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Adipose tissue and circulating endothelial cell specific molecule-1 in human obesity

Item Type:Article
Title:Adipose tissue and circulating endothelial cell specific molecule-1 in human obesity
Creators Name:Janke, J. and Engeli, S. and Gorzelniak, K. and Feldpausch, M. and Heintze, U. and Boehnke, J. and Wellner, M. and Herse, F. and Lassalle, P. and Luft, F.C. and Sharma, A.M.
Abstract:Adipocytes produce the endothelial-cell specific molecule-1 (ESM-1), which inhibits leukocyte adhesion and migration through the endothelium. This study investigates ESM-1 expression and regulation in human adipose tissue. Subcutaneous abdominal adipose tissue was obtained from seventy postmenopausal women. Fourteen women subsequently underwent non-pharmacological weight reduction. In vitro experiments were performed on adipocytes isolated from human mammary adipose tissue. We determined gene expression by TaqMan RT-PCR and measured ESM-1 levels in serum and cell culture medium by ELISA. Mature adipocytes produced ESM-1. ESM-1 gene expression was higher in adipocytes than in preadipocytes. Cortisol inhibited ESM-1 gene expression in preadipocytes. Insulin and cortisol inhibited adipocyte ESM-1 production in adipocytes. This inhibitory effect of insulin was attenuated by insulin resistance, as ESM-1 gene expression in subcutaneous adipose tissue was increased in obese, hyperinsulinemic women. In contrast, ESM-1 serum levels were reduced in obese women and inversely correlated to C-reactive protein levels. Five percent weight loss did not markedly change gene expression. Circulating ESM-1 levels increased significantly, albeit modestly. ESM-1 is actively produced by adipocytes. However, since ESM-1 adipocyte gene expression and circulating plasma levels are not correlated, other sources of ESM-1 may be more important. Circulating ESM-1 levels are reduced in the overweight and obese, consistent with the notion that ESM-1 may play some role in obesity-associated vascular disease.
Keywords:ESM-1, Adipocytes, Preadipocytes, Adipogenesis, Insulin resistance
Source:Hormone and Metabolic Research
Page Range:28-33
Date:January 2006
Official Publication:https://doi.org/10.1055/s-2006-924973
PubMed:View item in PubMed

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