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 influence of vigorous activity in man on plasma lipids and lipoproteins is reviewed, with particular emphasis on high density lipoproteins. Both cross sectional and longitudinal (or training) studies have been reported, many of them of less than ideal design. Nonetheless, a consistent pattern emerges in which increased exercise levels lead to lower plasma concentrations of triglycerides and very low density lipoproteins, and of low density lipoproteins. High density lipoprotein levels increase. Sometimes, but not uniformly, plasma total cholesterol level falls as the result of these changes. The increase in plasma high density lipoprotein appears to be the result largely of an increase in the less dense HDL2 subfraction. Plasma apolipoprotein A-I levels (but not apo-A-II levels) seem to increase concomitantly. The precise biochemical mechanism responsible for these changes has not been elucidated; but the recent finding of increased lipoprotein lipase activity in adipose tissue and muscle of endurance runners suggests that increased lipolytic rate of triglyceride-rich lipoproteins may be an initial step in a sequence of events leading to higher plasma levels of HDL-2.
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PMID:The effect of exercise on plasma high density lipoproteins. 22 Apr 92

The monolayer technique has been used to study the interaction of lipids with plasma apolipoproteins. Apolipoprotein C-II and C-III from human very low density lipoproteins, apolipoprotein A-I from human high density lipoproteins and arginine-rich protein from swine very low density lipoproteins were studied. The injection of each apoprotein underneath a monolayer of egg phosphatidy[14C]choline at 20 mN/m caused an increase in surface pressure to approximately 30 mN/m. With apolipoprotein C-II and apolipoprotein C-III there was a decrease in surface radioactivity indicating that the apoproteins were removing phospholipid from the interface; the removal of phospholipid was specific for apolipoprotein C-II and apolipoprotein C-III. Although there was a removal of phospholipid from the monolayer, the surface pressure remained constant and was due to the accumulation of apoprotein at the interface. The rate of surface radioactivity decrease was a function of protein concentration, required lipid in a fluid state and, of the lipids tested, was specific for phosphatidylcholine. Cholesterol and phosphatidylinositol were not removed from the interface. The addition of 33 mol% cholesterol to the phosphatidylcholine monolayer did not affect the removal of phospholipids by apolipoprotein C-III. The addition of phospholipid liposomes to the subphase greatly facilitated the apolipoprotein C-II-mediated removal of phospholipid from the interface. Although apolipoprotein A-I and arginine-rich protein gave surface pressure increases, phospholipid was only slightly removed fromthe interface by the addition of liposomes. Based on these findings, we conclude that the apolipoproteins C interact specifically with phosphatidylcholine at the interface. This interaction is important as it relates to the transfer of the apolipoproteins C and phospholipids from very low density lipoproteins to other plasma lipoproteins. The addition of human plasma high density lipoproteins or very low density lipoproteins to the subphase increased the apolipoprotein C-mediated removal of phosphatidyl[14C]choline from the interface 3--4 fold. Low density lipoproteins did not affect the rate of decrease. During lipolysis of very low density lipoproteins to the subphase increased the apolipoprotein C-mediated removal of with the lipid monolayer. Lipolysis experiments were performed in a monolayer trough containing a surface film of egg phosphatidyl[14C]choline and a subphase of very low density lipoproteins and bovine serum albumin. Lipolysis was initiated by the addition of purified milk lipoprotein lipase to the subphase. As a result of lipolysis, there was a decrease in surface radioactivity of phosphatidylcholine. The pre-addition of high density lipoproteins decreased the rate of decrease in surface radioactivity...
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PMID:Interaction of plasma apolipoproteins with lipid monolayers. 22 40

