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’ transcription factors such as peroxisome proliferator‐activated receptor‐γ (PPARγ). By contrast, hepatocytes undergo a micro‐ and macro‐vesicular steatosis, reflecting the accumulation of triacylglycerol, and associated with chronic inflammation and fibrosis. These paradoxical findings are extended in this issue: Kang and Chen demonstrate that while low‐density lipoproteins (LDL) can activate HSCs, curcumin can inhibit this process by activation of PPARγ, which not only represses gene expression of SREBP‐2 and LDLR , but via induction of expression of SREBP‐1c , restores the lipid storage capacity characteristic of quiescent HSCs, suggesting that curcumin may be of therapeutic usage in protecting against liver steatosis and fibrosis.