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A Transgenic Model of Visceral Obesity and the Metabolic Syn


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A Transgenic Model of Visceral Obesity and the Metabolic Syndrome

Hiroaki Masuzaki,1 Janice Paterson,23 Hiroshi Shinyama,1 Nicholas M. Morton,2 John J. Mullins,3 Jonathan R. Seckl,2 Jeffrey S. Flier1*

The adverse metabolic consequences of obesity are best predicted by the quantity of visceral fat. Excess glucocorticoids produce visceral obesity and diabetes, but circulating glucocorticoid levels are normal in typical obesity. Glucocorticoids can be produced locally from inactive 11-keto forms through the enzyme 11 hydroxysteroid dehydrogenase type 1 (11 HSD-1). We created transgenic mice overexpressing 11 HSD-1 selectively in adipose tissue to an extent similar to that found in adipose tissue from obese humans. These mice had increased adipose levels of corticosterone and developed visceral obesity that was exaggerated by a high-fat diet. The mice also exhibited pronounced insulin-resistant diabetes, hyperlipidemia, and, surprisingly, hyperphagia despite hyperleptinemia. Increased adipocyte 11 HSD-1 activity may be a common molecular etiology for visceral obesity and the metabolic syndrome.

1 Division of Endocrinology and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, MA, 02215, USA.

2 Endocrinology Unit, Molecular Medicine Center, University of Edinburgh, Edinburgh, EH4 2XU, Scotland, UK.

3 Molecular Physiology Laboratory, University of Edinburgh, Edinburgh, EH8 9AG, Scotland, UK.

*   To whom correspondence should be addressed. E-mail: jflier@caregroup.harvard.edu

(Edited by Kristy at 9:57 am on Dec. 10, 2001)

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