A comprehensive assessment of lipoprotein compositional/metabolic response to incremental caloric ethanol (EtOH) doses ranging from low to moderate to high was undertaken using male squirrel monkeys. Control monkeys were maintained on a chemically defined, isocaloric liquid diet, while experimental primates wee fed increasing doses of alcohol (6, 12, 18, 24, 30, and 36% of energy) substituted isocalorically for carbohydrate at 3-month intervals. Liver function tests and plasma triglyceride were normal for all animals. Plasma cholesterol showed a transient increase at the 12% caloric dose that was attributed solely to an increase in high density lipoprotein (HDL). A more pronounced increase in plasma sterol, beginning at 24% and continuing to 36% EtOH, was the result of increments in both HDL and low density lipoprotein (LDL) cholesterol, although the contribution by the latter was substantial primarily at the 36% dose. Plasma apolipoprotein elevations (HDL apolipoprotein A-I, LDL apolipoprotein B) generally accompanied the lipoprotein lipid increases, although the first atherogenic response for LDL became manifest as a significant increase in apolipoprotein B at 18% EtOH calories. Postheparin plasma lipoprotein lipase was not affected by dietary alcohol, whereas hepatic triglyceride lipase activity showed significant increases at higher (24 and 36%) EtOH doses. Plasma lecithin-cholesterol acyltransferase activity was normal at the 6 and 12% EtOH doses, but exhibited a significant reduction beginning at 18% and continuing to 36% EtOH. Alterations in these key lipoprotein regulatory enzymes may represent the underlying metabolic basis for the observed changes in lipoprotein levels and our earlier findings of HDL2/HDL3 subfraction modifications. Results from our study indicate that in squirrel monkeys, moderate (12%) EtOH caloric intake favors an antiatherogenic lipoprotein profile (increases HDL, normal LDL levels, and lecithin-cholesterol acyltransferase activity), whereas higher doses (24-36%) produce both coronary-protective (increases HDL) and atherogenic (increases LDL) responses. Moreover, the 18% EtOH level represents an important transition dose which signals early adverse alterations in lipoprotein composition (increases apolipoprotein B) and metabolism (decreases lecithin-cholesterol acyltransferase).
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PMID:Alcohol produces dose-dependent antiatherogenic and atherogenic plasma lipoprotein responses. 157 Mar 59

We examined the changes in high-density-lipoprotein (HDL) metabolism in eight female obese patients undergoing a very-low-calorie diet (VLCD). In the first half of the study, HDL cholesterol (HDL-C), apolipoprotein A-I (apo A-I), and apo A-II showed a parallel decrease. Although lipoprotein lipase (LPL) and hepatic lipase (HTGL) did not change, lecithin: cholesterol acyltransferase (LCAT) decreased. In the latter half of the protocol, HDL-C and apo A-I increased whereas apo A-II decreased, resulting in increased apo A-I-A-II ratios. There was no change in LPL, HTGL, or LCAT. LCAT and apolipoprotein composition may be important in HDL-C changes after VLCD.
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PMID:High-density-lipoprotein metabolism during a very-low-calorie diet. 161 10

Controversy as to which lipoprotein subfraction of high-density lipoprotein (HDL) increases during alcohol consumption prompted the current study of the effects of two alcohol doses over varying time intervals on plasma lipoproteins and lipolytic enzymes. Measurements were made in 49 healthy men before and after three weeks of abstinence from alcohol and after consumption of one or three 12-ounce cans of beer per day. We found that HDL (10%), HDL2 (14%), and HDL3 (9%) cholesterol, and apolipoprotein A-I (7%) decreased with abstinence from alcohol and then increased with its consumption. These increases were not significant until after 3 weeks of daily alcohol intake, but they were significant in both the one-can and three-cans of beer per day groups. In the 23 inactive subjects HDL and HDL2 cholesterol decreased with abstinence but did not increase significantly with alcohol intake. Lipolytic enzymes were not changed by alcohol manipulation, but the level of lipoprotein lipase was higher and that of hepatic lipase was lower at each measurement point in the 26 habitually active versus the 23 inactive subjects. Adjustment for weight or skinfold thickness did not affect lipoprotein changes over time within groups but did eliminate many of the differences between activity groups. Alcohol consumption seems to be related to possibly beneficial influences on plasma HDL and HDL2 cholesterol, and may thus impact the risk of heart disease.
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PMID:Effect of alcohol dose on plasma lipoprotein subfractions and lipolytic enzyme activity in active and inactive men. 210 42

