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A Transgenic Model of Visceral Obesity and the Metabolic Syndrome
Hiroaki Masuzaki,1Janice Paterson,23Hiroshi Shinyama,1Nicholas M. Morton,2John J. Mullins,3Jonathan R. Seckl,2Jeffrey S. Flier1*
The adverse metabolic consequences of obesity are best
predicted by the quantity of visceral fat. Excess glucocorticoids
producevisceral obesity and diabetes, but circulating glucocorticoidlevels are normal in typical obesity. Glucocorticoids can be producedlocally from inactive 11-keto forms through the enzyme 11
hydroxysteroiddehydrogenase type 1 (11 HSD-1). We created
transgenic mice overexpressing11 HSD-1 selectively in adipose
tissue to an extent similar tothat found in adipose tissue from obese
humans. These mice hadincreased adipose levels of corticosterone and
developed visceralobesity that was exaggerated by a high-fat diet. The
mice alsoexhibited pronounced insulin-resistant diabetes,
hyperlipidemia,and, surprisingly, hyperphagia despite hyperleptinemia.
Increasedadipocyte 11 HSD-1 activity may be a common molecular
etiologyfor 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{at}caregroup.harvard.edu
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