This Article Full Text Full Text (PDF) Data Supplement All Versions of this Article: 25/5/1002    most recent 01.ATV.0000160611.68791.c6v1 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 Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Maquoi, E. Articles by Lijnen, H. R. Search for Related Content PubMed PubMed Citation Articles by Maquoi, E. Articles by Lijnen, H. R. Pubmed/NCBI databases Gene GEO Profiles HomoloGene UniGene Substance via MeSH Medline Plus Health Information Nutrition Obesity Related Collections Animal models of human disease Energy metabolism Gene expression Genetically altered mice

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:1002.)
© 2005 American Heart Association, Inc.

Atherosclerosis and Lipoproteins

Role of Gas-6 in Adipogenesis and Nutritionally Induced Adipose Tissue Development in Mice

Erik Maquoi; Gabor Vörös; Peter Carmeliet; Désiré Collen; H. Roger Lijnen

From the Center for Molecular and Vascular Biology (E.M, G.V., D.C., H.R.L.), KU Leuven and the Center for Transgene Technology and Gene Therapy (P.C.), Flanders Interuniversity Institute for Biotechnology, Campus Gasthuisberg O & N, Leuven, Belgium.

Correspondence to H. Roger Lijnen, Center for Molecular and Vascular Biology, KU Leuven, Campus Gasthuisberg, O & N, Herestraat 49, B-3000 Leuven, Belgium. E-mail roger.lijnen{at}med.kuleuven.ac.be

Objective— A potential role of growth arrest-specific gene 6 (Gas-6) in energy storage in adipose tissue was investigated in murine models of obesity. Gas-6 is a ligand for the Axl, C-Mer, and Sky family of tyrosine kinase receptors.

Methods and Results— Whereas Gas-6, C-Mer, and Sky were expressed in mature murine adipocytes, the expression of Axl was restricted to the stromal-vascular fraction, which includes pre-adipocytes. During the in vitro conversion of adipogenic 3T3-F442A cells into mature adipocytes, the expression of Gas-6 increased in undifferentiated confluent pre-adipocytes during a transient phase of growth arrest. On treatment of these cells with an adipogenic medium, Gas-6 expression decreased sharply, coinciding with expression of early adipocytes markers. This modulation was not observed in the nonadipogenic 3T3-C2 cells. The Gas-6 mRNA level was transiently downregulated during nutritionally induced expansion of adipose tissues in vivo. When kept on a standard diet, no significant difference in either total body weight or weight of gonadal or subcutaneous fat pads was observed between Gas-6 deficient and wild-type mice. On exposure to a high-fat diet, however, Gas-6-deficient mice had significantly less fat mass than their wild-type counterparts.

Conclusions— Gas-6 enhances the accumulation of adipose tissue in diet-induced obese mice.

A role of Gas-6 in adipose tissue homeostasis was investigated in murine models of obesity. Gas-6 expression was transiently downregulated during nutritionally induced expansion of adipose tissues. On exposure to a high-fat-diet, Gas-6 mice were leaner than their wild-type counterparts, suggesting that Gas-6 enhances the accumulation of adipose tissue in diet-induced obesity.

Key Words: adipogenesis • adipose tissue • Gas-6 • high-fat diet • obesity

This article has been cited by other articles:

				S. B. English and A. J. Butte Evaluation and integration of 49 genome-wide experiments and the prediction of previously unknown obesity-related genes Bioinformatics, November 1, 2007; 23(21): 2910 - 2917. [Abstract] [Full Text] [PDF]