Apolipoprotein C-III deficiency accelerates triglyceride hydrolysis by lipoprotein lipase in wild-type and apoE knockout mice.

摘要: Previous studies with hypertriglyceridemic APOC3 transgenic mice have suggested that apolipoprotein C-III (apoC-III) may inhibit either the apoE-mediated hepatic uptake of TG-rich lipoproteins and/or lipoprotein lipase (LPL)-mediated hydrolysis TG. Accordingly, apoC3 knockout (apoC3-/-) are hypotriglyceridemic. In present study, we attempted to elucidate mechanism(s) underlying these phenomena by intercrossing apoC3-/- apoE-/- study effects apoC-III deficiency against a hyperlipidemic background. Similar apoE+/+ mice, exhibited marked reduction in VLDL cholesterol and TG, indicating which exerts its lipid-lowering effect act independent apoE. On both backgrounds, showed normal intestinal lipid absorption TG secretion. However, turnover TG-labeled emulsion particles were cleared much more rapidly whereas clearance apoB, as marker for whole particle liver, was not affected. Furthermore, it shown cholesteryl oleate-labeled also faster mice. Thus mechanisms hypolipidemia involve efficient well an enhanced selective esters from plasma. summary, our support concept is effective inhibitor reveal potential regulating role respect esters. Chemicals/CAS: Apolipoprotein C-III; Apolipoproteins C; E; Chylomicrons; Lipoprotein Lipase, EC 3.1.1.34; Lipoproteins, VLDL; Triglycerides