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Capsiate, a nonpungent ingredient of CH-19 Sweet, exhibits anti-obesity effects on animals and humans. This study investigated the effects and molecular mechanism of capsiate on lipid and glucose metabolism in PA-treated HepG2 cells. Results showed that compared with the PA-alone group, 100 μM capsiate inhibited lipid accumulation, decreased TG (0.0562 ± 0.0142 vs 0.0381 ± 0.0055 mmol/g of protein; P = 0.024) and TC (0.1087 ± 0.0037 vs 0.0359 ± 0.0059 mmol/g of protein; P = 0.000) levels, and increased the HDL-C level (0.0189 ± 0.0067 vs 0.1050 ± 0.0106 mmol/g of protein; P = 0.000) and glycogen content (0.0065 ± 0.0007 vs 0.0146 ± 0.0008 mg/10 6 cells; P = 0.000) of PA-treated HepG2 cells; 100 μM capsiate also upregulated the level of CD36 ( P = 0.000), phosphorylation of ACC ( P = 0.034), and expression of CPT1 ( P = 0.013) in PA-treated HepG2 cells, leading to an enhancement of lipid metabolism. Meanwhile, 100 μM capsiate upregulated the levels of GLUT1, GLUT4, GK, and phosphorylation of GS ( P = 0.001, 0.029, 0.000, and 0.045, respectively) and downregulated the PEPCK level ( P = 0.001) to improve glucose metabolism in PA-treated HepG2 cells. Furthermore, the levels of phosphorylation of AMPK and expression of SIRT1 in HepG2 cells were increased by a 100 μM capsiate treatment ( P = 0.001 and 0.000, respectively), while the FGF21 level was decreased ( P = 0.003). Most of these effects were reversed by pretreatment with compound C, a selective AMPK inhibitor. Thus, capsiate might improve lipid and glucose metabolism in HepG2 cells by activating the AMPK/SIRT1 signaling pathway.

Improvement of Lipid and Glucose Metabolism by Capsiate in Palmitic Acid-Treated HepG2 Cells via Activation of the AMPK/SIRT1 Signaling Pathway