Abstract

New function of retinol-binding protein 4 (RBP4) was identified in addition to the traditional role as a vitamin A transport protein. In the state of insulin resistance even before the onset of type 2 DM, GLUT4 expression by adipocytes is decreased, but those by skeletal muscle is well preserved. Decreased adipocyte GLUT4 causes expression of RBP4 by adipocytes, thus increasing serum RBP4 levels. Increased RBP4 induces insulin resistance on liver and skeletal muscle, thus acting as a diabetogenic signal from adipose tissue. Glucose disposal rate examined by clamp study is inversely related with serum RBP4 levels in humans. In this section, recent works on the metabolism and function of RBP4 were summarized.