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

---

Query: EC:3.1.1.34 (lipoprotein lipase)
7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lipoprotein concentration and composition before and after Intralipid infusion were investigated in seven adult surgical patients receiving continuous total parenteral nutrition. Plasma samples were obtained prior to parenteral alimentation, after 7 days of glucose/amino acid solution without Intralipid, and again following 5 days of daily Intralipid. Cholesterol, triglyceride, protein, and phospholipid concentrations were determined on very low-, low-, and high-density lipoprotein from each specimen. After Intralipid very low-density lipoprotein concentration fell to 29% (p less than 0.015) of pre-Intralipid levels. There was no substantial increase in low-density lipoprotein phospholipid post-Intralipid to suggest the presence of lipoprotein-X. Plasma total triglyceride levels declined by 33% after Intralipid (p less than 0.01) and plasma total cholesterol levels rose by 40% (p less than 0.02). In our patients, in whom metabolic mechanisms were not saturated, it would appear that Intralipid was metabolized by activated lipoprotein lipase pathways, without the appearance of hyperlipidemia or abnormal lipoproteins.
...
PMID:Human plasma lipoproteins and total parenteral nutrition with intravenous fat emulsion. 643 30

The study was conducted in mice in order to elucidate whether psycho-social stimulation produced in an interconnecting box system was able to induce alterations in some circulating lipid fractions and in heart lipoprotein lipase (LPL) activity. Two groups of male mice were studied: A--a group isolated in glass jars from weaning to the age of 12-13 weeks and then transferred to the interconnecting box system with a reduced number of female mice, to 26 weeks of age; B--a second group isolated from weaning to 26 weeks of age, as an extremely opposite situation to group A. Control mice were kept in standard cages from weaning to the end of the experiment. Total cholesterol and triglycerides were determined in blood plasma, and heart LPL activity was determined in small portions of the ventricles. Cholesterol decreased significantly in group A (p less than 0.002) and in group B (p less than 0.05) vs. controls. No alterations were observed either in plasma triglycerides or in LPL activity in either of the two groups.
...
PMID:Plasma lipid levels and heart lipoprotein lipase activity in mice under social stress. 654 55

The effect of lipid composition and structure on the lipoprotein lipase-catalyzed hydrolysis of triacylglycerols was determined in a monolayer system consisting of purified bovine milk lipoprotein lipase and fatty acid-free albumin. In a monolayer of dioleoylphosphatidylcholine containing 1-6 mol% of either tri[14C]oleoylglycerol or tri[14C] palmitoylglycerol , lipoprotein lipase catalyzed the hydrolysis of the unsaturated triacylglycerol at a higher rate than the saturated lipid and in either the presence or absence of apolipoprotein C-II, the activator protein for the enzyme. For example, with 3 mol% triacylglycerol and in the presence of apolipoprotein C-II, the rate of the lipoprotein lipase-catalyzed hydrolysis of tri[14C]oleoylglycerol was 27 mumol oleic acid produced/h per mg enzyme vs. 12 mumol for tri[14C] palmitoylglycerol . The effect of phospholipid fatty acyl chain length and unsaturation/saturation, polar head group and surface density on the lipoprotein lipase-catalyzed hydrolysis of tri[14C]oleoylglycerol was determined. The rate of enzyme hydrolysis of triacylglycerol was similar whether the phospholipid was a diester or diether lipid or the polar head group was ethanolamine or choline. In general, phospholipids with shorter and unsaturated fatty acyl chains gave higher rates of lipoprotein lipase hydrolysis of triacylglycerol than the corresponding longer and saturated lipids. However, with all phospholipids tested, the rate of enzyme hydrolysis decreased with increasing surface density. Lipoprotein lipase showed no activity toward triacylglycerol in a monolayer of sphingomyelin; addition of dioleoylphosphatidylcholine to the monolayer enhanced the rate of enzyme catalysis. Cholesterol (50 mol%) in a dipalmitoylphosphatidylcholine monolayer increased the rate of the lipoprotein lipase-catalyzed hydrolysis of tri[14C]oleoylglycerol, whereas cholesterol decreased the rate in a dioleoylphosphatidylcholine monolayer. The effect of phospholipid structure and surface density on lipoprotein lipase activity could not be accounted for by the amount of apolipoprotein C-II which was present at the interface. Based on these findings and other reports in the literature, we suggest that the catalytic activity of lipoprotein lipase toward tri[14C] oleylglycerol in various monolayers is dependent on the conformation or appropriate physical state of the triacylglycerol substrate at the lipid interface.
...
PMID:Effect of monolayer lipid structure and composition on the lipoprotein lipase-catalyzed hydrolysis of triacylglycerol. 671 77

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.
...
PMID:Lipid disorders in diabetes. 675 32

Data now available suggest that a dynamic equilibrium exists in the plasma lipoproteins. Chylomicrons and very low density lipoproteins (VLDL) are primary secretory products of cells and carry triglycerides through the blood stream. As intravascular triglyceride hydrolysis occurs via the action of lipoprotein lipase (LPL), the further metabolism of nontriglyceride constituents of chylomicrons and VLDL can be followed along two interrelated pathways. Along the core pathway, cholesterol ester increasingly becomes a major core lipid with resultant formation of intermediate density (IDL, or remnant particles) and eventually low density (LDL) lipoprotein. Concomitant with reduction of core volume, redundant surface lipids and proteins move along a surface pathway and either form high density (HDL) lipoprotein precursors, or become associated with existing HDL particles. Cholesterol esters are formed via the action of lecithin: cholesterol acyltransferase (LCAT) in HDL. Therefore, action of LPL and LCAT on triglyceride-rich lipoproteins and their catabolic products is sufficient and necessary for formation, in plasma, of LDL and HDL. Once formed, all plasma lipoproteins are further remodelled by the activity of exchange and transfer reactions. In humans, a major remodelling occurs through exchange of LDL and HDL cholesterol ester by VLDL (and chylomicrons) triglyceride. The reaction is the main source of cholesterol esters in triglyceride-rich lipoproteins and is responsible for the enrichment of LDL and HDL with triglycerides. When followed by triglyceride lipolysis, this cycle results in limitation of size and cholesterol content of both LDL and HDL. The physiology and pathophysiology of the plasma lipid transport system in humans can therefore be fully appreciated only when the interrelations of all these metabolic reactions is taken into account.
...
PMID:Lipoproteins and lipoprotein metabolism. A dynamic evaluation of the plasma fat transport system. 684 39

Lipoprotein lipase activity was measured in heparin extracts of aortic intima and adventitia from normal and cholesterol-fed turkeys. This lipolytic activity showed typical characteristics of lipoprotein lipase i.e., requirement of serum for activity and a 92% inhibition by protamine sulfate. The highest lipoprotein lipase activity was found in the adventitia of the abdominal aorta. Lipoprotein lipase activity was greater in the intima of the thoracic aorta than in the intima of the abdominal aorta. This higher activity of thoracic intima was not correlated with development of fibrous plaques which were found only in abdominal aorta. Cholesterol-feeding resulted in plasma very low density lipoproteins enriched in cholesterol-ester but had no effect on the level of lipoprotein lipase activity of aortic intima. Cholesterol-feeding, although altering lipoprotein composition, did not increase aortic intima lipoprotein lipase activity.
...
PMID:Lipoprotein lipase activity in turkey aorta. 715 23

Diabetes mellitus was induced in the rats with streptozotocin. Lipoproteins obtained by ultracentrifugation and column chromatography were analyzed. Some groups of rats fed on high cholesterol diet for 3 weeks, others were fed on normal chow. I) In diabetic rats fed on normal chow, the following results were obtained. i) Hypertriglyceridemia, even in fasting state, occurred in the rats whose fasting blood sugar exceeded 270 mg/dl. High density lipoprotein (HDL)-Cholesterol was neither increased, nor decreased. ii) An apoCII peptide, known as the activator of lipoprotein lipase, was decreased in plasma HDL of diabetic rats with hypertriglyceridemia (48% of norm). In diabetic rats without hypertriglyceridemia, the CII peptide was not decreased. iii) An apo E peptide in HDL was decreased significantly (28%-41% of norm). iv) The potency of apoHDL derived from diabetic rats with hypertriglyceridemia for activating lipoprotein lipase was considerably decreased, compared to normal apoHDL. II) In diabetic rats fed on high cholesterol diet (DMC-rats), striking alterations in plasma lipoproteins occurred. i) Compared to normal fed on high cholesterol diet, plasma total cholesterol level rose significantly (7 fold), with an appreciable increase in levels of phospholipids and triglycerides. HDL-cholesterol was decreased. ii) An abnormal peak appeared on agarose column chromatogram. This lipoprotein was estimated to possess an apoE-AII peptide complex, addition to apoB, E, C, AI and AIV, and showed one major band (having a slightly slower mobility than VLDL) and one minor band (alpha mobility) on electrophoresis, and exhibited two types of particles on electronmicroscopy. Diameters of these particles were 40.6 +/- 36.7 A, and 240.3 +/- 47.4 A. iii) The HDL of DMC-rats also had the apoE-AII complex. These results may suggest that the decrease in apoCII in HDL cause the diabetic hypertriglyceridemia, and the apoE-AII complexes observed in cholesterol feeding hinder the incorporation of lipoproteins into the liver.
...
PMID:[On the etiology of diabetic hyperlipidemia from the aspects of the metabolism of ApoHDL (author's transl)]. 731 64

Effects of a combination therapy of fluvastatin, a new inhibitor of HMG-CoA reductase, and niceritrol on lipid metabolism were investigated measuring a wide range of parameters in 42 patients with primary hypercholesterolemia. After a wash-out period patients were randomly allocated to 1 of the 2 groups, the fluvastatin-preceding group (G-1) and the niceritrol-preceding group (G-2). In G-1 fluvastatin monotherapy (30 mg/day) significantly decreased total cholesterol (TC) and LDL-cholesterol (LDL-C). There was no significant change in HDL-cholesterol (HDL-C), triglyceride (TG) and lipoprotein (a) (Lp(a)). Further effect in HDL-C and TG was observed after the addition of niceritrol (750 mg/day). On the other hand, in G-2, while niceritrol alone (750 mg/day) produced no significant change in TC, LDL-C, HDL-C, TG and Lp(a), the addition of fluvastatin (30 mg/day) reduced TC and LDL-C levels significantly. Cholesterol ester transfer (CET) activity was significantly reduced by niceritrol monotherapy. After the concomitant use of the 2 drugs CET activity was significantly reduced only in G-2. No significant change in lipoprotein lipase and hepatic triglyceride lipase activities were observed in the 2 groups at either point in time. No serious adverse effect was observed in this study. It is concluded that fluvastatin is an effective drug for lowering LDL-cholesterol and causes no adverse alteration in lipid metabolism. Combination with niceritrol at a dose of 750 mg/day dose not appear to augment or attenuate beneficial effects of fluvastatin.
...
PMID:Effects of fluvastatin, a new inhibitor of HMG-CoA reductase, and niceritrol on serum lipids, lipoproteins and cholesterol ester transfer activity in primary hypercholesterolemic patients. 758 1

