COMMENTARY Curcumin adds spice to the debate: lipid metabolism in liver disease

Activated hepatic stellate cells (HSCs), the major source of the collagens involved in fibrosis and non-alcoholic fatty liver disease(NAFLD), undergo a profound loss of lipid and vitamin A storage capacity, as a consequence of a decline in expression of‘adipogenic’transcriptionfactorssuchasperoxisomeproliferator-activatedreceptor-g(PPARg).Bycontrast,hepatocytesundergoa micro- and macro-vesicular steatosis, reflecting the accumulation of triacylglycerol, and associated with chronic inflammationand fibrosis. These paradoxical findings are extended in this issue: Kang and Chen demonstrate that while low-densitylipoproteins (LDL) can activate HSCs, curcumin can inhibit this process by activation of PPARg, which not only represses geneexpression of