出版社：American Society for Biochemistry and Molecular Biology
摘要：CD36 is involved in high-affinity peripheral FFA uptake. CD36-deficient ( cd36 −/−) mice exhibit increased plasma FFA and triglyceride (TG) levels. The aim of the present study was to elucidate the cause of the increased plasma TG levels in cd36 −/− mice. cd36 −/− mice showed no differences in hepatic VLDL-TG production or intestinal [3H]TG uptake compared with wild-type littermates. cd36 −/− mice showed a 2-fold enhanced postprandial TG response upon an intragastric fat load ( P P cd36 −/− mice may impair LPL-mediated TG hydrolysis. Postheparin LPL levels were not affected. However, the in vitro LPL-mediated TG hydrolysis rate as induced by postheparin plasma of cd36 −/− mice in the absence of excess FFA-free BSA was reduced 2-fold compared with wild-type plasma ( P cd36 −/− mice by infusion prolonged the plasma half-life of glycerol tri[3H]oleate-labeled VLDL-like emulsion particles by 2.5-fold ( P We conclude that the increased plasma TG levels observed in cd36 −/− mice are caused by decreased LPL-mediated hydrolysis of TG-rich lipoproteins resulting from FFA-induced product inhibition of LPL.
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