Introduction Serum retinol-binding protein (RBP4) is secreted by the liver andadipocytes and is implicated in systemic insulin resistance. RBP4transports retinol and circulates in the plasma by binding to the largertransthyretin (TTR) homotetramer, forming a protein complex that reducesrenal clearance of RBP4. In insulin-resistant ob/ob mice, urinaryfractional excretion of RBP4 was reduced, consistent with increasedretention; while TTR level is elevated (1). RBP4 is encoded by the RBP4 gene that maps to chromosome 10q23-q24 linked to increased risk for type2 diabetes in different populations (2 - 3). Transgenic overexpressionof RBP4 or injection of recombinant RBP4 in normal mice causes insulinresistance. Conversely, genetic deletion of RBP4 enhances insulinsensitivity. Increasing serum RBP4 induces hepatic expression of thegluconeogenic enzyme phosphoenolpyruvate carboxykinase and impairsinsulin signaling in muscle tissue (4). Expression of RBP4 is induced inadipose tissue as a consequence of decreased glucose transporter GLUT4expression. Increased serum RBP4 is associated with insulin resistance,Type II diabetes, and metabolic syndrome such as obesity, glucoseintolerance, dyslipidemia, and hypertension (5 - 6). Plasma RBP4concentration might be a biomarker of nephropathy and cardiovasculardisease in type 2 diabetic subjects (7).