METTL3 is required for maintaining β-cell function

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. (C) 2021 Elsevier Inc. All rights reserved.

Automated summary

This study found that under inflammatory and oxidative stress conditions, METTL3 is downregulated, and deletion of Mettl3 induces beta-cell failure and hyperglycemia. This suggests that METTL3 may be a potential drug target for the treatment of beta-cell failure in diabetes.