Abstract
Background and Aims: Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease and share common risk factors with atherosclerosis. Excessive hepatic lipid accumulation promotes macrophages/Kupffer cells activation, resulting in exacerbation of insulin resistance and progression of nonalcoholic steatohepatitis (NASH). The purpose of this study was to investigate the impact of a myeloid deletion of lysophosphatidylcholine acyltransferase 3 (LPCAT3) on these metabolic disorders. This enzyme, involved in phospholipid remodeling, inserts mainly arachidonic acid (AA) into cell membranes.,
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