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Retinol Binding Protein 4
An Adipokine potential contribution to pathophysiology of obesity



Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes.

In obesity and type 2 diabetes, expression of the GLUT4 glucose transporter is decreased selectively in adipocytes. Adipose-specific Glut4 (also known as Slc2a4) knockout (adipose-Glut4(-/-)) mice show insulin resistance secondarily in muscle and liver. Here we show, using DNA arrays, that expression of retinol binding protein-4 (RBP4) is elevated in adipose tissue of adipose-Glut4(-/-) mice. We show that serum RBP4 levels are elevated in insulin-resistant mice and humans with obesity and type 2 diabetes. RBP4 levels are normalized by rosiglitazone, an insulin-sensitizing drug. Transgenic overexpression of human RBP4 or injection of recombinant RBP4 in normal mice causes insulin resistance. Conversely, genetic deletion of Rbp4 enhances insulin sensitivity. Fenretinide, a synthetic retinoid that increases urinary excretion of RBP4, normalizes serum RBP4 levels and improves insulin resistance and glucose intolerance in mice with obesity induced by a high-fat diet. Increasing serum RBP4 induces hepatic expression of the gluconeogenic enzyme phosphoenolpyruvate carboxykinase (PEPCK) and impairs insulin signalling in muscle. Thus, RBP4 is an adipocyte-derived 'signal' that may contribute to the pathogenesis of type 2 diabetes. Lowering RBP4 could be a new strategy for treating type 2 diabetes.
Yang Q, et al. Nature. 2005 Jul 21;436(7049):356-62.
 
Metabolism: A is for adipokine
Adipokines are hormones that signal changes in fatty-tissue mass and energy status so as to control fuel usage. A fat-derived adipokine that binds to vitamin A provides a new link between obesity and insulin resistance. Clearly, the study by Yang et al.2 moves the adipocyte and its secreted factors closer to the epicentre of the diabetes and obesity epidemic.
Deborah M. Muoio1 and Christopher B. Newgard1. Nature. 2005 Jul 21;436(7049):337-8.

In normal individuals, binding of insulin to its receptor on the cell membrane stimulates glucose uptake into muscle and fat cells through the GLUT4 transporter. It also inhibits glucose production in liver, thereby maintaining normal glucose levels in the blood. In adipose tissue, glucose provides fuel for the synthesis of fat stores, which serve as the body's main energy reservoir. Yang et al.2 found that the decrease in GLUT4 expression that occurs in the fatty tissue of obese animals is accompanied by increased expression and secretion of the fat-derived factor RBP4. This factor, possibly working in concert with retinol (vitamin A), impairs insulin signalling in muscle, inhibiting glucose uptake, and interferes with insulin-mediated suppression of glucose production in the liver, causing blood glucose levels to rise.
Deborah M. Muoio1 and Christopher B. Newgard1. Metabolism: A is for adipokine. Nature 436, 337-338 (21 July 2005) | doi: 10.1038/436337a


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