Glycycoumarin prevents hepatic steatosis through activation of adenosine 5,-monophosphate (AMP)-activated protein kinase signaling pathway and up-regulation of BTG1/Tob-1

- Glycycoumarin inhibits lipid accumulation induced by OA/PA in cultured liver cells.
- Glycycoumarin prevents hepatic steatosis induced by MCD diet in a mouse model.
- Glycycoumarin prevents hepatic steatosis through activating AMPK signaling pathway.

Glycycoumarin (GCM) is a representative of coumarin compounds isolated from licorice, a popular herbal plant which is widely used to treat various diseases including liver diseases. This study was designed to evaluate the protective effects of GCM on hepatic steatosis in the setting of non-alcoholic fatty liver disease using both cell culture model of OA(oleic acid)/PA(palmitate acid)-induced lipids accumulation and a murine model of hepatic steatosis induced by a methionine-choline-deficient (MCD) diet. Results showed that GCM was highly effective in removing lipids droplets in both in vitro and in vivo models. Mechanistically, we demonstrated that activation of adenosine 5,-monophosphate (AMP)-activated protein kinase (AMPK)-mediated lipophagy, lipogenesis inhibition and enhanced fatty acid oxidation contributed to the anti-lipogenic effect of GCM. Our findings support a possible usefulness of GCM as a novel agent to mitigate hepatic steatosis.