METTL3 is required for maintaining β-cell function.

N6-methyladenosine (m⁶A) mRNA methylation has been shown to regulate obesity and type 2 diabetes. However, whether METTL3, the key methyltransferase for m⁶A mRNA methylation, regulates β-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 β-cell-specific deletion of Mettl3 induces β-cell failure and hyperglycemia, which is likely due to decreased m⁶A modification and reduced expression of insulin secretion-related genes. Overall, METTL3 might be a potential drug target for the treatment of β-cell failure in diabetes.

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