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Increased Levels of Acylation-Stimulating Protein in Interleukin-6-Deficient (IL-6^–/–) Mice

Research Center for Endocrinology and Metabolism (I.W., B.O., M.J., L.M.S.C., K.W., V.W.), Wallenberg Laboratory (I.W., V.W.), Lundberg Laboratory for Diabetes Research (U.S.), Departments of Internal Medicine and Surgery (V.W.), Sahlgrenska Academy, Sahlgrenska University Hospital, SE-41345 Goteborg, Sweden; and Centre de Recherche de l’Hôpital Laval, Université Laval (S.P., K.C.), Québec, Canada G1V 4G5

Address all correspondence and requests for reprints to: Dr. Ville Wallenius, Department of Surgery, Sahlgrenska University Hospital, Bruna Stråket 11, SE-41345 Goteborg, Sweden. E-mail: ville.wallenius{at}medic.gu.se.

IL-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 preobese IL-6^–/– were compared with those of IL-6^+/+ mice using DNA arrays. Genes that were up-regulated in IL-6^–/– mice included the factors transthyretin and properdin in white adipose tissue 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 in adipocytes, and ASP-deficient mice are resistant to diet-induced obesity. In line with the increases in 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 in IL-6^–/– mice decreased ASP levels significantly by 25–60%. In conclusion, ASP levels are increased in preobese IL-6^–/– mice. This increase may result in increased triacylglycerol formation and uptake in IL-6^–/– adipocytes and thereby contribute to the development of obesity in IL-6^–/– mice.

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