Because the apparent reduction in cardiovascular risk noted in nondiabetic populations that ingest diets rich in marine lipids containing omega-3 fatty acids is believed to result in part from their capacity to modify the composition and physicochemical behavior of lipoproteins, we sought to determine whether dietary supplementation with marine lipids might favorably affect lipoprotein composition in insulin-dependent diabetes mellitus (IDDM). Eight normolipidemic IDDM women (mean +/- SD age 29.8 +/- 4.7 yr) were studied before and 3 mo after receiving a marine-lipid concentrate (Super-EPA) containing 6 g omega-3 fatty acids and a total of 12 mg of cholesterol daily. Weight, insulin requirements, and glycosylated hemoglobin remained stable. After treatment, mean +/- SD plasma triglyceride (TG) levels fell (before, 81.7 +/- 22 mg/dl; after, 69.19 +/- 17; P less than 0.025). High-density lipoprotein2 (HDL2) cholesterol (before, 10.98 +/- 5.45 mg/dl; after, 18.43 +/- 7.93; P less than 0.01), its major apolipoprotein A-I (apoAI), and the major phospholipids (sphingomyelin and lecithin) all rose significantly. ApoB and plasma and low-density lipoprotein cholesterol levels and HDL3 composition were unchanged. Postheparin hepatic and lipoprotein lipase activities were unaffected by marine lipids. These data indicate that women with IDDM experience apparently beneficial effects on TG and HDL2 from dietary supplementation with omega-3 fatty acids administered in a low-cholesterol-containing oil without adversely affecting overall diabetes management. If these changes in lipoprotein concentration and composition prove to have antiatherogenic consequences and are free of long-term toxicity, these agents may have a role in the therapy of IDDM patients.
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PMID:Effects of omega-3 fish oils on plasma lipids, lipoprotein composition, and postheparin lipoprotein lipase in women with IDDM. 231 45

When bezafibrate therapy was interrupted in patients who had been on continuous treatment for hyperlipoproteinemia for 4-10 years, there were significant increases in the serum cholesterol, triglyceride and apolipoprotein B concentrations corresponding to an increase of the very low density lipoprotein (VLDL) levels by approximately 50%. This increase of VLDL was accompanied by reduced levels of the post-heparin lipoprotein lipase activity (LPLA) (P = 0.07) and hepatic lipase (P = 0.05) activity with a significant reduction of the skeletal muscle LPLA (P less than 0.05), but not the adipose tissue LPLA, and a retarded removal of an i v injected fat emulsion (P less than 0.01). There were no significant changes of the low or high density lipoprotein cholesterol or the apolipoprotein A-I or A-II concentrations. Three months after bezafibrate treatment the content of linoleic and gammalinoleic acid in the plasma cholesterol ester had increased significantly, while the palmitoleic and oleic acids were reduced in spite of unchanged dietary treatment. Taken together, the data indicate that a lipid-lowering effect of bezafibrate, particularly on the VLDL lipids, is maintained throughout long treatment periods. One mechanism for the reduced level of the triglyceride-rich lipoproteins is an increased activity of the lipoprotein-lipase activity in the skeletal muscle, which decreased when the treatment was interrupted. The significance of the changes of the plasma lipid fatty acid spectrum during bezafibrate treatment remains unclear.
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PMID:Interruption of long-term lipid-lowering treatment with bezafibrate in hypertriglyceridaemic patients. Effects on lipoprotein composition, lipase activities and the plasma lipid fatty acid spectrum. 236 Sep 15

