Beta-very low density lipoprotein induces triglyceride accumulation through receptor mediated endocytotic pathway in 3T3-L1 adipocytes.

ATHEROSCLEROSIS(1997)

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摘要
To elucidate the mechanism of triglyceride (TG) accumulation in adipocytes induced by TG-rich lipoproteins, we examined the effect of beta-very low density lipoprotein (beta-VLDL) on TG accumulation in 3T3-L1 adipocytes. beta-VLDL did not induce TG accumulation in 3T3-L1 preadipocytes but in 3T3-L1 adipocytes. TG accumulation was significantly inhibited by cytochalasin B, an inhibitor of receptor mediated endocytosis. In contrast, cytochalasin B did not inhibit free fatty acid induced TG accumulation in adipocytes. The binding of [I-125]beta-VLDL to preadipocytes was inhibited completely by both beta-VLDL and LDL. In sharp contrast, the binding of [I-125]beta-VLDL to adipocytes was inhibited completely by beta-VLDL, but partially by LDL. The VLDL receptor mRNA was only expressed in adipocytes. These results suggest that beta-VLDL induced TG accumulation in adipocytes may be mediated through the VLDL receptor pathway. (C) 1997 Elsevier Science Ireland Ltd.
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关键词
very low density lipoprotein receptor,beta-VLDL,3T3-L1 cells,triglyceride accumulation,lipoprotein lipase
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