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

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Item Type:	Article
Title:	Adipose tissue and circulating endothelial cell specific molecule-1 in human obesity
Creators Name:	Janke, J., Engeli, S., Gorzelniak, K., Feldpausch, M., Heintze, U., Boehnke, J., Wellner, M., Herse, F., Lassalle, P., 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
ISSN:	0018-5043
Volume:	38
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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