Gut-derived bacterial endotoxins, such as lipopolysaccharide (LPS), contribute to the
pathogenesis of steatosis and steatohepatitis by activating Kupffer cells, the resident liver
macrophages. Exposure of macrophages to low doses of LPS causes hyporesponsiveness
upon subsequent endotoxin challenge, a phenomenon termed endotoxin or LPS tolerance.
In the present study, we aimed to examine whether LPS-induced lipid accumulation is
affected by endotoxin tolerance. LPS pretreatment reduced the expression of …