| First Author | Wernstedt I | Year | 2006 |
| Journal | Endocrinology | Volume | 147 |
| Issue | 6 | Pages | 2690-5 |
| PubMed ID | 16513824 | Mgi Jnum | J:129659 |
| Mgi Id | MGI:3769950 | Doi | 10.1210/en.2005-1133 |
| Citation | Wernstedt I, et al. (2006) Increased levels of acylation-stimulating protein in interleukin-6-deficient (IL-6(-/-)) mice. Endocrinology 147(6):2690-5 |
| abstractText | 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. |
