THURSDAY, April 2 (HealthDay News) -- The ability of curcumin, an antioxidant from turmeric, to reduce liver fibrosis in patients with non-alcoholic steatohepatitis is due to its ability to suppress leptin signaling in hepatic stellate cells, according to the results of a study published online March 19 in Endocrinology.
Youcai Tang and colleagues from Saint Louis University investigated how curcumin suppressed the activation of rat hepatic stellate cells, which are largely responsible for liver fibrogenesis. They hypothesized that this fibrogenesis could be activated by leptin, since patients with non-alcoholic steatohepatitis are often obese with hyperleptinemia and hepatic fibrosis.
The researchers found that curcumin interrupted leptin signaling by modifying its receptor and downstream effectors, as well as reducing the expression of the receptor. Suppressing receptor expression required the activation of peroxisome proliferator-activated receptor-gamma and synthesis of glutathione, the authors note.
"These results provide novel insights into therapeutic mechanisms of curcumin in inhibiting hepatic stellate cell activation and intervening liver fibrogenesis associated with hyperleptinemia in non-alcoholic steatohepatitis patients," Tang and colleagues conclude.
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