![]() Atorvastatin significantly increased ( P < 0.002) the fractional catabolic rate (FCR) of VLDL apoB, IDL apoB, and LDL apoB but did not affect the production of apoB in any lipoprotein fraction or in the turnover of apoAI. Fenofibrate significantly decreased ( P < 0.001) plasma triglyceride and VLDL apoB and elevated HDL 2 cholesterol ( P < 0.001), HDL 3 cholesterol ( P < 0.01), apoAI ( P = 0.01), and apoAII ( P < 0.001) concentrations, but it did not significantly alter LDL cholesterol. Compared with placebo, atorvastatin significantly decreased ( P < 0.001) plasma concentrations of cholesterol, triglyceride, LDL cholesterol, VLDL apoB, intermediate-density lipoprotein (IDL) apoB, and LDL apoB. ApoAI and apoB kinetics were studied following intravenous d 3-leucine administration using gas-chromatography mass spectrometry with data analyzed by compartmental modeling. The effects of atorvastatin (40 mg/day) and micronised fenofibrate (200 mg/day) on the kinetics of apoAI and apoB were investigated in a controlled cross-over trial of 11 dyslipidemic men with the metabolic syndrome. The metabolic syndrome is characterized by insulin resistance and abnormal apolipoprotein AI (apoAI) and apolipoprotein B-100 (apoB) metabolism that may collectively accelerate atherosclerosis.
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