β-very low density lipoprotein induces triglyceride accumulation through receptor mediated endocytotic pathway in 3T3-L1 adipocytes Original Research Article Pages 57-64 Toshihiro Yano, Shozo Kobori, Masakazu Sakai, Yoshichika Anami, Takeshi Matsumura, H

To elucidate the mechanism of triglyceride (TG) accumulation in adipocytes induced by TG-rich lipoproteins, we examined the effect of β-very low density lipoprotein (β-VLDL) on TG accumulation in 3T3-L1 adipocytes. β-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 [125I]β-VLDL to preadipocytes was inhibited completely by both β-VLDL and LDL. In sharp contrast, the binding of [125I]β-VLDL to adipocytes was inhibited completely by β-VLDL, but partially by LDL. The VLDL receptor mRNA was only expressed in adipocytes. These results suggest that β-VLDL induced TG accumulation in adipocytes may be mediated through the VLDL receptor pathway.