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This Article Full Text Full Text (PDF) All Versions of this Article: 290/6/E1068    most recent 00374.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Linscheid, P. Articles by Müller, B. Search for Related Content PubMed PubMed Citation Articles by Linscheid, P. Articles by Müller, B.

Cytokine-induced metabolic effects in human adipocytes are independent of endogenous nitric oxide

¹Department of Research, ²Division of Endocrinology, Diabetology, and Clinical Nutrition, ³Institute for Surgical Research and Hospital Management, University Hospital, CH-4031 Basel; and ⁴Division of Clinical Chemistry and Biochemistry, University Children's Hospital, Zurich, Switzerland

Submitted 11 August 2005 ; accepted in final form 20 December 2005

Nitric oxide (NO) has been recognized as a potential mediator of inflammation-induced metabolic alterations, including insulin resistance. However, expression mechanisms and potential roles of endothelial and inducible NO synthases (eNOS and iNOS, respectively) in human adipocytes are poorly understood. In the present study, we aimed to analyze several aspects of NO-related gene expression and metabolite synthesis in basal and inflammation-activated human adipocyte models. eNOS mRNA was highly expressed in omental and to a lesser extent in human subcutaneous adipose tissue biopsies, but not in purified adipocytes, in mesenchymal stem cell (MSC)- and in preadipocyte-derived adipocytes, respectively. Trace amounts of iNOS mRNA were detected in adipose tissue samples of donors with abdominal infection, as opposed to noninfected subjects. Interferon-, in combination with interleukin-1 or lipopolysaccharide, evoked a transient (4 h < time < 24 h) iNOS mRNA expression in human MSC and preadipocyte-derived adipocytes, respectively. This induction was preceded by cytokine-specific mRNAs. In addition, it was accompanied by an activation of the tetrahydrobiopterin synthesis pathway and by inhibition of peroxisome proliferator-activated receptor-2. In contrast to murine 3T3-L1-derived adipocytes, iNOS protein and NO oxidation products remained undetectable in iNOS mRNA-positive human adipocytes. Accordingly, coadministration of NOS inhibitors (i.e., N-nitro-L-arginine methyl ester, N-monomethyl-L-arginine, and 1400W) had no effects on insulin-mediated glucose uptake and lipolysis. We conclude that, in human adipocytes, endogenous NO is not involved in metabolic regulation during either basal or cytokine-activated conditions.

adipose tissue; nitric oxide synthase; insulin resistance; cytokines; lipolysis

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