| First Author | Mikkonen L | Year | 2013 |
| Journal | Endocrinology | Volume | 154 |
| Issue | 2 | Pages | 698-708 |
| PubMed ID | 23270804 | Mgi Jnum | J:194662 |
| Mgi Id | MGI:5474493 | Doi | 10.1210/en.2012-1846 |
| Citation | Mikkonen L, et al. (2013) SUMO-1 regulates body weight and adipogenesis via PPARgamma in male and female mice. Endocrinology 154(2):698-708 |
| abstractText | Properly functioning adipose tissue is essential for normal insulin sensitivity of the body. When mice are kept on high-fat diet (HFD), adipose tissue expands, adipocytes increase in size and number, and the mice become obese. Many of these changes are mediated by the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARgamma), the activity of which is regulated by multiple posttranslational modifications, including SUMOylation. To address the role of small ubiquitin-like modifier-1 (SUMO-1) in PPARgamma function in vivo, particularly in fat cell biology, we subjected Sumo1-knockout mice to HFD. Sumo1-null mice gained less weight and had smaller and fewer adipocytes in their gonadal fat tissue on HFD, but their glucose tolerance was similar to that of wild-type littermates. Adipogenesis was impaired in Sumo1-null cells, and expression of PPARgamma target genes was attenuated. In addition, both Sumo1-null cells and Sumo1-null mice responded less efficiently to rosiglitazone, a PPARgamma agonist. These findings indicate that SUMO-1 is important also for transcriptional activation by the PPARgamma signaling pathway and not only for trans-repressive functions of PPARgamma as previously reported. |
