Coompo Research Chemicals

The alimentary obesity model was established by hyperalimentation. The wet weight of fat,fat index, number of fat cells per unit visual field, Lee's index, jejunum microvillus area,serum triglyceride and cholesterol were selected to observe the anti-obesity effect of phillyrin. Phillyrin could lower wet weight of fat (P < 0.01), fat index (P < 0.05 or P < 0.01),diameter of fat cell and Lee's index (P < 0.05), decrease the jejunum microvillus area,lower the level of serum triglyceride and cholesterol. Phillyrin has anti-obesity effect in
nutritive obesity mice.

Phillyrin suppressed high glucose-induced lipid accumulation in HepG2 cells. Phillyrin strongly inhibited high glucose-induced fatty acid synthase (FAS) expression by mmodulating sterol regulatory element-binding protein-1c (SREBP-1c) activation. Moreover, use of the pharmacological AMP-activated protein kinase (AMPK) inhibitor compound C revealed that AMPK is essential for suppressing SREBP-1c expression in phillyrin-treated cells. Liver kinase B1 (LKB1) phosphorylation is required for the phillyrin-enhanced activation of AMPK in HepG2 hepatocytes. These results indicate that phillyrin prevents lipid accumulation in HepG2 cells by blocking the expression of SREBP-1c and FAS through LKB1/AMPK activation, suggesting that phillyrin is a novel AMPK activator with a role in the prevention and treatment of obesity.

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