Effects of baicalin on Akt /TBC1D1 phosphorylation in mouse skeletal muscle (1142.13)

Abstract

Insulin resistance is a common pathophysiological basis of type 2 diabetes. Related studies have confirmed that high lipid environment can decrease insulin sensitivity in liver, fat and skeletal muscle. TBC1D1 was recently discovered as a member of the TBC1 Rab‐GTPase family, which involved in the regulation of glucose transport and highly expressed in skeletal muscle.The phosphorylation of TBC1D1 may play a key role in regulating insulin‐stimulated glucose transport. TBC1D1 Thr590 is match for the Akt recognition motifs. Akt may activate its downstream substrate TBC1D1 Thr590 phosphorylation, and trigger glucose transporter protein GLUT4 translocation to cell surface. Baicalin is a natural compound extracted from scutellaria root, which is a kind of flavonoids. It has been reported that baicalin can show improvement diabetic rats, and also increase the glucose uptake in fat cells. However ,the effect of baicalin on skeletal muscle less reported. The aim of our study was to identify whether the beneficial effects of baicalin are related to regulate the phosphorylation of Akt and TBC1D1 in skeletal muscle. Our study results showed that baicalin can improve blood lipid, reduce the fasting blood glucose and postprandial glucose tolerance, and simultaneously increase Akt and TBC1D1 phosphorylation in skeletal muscle. These data demonstrate for the first time that intervention with baicalin may improve insulin sensitivity in skeletal muscle, which is related in part to regulate Akt /TBC1D1 signaling pathway.