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 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