HMG CoA reductase inhibitors lower LDL cholesterol without reducing Lp(a) levels.

Abstract

Lp(a) is a plasma lipoprotein particle consisting of a plasminogenlike protein [apo(a)

Tetrahydrocurcumin: Beneficial Effects on HMG-CoA Reductase enzyme and Lipoprotein Lipase Enzymes in High-fat diet-induced Hypercholesteremia Rabbits

“…However, increases in HMG-CoA reductase synthesis shortly after statin therapy restore cellular VLDL levels, and the ultimate effect of reductase inhibition is enhanced LDL receptor expression and lower plasma LDL in the setting of normal cellular cholesterol content. 20 The same inference could be attained in our study in the animal treated with the high dose of THC. The depletion of free radical scavenger system due to increased oxidative stress in the cell in high fat diet induced hyperlipidemia in animals.…”

“…[1,2] Elevation of the blood cholesterol level results in abnormal cholesterol loads into lipoproteins, which in turn results in the deposit of cholesterol on the coronary arteries. Such deposition, eventually leading to atherosclerosis, is a foremost contributory factor in diseases of the coronary arteries [3] Lipoprotein lipase (LPL) is a glycoprotein located on luminal surface of capillary endothelial cells. The role of LPL in atherosclerosis is clinically relevant because genetic defects as well as surplus of this enzyme are unpredictably frequent.…”

Cholesterol-lowering therapy may retard the progression of diabetic nephropathy

“…The satisfactory reductions in total cholesterol, LDL-cholesterol and apo B levels observed in our lovastatin-treated patients are in keeping with observations in Caucasian patients with NIDDM and hyperlipidaemia [11]. An increase in Lp(a) levels was previously reported in non-diabetic patients after 9 months of lovastatin therapy [27]. In our patients treated with lovastatin, no significant increase in plasma apo(a) and, by implication, of Lp(a) was observed during the 24-month study period, in agreement with the findings of a short-term study in Chinese patients with uraemia [28].…”

Evaluation of Pharmacokinetics of Simvastatin and Its Pharmacologically Active Metabolite from Controlled-Release Tablets of Simvastatin in Rodent and Canine Animal Models

“…However, SV is an inactive lactone prodrug which after administration is primarily metabolized into pharmacologically active metabolite simvastatin β-hydroxy acid (SVA). SVA formed in vivo is a specifi c and competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase enzyme responsible for conversion of HMG-CoA to mevalonate, which is an early and rate-limiting step in the biosynthesis of cholesterol (Gotto, 1997;Hebert et al, 1997;Kostner et al, 1989).…”