Rosiglitazone balances insulin-induced exo- and endocytosis in single 3T3-L1 adipocytes.

Rosiglitazone (Rosi) improves insulin sensitivity and increases the translocation of glucose transporter 4 (GLUT4) to the plasma membrane (PM). This involves the fusion of membrane-bound compartments with the plasma membrane, thus increasing the plasma membrane area. However, recent work has shown that in Rosi-pretreated 3T3-L1 adipocytes membrane area did not increase following insulin application, suggesting that the rates of exo- and endocytosis are balanced. Here we examined whether Rosi differentially affects the rates of exo- and endocytosis in 3T3-L1 adipocytes. The immunolabelling of GLUT4 revealed the 3.1-fold increase in PM-resident GLUT4 in Rosi-pretreated, insulin-stimulated cells. By monitoring cumulative exocytosis and endocytosis we found that in Rosi-pretreated cells insulin substantially stimulated the rate of exocytosis and to a similar extent also the rate of endocytosis. We conclude that Rosi-pretreatment balances insulin-stimulated exocytosis and endocytosis, which may prevent insulin-mediated adipocyte cell size increase.