Mogrol, a biometabolite of mogrosides, functions by inhibiting the ERK1/2 and STAT3 pathways, diminishing CREB activation, and activating AMPK signaling.

Mogrol, but not mogrosides, suppressed triglyceride accumulation by affecting early (days 0 2) and late (days 4 8), but not middle (days 2 4), differentiation stages.?At the late stage, mogrol increased AMP-activated protein kinase (AMPK) phosphorylation and reduced glycerol-3-phosphate dehydrogenase activity.?At the early stage, mogrol promoted AMPK phosphorylation, inhibited the induction of CCAAT/enhancer-binding protein β (C/EBPβ;?a master regulator of adipogenesis), and reduced 3T3-L1 cell contents (e.g., clonal expansion).?In addition, mogrol, but not the AMPK activator AICAR, suppressed the phosphorylation and activity of the cAMP response element-binding protein (CREB), which regulates C/EBPβ expression.?Mogrol suppressed adipogenesis by reducing CREB activation in the initial stage of cell differentiation and by activating AMPK signaling in both the early and late stages of this process[2].