| First Author | Lee CC | Year | 2019 |
| Journal | Mol Cell | Volume | 76 |
| Issue | 3 | Pages | 500-515.e8 |
| PubMed ID | 31422874 | Mgi Jnum | J:283767 |
| Mgi Id | MGI:6376895 | Doi | 10.1016/j.molcel.2019.07.026 |
| Citation | Lee CC, et al. (2019) Naa10p Inhibits Beige Adipocyte-Mediated Thermogenesis through N-alpha-acetylation of Pgc1alpha. Mol Cell 76(3):500-515.e8 |
| abstractText | Diet-induced obesity can be caused by impaired thermogenesis of beige adipocytes, the brown-like adipocytes in white adipose tissue (WAT). Promoting brown-like features in WAT has been an attractive therapeutic approach for obesity. However, the mechanism underlying beige adipocyte formation is largely unknown. N-alpha-acetyltransferase 10 protein (Naa10p) catalyzes N-alpha-acetylation of nascent proteins, and overexpression of human Naa10p is linked to cancer development. Here, we report that both conventional and adipose-specific Naa10p deletions in mice result in increased energy expenditure, thermogenesis, and beige adipocyte differentiation. Mechanistically, Naa10p acetylates the N terminus of Pgc1alpha, which prevents Pgc1alpha from interacting with Ppargamma to activate key genes, such as Ucp1, involved in beige adipocyte function. Consistently, fat tissues of obese human individuals show higher NAA10 expression. Thus, Naa10p-mediated N-terminal acetylation of Pgc1alpha downregulates thermogenic gene expression, making inhibition of Naa10p enzymatic activity a potential strategy for treating obesity. |
