesterol acyltransferase (LCAT) activities. Simvastatin was well tolerated and no critical side effects were noted in the eight-month study period. These data indicate that simvastatin, even at a low dose of 2.5 to 5 mg daily, causes consistent reductions in serum TC, LDL-C, apo B, and TG, and a rise in HDL-C and antiatherogenic lipoproteins.
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PMID:Low-dose effect of simvastatin (MK-733) on serum lipids, lipoproteins, and apolipoproteins in patients with hypercholesterolemia. 273 71

A lower accessibility to water-soluble quenchers of tryptophanyls of VLDL apolipoproteins B, E, C as compared to LDL apoB chromophores has been detected by a fluorescence quenching technique. The dynamic behaviour of the tryptophanyls of VLDL amphipathic apolipoproteins E and C did not change in the presence of a detergent, Tween-20, at sub-lytic concentrations. However, a reversible structural transition registered by the 'red' shift of the emission spectrum maximum and the changes in the quenching pattern by I- occurred under these conditions. The increase in the VLDL tryptophanyl accessibility to acrylamide and the decrease in the quenching constant were observed at partial and complete solubilization of the VLDL particles by the detergent. Dissociation of apolipoproteins from VLDL occurred after their treatment with Tween-20 or lipoprotein lipase isolated from bovine milk, and the tryptophanyl population not participating in fluorescence energy transfer on lipid phase-localized fluorescent probe pyrene appeared. In the presence of Tween-20, the relative affinity of apoE for the lipid matrix of VLDL was lower than that of apoC. Besides, the uncompetitive mode of inhibition of the LPL activity by apoC-III has been demonstrated. It is suggested that: (1) the amphipathic apolipoproteins E and C are organized as clusters on the VLDL surface and/or partially shielded by apolipoprotein B: (2) self-regulation of lypolysis may exist involving detergent-like reaction product accumulation and changes in relative apolipoprotein contents.
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PMID:Topo-dynamic characteristics of human plasma VLDL apolipoproteins and efficiency of triacylglycerol hydrolysis by lipoprotein lipase. 277 63

In severe cystic acne we found low levels of high density lipoprotein-cholesterol (HDL-C) and apolipoprotein A (Apo-A) in the presence of normal total lipids. In a larger number of patients, we always observed significantly lower levels of HDL-C and Apo-A than in either age-matched controls or subjects with acne vulgaris. Since lipoprotein lipase is one major determinant of HDL concentration, we assayed the lipase activity in liver and extra-hepatic tissues by the method of Krauss et al. There was highly significant less total and hepatic lipase activity than in age-matched controls. HDL distribution was examined by zonal ultracentrifugation and a decrease in the HDL2 subclass was discovered. Since HDL are inversely correlated to atherosclerosis, cystic acne is one risk factor for atherosclerosis. The linkage between low HDL levels and severe cystic acne should be further investigated.
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PMID:Lipoprotein metabolism and lipoprotein lipase in severe cystic acne. 293 79

We have recently reported that patients with severe nodular cystic acne have much lower levels of HDL-cholesterol, apolipoprotein A and hepatic lipoprotein lipase than healthy controls or subjects with acne vulgaris. Since isotretinoin is very effective in the treatment of the nodular cystic acne but has been shown to increase blood lipid levels, we decided to compare its clinical effectiveness and its effects on lipid metabolism with those of minocycline in patients with nodular cystic acne. After 20 weeks, the number and mean diameter of the cysts were definitely decreased in both groups, but the improvement was more striking in the isotretinoin-treated group. At the end of the treatment, the HDL-C and hepatic lipoprotein lipase levels in this group were increased toward normal, but not in the minocycline-treated group. Our study showed a significant remission in the acne of patients treated with isotretinoin but not in that of the minocycline-treated patients. Furthermore isotretinoin can also correct the altered lipid metabolism in these patients.
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PMID:Isotretinoin versus minocycline in cystic acne: a study of lipid metabolism. 293 93


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