The m⁶A Methyltransferase METTL3 Ameliorates Methylglyoxal-Induced Impairment of Insulin Secretion in Pancreatic β Cells by Regulating MafA Expression.

ABSTRACT: Methylglyoxal, a major precursor of advanced glycation end products, is elevated in the plasma of patients with type 2 diabetes mellitus. Islet β-cell function was recently shown to be regulated by N⁶-methyladenosine (m⁶A), an RNA modification consisting of methylation at the N6 position of adenosine. However, the role of m⁶A methylation modification in methylglyoxal-induced impairment of insulin secretion in pancreatic β cells has not been clarified. In this study, we showed that treatment of two β-cell lines, NIT-1 and β-TC-6, with methylglyoxal reduced m⁶A RNA content and methyltransferase-like 3 (METTL3) expression levels. We also showed that silencing of METTL3 inhibited glucose-stimulated insulin secretion (GSIS) from NIT-1 cells, whereas u

SUBMITTER: Cheng Y 

PROVIDER: S-EPMC9304699 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature