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Papers In Press, published online ahead of print March 14, 2006
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Endocrinology and Metabolism, Leiden University Medical Center, Leiden 2333 ZA
Corresponding Author: M.Westerterp{at}lumc.nl
Previous studies have shown that overexpression of human apoCI results in moderate hypercholesterolemia and severe hypertriglyceridemia in mice, in the presence and absence of apoE. We assessed whether physiological endogenous apoCI levels are sufficient to modulate plasma lipid levels, independently of effects of apoE on lipid metabolism, by comparing apoe-/-apoc1-/-, apoe-/-apoc1+/-, and apoe-/-apoc1+/+ mice. Presence of apoCI gene-dose-dependently increased plasma cholesterol (+45%; P<0.001) and triglycerides (TG) (+137%; P<0.001), both specific for VLDL. Whereas apoCI did not affect the intestinal [3H]TG absorption, apoCI increased the production rate of hepatic VLDL-TG (+35%, P<0.05) and VLDL-35S-apoB (+39%, P<0.01). In addition, apoCI increased the postprandial TG response to an intragastric olive oil load (+120%; P<0.05), and decreased the uptake of [3H]TG-derived free fatty acids (FFA) from intravenously administered VLDL-like emulsion particles by gonadal and perirenal white adipose tissue (WAT) (-34% and -25%, respectively; P<0.05). As LPL is the main enzyme involved in clearance of TG-derived FFA by WAT, and total post-heparin plasma LPL levels were unaffected, these data demonstrate that endogenous apoCI suffices to attenuate the lipolytic activity of LPL. We thus conclude that endogenous plasma apoCI increases VLDL-TC and VLDL-TG dose-dependently in apoe-/- mice, resulting from increased VLDL-particle production and LPL-inhibition.
Revised on February 23, 2006
Accepted on March 13, 2006
Endogenous apoCI increases hyperlipidemia in apoE-knockout mice by stimulating VLDL production and inhibiting LPL
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