The Compound of Mangiferin-Berberine Salt Has Potent Activities in Modulating Lipid and Glucose Metabolisms in HepG2 Cells

Figure 10

A schematic figure summarizes the activities and possible pathways of MB salt in modulating lipid and glucose metabolisms. In HepG2 cells, MB salt could activate AMPK potently, during which M (in red lines) and B (in green lines) might have different modes of actions. AMPK activation could cause the phosphorylation and inhibition of ACC, which in turn stimulated cellular CPT1 activity and suppressed TG accumulation. On the other hand, AMPK activation could result in the downregulation of lipogenic genes, which could reduce intracellular TG as well. PEPCK and G6Pase mRNA expression levels cloud also be downregulated by AMPK activation, which could cause inhibition of gluconeogenesis. M and B might enhance basal glucose consumption through different mechanisms. While B was proved to increase glycolysis and basal glucose consumption in an AMPK-independent manner, the activity of M on basal glucose consumption was AMPK dependent. M was shown to stimulate glucose metabolism by increasing membrane translocation of GLUTs and enhancing glucose oxidation, two processes that were able to be modulated by AMPK. In addition, MB salt could enhance insulin sensitivity potently, although M and B might act through different mechanisms. Dashed lines and question marks represent pathways and mechanisms that need further investigation and validation.