Helicobacter pylori infection aggravates hepatic steatosis by lactylation-driven WTAP-mediated m6A modification

Helicobacter pylori (H. pylori) infection has been investigated as a potential risk factor for extragastric diseases, including metabolic dysfunction-associated fatty liver disease (MASLD). However, the details of the underlying mechanisms remain inadequately understood. In this study, we elucidate that H. pylori infection exacerbates hepatic metabolic disorders both in vitro and in vivo, manifesting as increased lipid deposition and insulin resistance. Mechanistically, H. pylori infection further upregulates m6A content, particularly increasing the expression of one of the m6A methyltransferases, WTAP. Overall design: The m6A-Seq analysis of the HepG2 cells co-cultivated with H.pylori and controls.