Several drugs used for antihypertensive therapy may interact with lipoprotein metabolism and may increase associated coronary risk levels. beta-Blocker monotherapy with selective or nonselective beta-blockers without intrinsic sympathomimetic activity (ISA) usually increases serum triglyceride and decreases high-density lipoprotein (HDL), especially HDL2 cholesterol concentration. With the exception of the nonselective beta-blocker sotalol, beta-blocker therapy has little influence on the serum total cholesterol or low-density lipoprotein (LDL) cholesterol concentrations. The magnitude of these changes in serum lipids did not distinctly differ between selective and nonselective beta-blockers. Two beta-blockers possessing ISA, acebutolol, and pindolol did not show the increase in serum triglycerides and in serum total cholesterol or LDL cholesterol. Acebutolol showed the nonsignificant decrease in HDL cholesterol level. Pindolol with marked ISA exhibited the most favorable lipid profile, increasing serum HDL cholesterol and the ratio of HDL cholesterol to total cholesterol. The concentration of apolipoprotein A-I increased slightly during pindolol therapy. beta-Blockers with the exception of pindolol decrease the concentration of serum free fatty acids. beta-blocker therapy has little influence on the adipose tissue lipoprotein lipase activity, but lecithin cholesterol acyltransferase activity may increase during pindolol therapy.
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PMID:Effects of beta-blockers on plasma lipids during antihypertensive therapy. 240 57

Several drugs used for antihypertensive therapy may interact with lipoprotein metabolism and increase associated coronary risk factors. Beta-blocker monotherapy with cardioselective or noncardioselective beta blockers without intrinsic sympathomimetic activity (ISA) usually increases serum triglyceride and decreases the concentration of high-density lipoprotein (HDL), especially HDL2 cholesterol. With the exception of the noncardioselective beta blocker sotalol, beta-blocker therapy has little influence on the serum total cholesterol or low-density lipoprotein (LDL) cholesterol concentrations. The magnitude of these changes in serum lipids does not significantly differ between cardioselective and noncardioselective beta blockers. Two beta blockers possessing ISA, acebutolol and pindolol, did not increase serum triglycerides and serum total cholesterol or LDL cholesterol. Acebutolol produced a nonsignificant decrease in HDL cholesterol level. Pindolol, with marked ISA, exhibited the most favorable lipid profile, increasing serum HDL cholesterol and the ratio of HDL cholesterol to total cholesterol. The concentration of apolipoprotein A-I increased slightly during pindolol therapy. Beta blockers, with the exception of pindolol, decrease the concentration of serum free fatty acids. Beta-blocker therapy has little influence on the adipose tissue lipoprotein lipase activity, but lecithin cholesterol acyltransferase activity may increase during pindolol therapy. Thus beta-blocking drugs possessing ISA, such as acebutolol and pindolol, might be desirable choices as antihypertensive agents, since they do not appear to produce adverse effects on the lipid profile.
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PMID:Effect of beta blockers on blood lipid profile. 285 84

Effects on plasma lipoproteins, lecithin:cholesterol acyltransferase (LCAT), and postheparin lipase (LPL and HTGL) activities were studied in 18 patients with familial hypercholesterolemia during 8-week treatment periods with colestipol (15 g/d), fenofibrate (0.25 g/d), and colestipol plus fenofibrate. Lipoprotein lipids and apolipoproteins were determined by standard procedures, LCAT by a self-substrate method, and lipases by nonradioisotopic methods. Colestipol and fenofibrate, each given independently, caused similar percentage decreases in LDL cholesterol and apolipoprotein B: -18.4% and -8.6% v -17.4% and -10.6% Colestipol increased the VLDL cholesterol concentration, whereas fenofibrate reduced this parameter but increased HDL cholesterol and apolipoprotein A-I levels. The combination of both drugs led to a substantial fall in LDL cholesterol (-36.8%) and in apolipoprotein B (-28.3%) and maintained the other effects of fenofibrate on VLDL and HDL. Colestipol, given independently or with fenofibrate, produced an increase of the fractional esterification rate of the LCAT enzyme (+25.3% and +36.2%). Fenofibrate stimulated the postheparin LPL enzyme by +16.1% and +21.7%, respectively. This study indicates the complementarity in effectiveness when both drugs were administered together. The appropriate reduction in LDL was combined with the favorable effects on HDL in familial hypercholesterolemia.
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PMID:Low-dose colestipol plus fenofibrate: effects on plasma lipoproteins, lecithin:cholesterol acyltransferase, and postheparin lipases in familial hypercholesterolemia. 291 46


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