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Ronadip R. Banerjee,1*Shamina M. Rangwala,1*Jennifer S. Shapiro,1A. Sophie Rich,1Ben Rhoades,1Yong Qi,1Juan Wang,1Michael W. Rajala,2Alessandro Pocai,2Phillipp E. Scherer,2Claire M. Steppan,1Rexford S. Ahima,1Silvana Obici,2Luciano Rossetti,2Mitchell A. Lazar1
The association between obesity and diabetes supports an endocrinerole for the adipocyte in maintaining glucose homeostasis. Herewe report that mice lacking the adipocyte hormone resistin exhibitlow blood glucose levels after fasting, due to reduced hepaticglucose production. This is partly mediated by activation ofadenosine monophosphateactivated protein kinase and decreasedexpression of gluconeogenic enzymes in the liver. The data thussupport a physiological function for resistin in the maintenanceof blood glucose during fasting. Remarkably, lack of resistindiminishes the increase in post-fast blood glucose normallyassociated with increased weight, suggesting a role for resistinin mediating hyperglycemia associated with obesity.
1 Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, and The Penn Diabetes Center, 611 CRB, 415 Curie Boulevard, Universityof Pennsylvania School of Medicine, Philadelphia, PA 19104, USA. 2 Department of Medicine, Diabetes Research and Training Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
* These authors contributed equally to this work.
To whom correspondence should be addressed: E-mail: lazar{at}mail.med.upenn.edu
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