Mettl3 deficiency leads to impaired insulin secretion via regulating Ire1a of mature β-cells in mice.

ABSTRACT: The modification of N6-methyladenosine (m⁶A) influences the translation and stability of transcripts, allowing for the coordination of gene regulation during cell state maintenance and transition. Deregulation of components in the m⁶A regulatory network is associated with glucose homeostasis and development of diabetes. In this study, we investigated the functional role of Mettl3, which is the key component of the m⁶A methyltransferase complex, in regulating β-cell identity and function in two pancreatic β-cell-specific Mettl3 knockout mouse models. The glucose metabolic phenotype, β-cell proliferation, islet architecture and insulin secretion were analyzed in vivo. We next analyzed the expression levels of genes associated with endoplasmic reticulum (ER) s

SUBMITTER: Zhang X 

PROVIDER: S-EPMC11953400 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature