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Journal of Lipid Research, Vol. 45, 1640-1648, September 2004
Copyright © 2004 by American Society for Biochemistry and Molecular Biology

Regulation of the nitric oxide system in human adipose tissue

Stefan Engeli^1,2,*, Jürgen Janke^1,*, Kerstin Gorzelniak^*, Jana Böhnke^*, Nila Ghose^*, Carsten Lindschau^*, Friedrich C. Luft^* and Arya M. Sharma

^* HELIOS-Klinikum Berlin, Franz Volhard Clinic, Charité University Medicine in Berlin, and Max Delbrück Center for Molecular Medicine, Berlin, Germany
Department of Internal Medicine, Hamilton General Hospital, McMaster University, Hamilton, Ontario, Canada

² To whom correspondence should be addressed. e-mail: engeli{at}fvk.charite-buch.de

Nitric oxide (NO) is involved in adipose tissue biology by influencing adipogenesis, insulin-stimulated glucose uptake, and lipolysis. The enzymes responsible for NO formation in adipose cells are endothelial NO synthase (eNOS) and inducible NO synthase (iNOS), whereas neuronal NO synthase (bNOS) is not expressed in adipocytes. We characterized the expression pattern and the influence of adipogenesis, obesity, and weight loss on genes belonging to the NO system in human subcutaneous adipose cells by combining in vivo and in vitro studies. Expression of most of the genes known to belong to the NO system (eNOS, iNOS, subunits of the soluble guanylate cyclase, and both genes encoding cGMP-dependent protein kinases) in human adipose tissue and isolated human adipocytes was detected. In vitro adipogenic differentiation increased the expression level of iNOS significantly, whereas eNOS expression levels were not influenced. The genes encoding eNOS, iNOS, and cGMP-dependent protein kinase 1 were expressed at higher levels in obese women. Expression of these genes, however, was not influenced by 5% weight loss. Insulin and angiotensin II (Ang II) increased NO production by human preadipocytes in vitro.

Increased eNOS and iNOS expression in adipocytes and local effects of insulin and Ang II may increase adipose tissue production of NO in obesity.

Supplementary key words adipocytes • obesity • hypertension • insulin resistance • adipogenesis

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