Furthermore, mechanism analysis suggested that Mettl3 deletion altered the expression pattern of hepatic lipid and glucose metabolic genes, and particularly extended the mRNA half-life of an important regulator of liver metabolism, Lpin1. Together, these findings reveal the critical role of Mettl3-mediated m6A modification in HFD-induced liver metabolic disorders and hepatogenous diabetes, supporting that m6A could be used as a potential therapeutic and diagnostic target for hepatic diseases. This evidence concerns the gene LPIN1 and liver disorder.