The current biology of resistin

Authors

  • Claire M. Steppan,

    1. From the Division of Endocrinology, Diabetes, and Metabolism, Departments of Medicine and Genetics, and The Penn Diabetes Center, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
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  • Mitchell A. Lazar

    1. From the Division of Endocrinology, Diabetes, and Metabolism, Departments of Medicine and Genetics, and The Penn Diabetes Center, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
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Mitchell A. Lazar MD, PhD, University of Pennsylvania School of Medicine, 611 CRB, 415 Curie Blvd., Philadelphia, PA 19104-6149, USA.
(fax: (215) 898-5408; e-mail: lazar@mail.med.upenn.edu)

Abstract.

Obesity and noninsulin-dependent diabetes mellitus are globally epidemic. Insulin resistance is a major contributor to the pathogenesis of type II diabetes and plays a role in numerous other metabolic disorders including hypertension, dyslipidaemia and atherosclerosis. Obesity, in particular visceral adiposity, is positively correlated with insulin resistance. Although this correlation between adiposity and insulin resistance is well established in human beings as well as in rodent models, the mechanisms involved in obesity-related insulin resistance are not fully defined. One mechanism is that factors secreted from adipocytes can affect peripheral insulin resistance. One candidate for such a factor is resistin, an adipocyte-secreted hormone that impairs glucose homeostasis and insulin action in the mouse. This review will summarize our current understanding of resistin and will attempt to provide a framework for future study of its role in rodent and human physiology.

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