Licorice extract suppresses adipogenesis through regulation of mitotic clonal expansion and adenosine monophosphate-activated protein kinase in 3T3-L1 cells.

Licorice, the root of Glycyrrhiza glabra, has been observed to possess an anti-obesity effect. Previous research has suggested that licorice acetone extract (LE) has an influence on mitotic clonal expansion (MCE) and adenosine monophosphate-activated protein kinase (AMPK), which play a key role in regulating adipogenesis. This study sought further insight into the molecular mechanism of LE's anti-obesity effect using 3T3-L1 adipocytes in vitro. LE inhibited 3T3-L1 adipogenesis, and the inhibitory effect of LE on adipogenesis was most significant in the early stage of adipogenic differentiation. LE inhibited the protein expression of cyclins and cyclin-dependent kinases in the MCE stage and arrested cells in the G1 phase of the cell cycle. Furthermore, it activated AMPK via phosphorylation. Moreover, the expression levels of lipid metabolism-related genes were regulated by LE. These findings suggest the anti-obesity effect of LE via MCE and AMPK regulation. PRACTICAL APPLICATIONS: Although the anti-obesity effects of licorice have been studied, the application of functional food-related anti-obesity effects of licorice has been less than that of other extracts. The present study increases the reliability of the anti-obesity effect of licorice by suggesting a new mechanism of action and expands the application of functional foods related to the anti-obesity effect of licorice. A new mechanistic insight will not only improve the scientific knowledge but will also help to predict the side effects of licorice's anti-obesity application.