| First Author | Lin X | Year | 2020 |
| Journal | iScience | Volume | 23 |
| Issue | 3 | Pages | 100928 |
| PubMed ID | 32151973 | Mgi Jnum | J:288453 |
| Mgi Id | MGI:6432273 | Doi | 10.1016/j.isci.2020.100928 |
| Citation | Lin X, et al. (2020) FAM13A Represses AMPK Activity and Regulates Hepatic Glucose and Lipid Metabolism. iScience 23(3):100928 |
| abstractText | Obesity commonly co-exists with fatty liver disease with increasing health burden worldwide. Family with Sequence Similarity 13, Member A (FAM13A) has been associated with lipid levels and fat mass by genome-wide association studies (GWAS). However, the function of FAM13A in maintaining metabolic homeostasis in vivo remains unclear. Here, we demonstrated that rs2276936 in this locus has allelic-enhancer activity in massively parallel reporter assays (MPRA) and reporter assay. The DNA region containing rs2276936 regulates expression of endogenous FAM13A in HepG2 cells. In vivo, Fam13a(-/-) mice are protected from high-fat diet (HFD)-induced fatty liver accompanied by increased insulin sensitivity and reduced glucose production in liver. Mechanistically, loss of Fam13a led to the activation of AMP-activated protein kinase (AMPK) and increased mitochondrial respiration in primary hepatocytes. These findings demonstrate that FAM13A mediates obesity-related dysregulation of lipid and glucose homeostasis. Targeting FAM13A might be a promising treatment of obesity and fatty liver disease. |
