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Zinc‐α 2 ‐glycoprotein, a lipid mobilizing factor, is expressed and secreted by human (SGBS) adipocytes
Author(s) -
Bao Yi,
Bing Chen,
Hunter Leif,
Jenkins John R.,
Wabitsch Martin,
Trayhurn Paul
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2004.11.042
Subject(s) - adipose tissue , endocrinology , medicine , adipokine , adipocyte , downregulation and upregulation , messenger rna , rosiglitazone , secretion , biology , tumor necrosis factor alpha , receptor , chemistry , leptin , biochemistry , gene , obesity
Zinc‐α 2 ‐glycoprotein (ZAG), a lipid mobilizing factor, is expressed in mouse adipose tissue and is markedly upregulated in mice with cancer cachexia. We have explored whether ZAG is expressed and secreted by human adipocytes, using SGBS cells, and examined the regulation of ZAG expression. ZAG mRNA was detected by RT‐PCR in mature human adipocytes and in SGBS cells post‐, but not pre‐, differentiation to adipocytes. Relative ZAG mRNA levels increased rapidly after differentiation of SGBS cells, peaking at day 8 post‐induction. ZAG protein was evident in differentiated adipocytes (by day 3) and also detected in the culture medium (by day 6) post‐induction. The PPARγ agonist rosiglitazone induced a 3‐fold increase in ZAG mRNA level, while TNF‐α led to a 4‐fold decrease. Human adipocytes express and secrete ZAG, with ZAG expression being regulated particularly through TNF‐α and the PPARγ nuclear receptor. ZAG is a novel adipokine, which may be involved in the local regulation of adipose tissue function.