| First Author | Li X | Year | 2021 |
| Journal | Metabolism | Volume | 116 |
| Pages | 154702 | PubMed ID | 33417895 |
| Mgi Jnum | J:305101 | Mgi Id | MGI:6681951 |
| Doi | 10.1016/j.metabol.2021.154702 | Citation | Li X, et al. (2021) METTL3 is required for maintaining beta-cell function. Metabolism 116:154702 |
| abstractText | N6-methyladenosine (m(6)A) mRNA methylation has been shown to regulate obesity and type 2 diabetes. However, whether METTL3, the key methyltransferase for m(6)A mRNA methylation, regulates beta-cell failure in diabetes has not been fully explored. Here, we show that METTL3 is downregulated under the inflammatory and oxidative stress conditions, and islet beta-cell-specific deletion of Mettl3 induces beta-cell failure and hyperglycemia, which is likely due to decreased m(6)A modification and reduced expression of insulin secretion-related genes. Overall, METTL3 might be a potential drug target for the treatment of beta-cell failure in diabetes. |