Elevated plasma intermediate density lipoprotein (IDL) is one of the features of uremic dyslipidemia which is potentially atherogenic. We examined the effects of pravastatin, an HMG-CoA reductase inhibitor, on IDL levels as well as other lipoprotein parameters in 19 uremic patients treated with hemodialysis (HD, n = 11) or continuous ambulatory peritoneal dialysis (CAPD, n = 8). The patients were administered 5 mg/day pravastatin for the initial 4 weeks and 10 mg/day for the subsequent 12 weeks. In the analysis of the total subjects, IDL-cholesterol was reduced by 31% as well as low density lipoprotein (LDL)-cholesterol. Cholesterol in very low density lipoprotein (VLDL) also decreased whereas that in high density lipoprotein (HDL) did not. Significant decrease of serum triglycerides was due mainly to reduced IDL- and LDL-triglycerides. Apolipoprotein (apo) A-I did not change, whereas apo A-II, B, C-II, C-III, E, and B/A-I ratio were significantly lowered. Pravastatin did not affect measured activity of lecithin: cholesterol acyltransferase, post-heparin plasma lipoprotein lipase or hepatic triglyceride lipase. HD and CAPD patients responded almost equally to the treatment. IDL elevation was present independent of serum total cholesterol, and it was lowered by pravastatin even in non-hypercholesterolemic subjects. There was no critical adverse effect besides transient and asymptomatic increase of serum creatine kinase level. We conclude that pravastatin can be a safe and effective approach to the management of dyslipidemia in uremic patients who have an elevated level of IDL.
...
PMID:Reduction of intermediate density lipoprotein by pravastatin in hemo- and peritoneal dialysis patients. 760 82

A series of 2-benzoyl-4,4-dialkyl-3,5-isoxazolidinediones proved to have potent hypolipidemic activity, lowering both serum cholesterol and triglyceride levels at 10 or 20 mg/kg/day, IP and orally in rodents. 2-(3,4,5-Trimethoxybenzoyl)-4,4-diethyl-3,5-isoxazolidinedione+ ++ (4) afforded the best hypolipidemic activity lowering normolipidemic CF1 mouse serum cholesterol levels 49% and serum triglyceride levels 34% at 20 mg/kg/day, IP. Compound 4 was selected as a typical derivative of the chemical class for further detailed studies. Serum cholesterol levels in normolipidemic Sprague Dawley male rats were reduced 45% after 8 weeks at 10 and 20 mg/kg/day of compound, orally. Serum triglyceride levels were reduced 38-49% at 10 and 20 mg/kg/day, orally. In vitro liver enzyme activities studies in normolipidemic CF1 mice showed the compound inhibited mitochondrial citrate exchange, acetyl CoA synthetase, HMG CoA reductase, acyl CoA cholesterol acyl transferase, acetyl CoA carboxylase, sn-glycerol-3-phosphate acyl transferase, phosphatidylate phosphohydrolase and heparin-induced lipoprotein lipase activities with increases in the activities of cholesterol ester hydrolase and ATP-dependent citrate lyase. Similar enzyme activities were inhibited in vivo except HMG CoA reductase activity was not inhibited in rat liver or small intestinal mucosa after 8 weeks drug administration. Cholesterol levels were reduced in tissues after 8 weeks administration of compound 4 in normolipidemic rats. Bile cholesterol and triglyceride levels were elevated after two weeks administration to rats at 20 mg/kg/day. Serum lipoprotein levels in normolipidemic and hyperlipidemic rats showed the cholesterol levels in VLDL and LDL fractions after 4, 6 and 8 weeks at 10 and 20 mg/kg/day were reduced whereas HDL-cholesterol levels were significantly elevated. Studies demonstrated that 3H-cholesterol and 14C-palmitic acid incorporation into lipids of the lipoprotein fraction was reduced by the drug but 32P-incorporation was generally elevated. The agent demonstrated no observable toxicity in rats after 8 weeks administration, orally. The acute toxicity study in normolipidemic mice at 20, 40 and 100 mg/kg/day, IP, demonstrated no observable harmful effects of the drug.
...
PMID:Investigation of 3,5-isoxazolidinediones as hypolipidemic agents in rodents. 772 85


<< Previous 1 2 3 4 5 6 7 Next >>

---