Pemt, or phosphatidylethanolamine N-methyltransferase, is an enzyme that catalyzes the production of phosphatidylcholine. This process is crucial for lipid metabolism, as phosphatidylcholine is an important component of cell membranes. The non-canonical synthesis pathway involving Pemt is part of the overall lipid-related biological pathways [2].

Reduced expression of hepatic Pemt in mice causes steatosis, inflammation, and fibrosis, suggesting its key role in maintaining liver health [1]. In HCV-infected cells, Pemt is induced, mediating steatosis and supporting virus replication. Knocking down Pemt with siRNA inhibits virus replication and reduces lipid content in these cells [2]. Also, in humans, Pemt rs7946 polymorphism exerts sex-specific effects on choline requirement and hepatic steatosis risk. For example, in postmenopausal Taiwanese women with the Pemt rs7946 GG genotype, current dietary choline intake may be inadequate to minimize hepatic steatosis risk, while in older men, high choline intake may increase the risk of non-alcoholic fatty liver disease [3].

In conclusion, Pemt is essential for lipid metabolism, especially in processes related to phosphatidylcholine synthesis. Its role in liver-related diseases such as non-alcoholic fatty liver disease and HCV-induced steatosis is significant. The study of Pemt using mouse models and human genetic polymorphism analysis helps to understand its function in maintaining normal physiological conditions and the pathogenesis of related diseases.