出版社：American Society for Biochemistry and Molecular Biology
摘要：Previous studies have shown that overexpression of human apolipoprotein C-I (apoC-I) results in moderate hypercholesterolemia and severe hypertriglyceridemia in mice in the presence and absence of apoE. We assessed whether physiological endogenous apoC-I levels are sufficient to modulate plasma lipid levels independently of effects of apoE on lipid metabolism by comparing apolipoprotein E gene-deficient/apolipoprotein C-I gene-deficient ( apoe −/− apoc1 −/−), apoe −/− apoc1 +/−, and apoe −/− apoc1 +/+ mice. The presence of the apoC-I gene-dose-dependently increased plasma cholesterol (+45%; P P 3H]TG absorption, it increased the production rate of hepatic VLDL-TG (+35%; P 35S]apoB (+39%; P P 3H]TG-derived FFAs from intravenously administered VLDL-like emulsion particles by gonadal and perirenal white adipose tissue (WAT) (−34% and −25%, respectively; P apoe −/− mice, resulting from increased VLDL particle production and LPL inhibition.
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