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This version published online on March 2, 2006
Endocrinology, doi:10.1210/en.2005-1133
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Submitted on September 7, 2005
Accepted on February 17, 2006

Increased levels of Acylation Stimulating Protein (ASP) in Interleukin-6-deficient (IL-6 -/-) mice

I. Wernsted, B. Olsson, M. Jernås, S. Paglialunga, L. M.S. Carlsson, U. Smith, K. Cianflone, K. Wallenius, and V. Wallenius*

Research Centre for Endocrinology and Metabolism, Wallenberg laboratory, The Lundberg Laboratory for Diabetes Research, Dept. Internal Medicine, and Dept. of Surgery, Sahlgrenska Academy at Sahlgrenska University Hospital, Göteborg, Sweden. Centre de Recherche de l'Hôpital Laval, Université Laval, Québec, Canada

* To whom correspondence should be addressed. E-mail: ville.wallenius{at}medic.gu.se.

Interleukin-6-deficient (IL-6 -) mice develop obesity at 6-7 months of age. To elucidate the mechanisms of this mature-onset obesity, global gene expression profiles of 3-month-old pre-obese IL-6 -/- were compared with IL-6 +/+ mice using DNA arrays. Genes that were upregulated in IL-6 -/- mice included the factors transthyretin and properdin in white adipose tissue (WAT), and adipsin in muscle. These factors have been shown to influence the formation of acylation stimulating protein (ASP), a cleavage product of complement C3. ASP stimulates the synthesis of triacylglycerol (TG) in adipocytes, and ASP-deficient mice are resistant to diet-induced obesity. In line with the increases of transthyretin, properdin and adipsin, ASP levels in serum were increased by 31-54% in IL-6 -/- compared with IL-6 +/+ mice. Furthermore, IL-6 replacement treatment to IL-6 -/- mice decreased ASP levels significantly by 25-60%. In conclusion, ASP levels are increased already in pre-obese IL-6 -/- mice. This increase may result in increased TG formation and uptake in IL-6 -/- adipocytes and thereby contribute to the development of obesity in the IL-6 -/- mice.
Key words: knockout • adipose tissue • triglyceride • complement C3




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