Adiponectin improves branched-chain amino acid catabolism of HepG2 cells via upregulation of AMPK
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Graphical Abstract
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Abstract
AIM:To investigate the promoter effect of adiponectin (APN) on the branched-chain amino acid (BCAA) catabolism of HepG2 cells and the underlying mechanism. METHODS: HepG2 cells randomly received a control, APN, APN+CpC and AICAR. Expressions of protein p-AMPK, AMPK, p-BCKD E1α and BCKD E1α were analyzed by Western blot and the BCAA level of supernatant from cultured HepG2 was detected by ELISA. RESULTS: Compared with that of vehicle, the supernatant BCAA level from cultured HepG2 significantly decreased (P<0.01) when APN or AICAR was administered, but the expression of p-AMPK protein from cells increased (P<0.01). Administration of CpC to HepG2 cells increased the supernatant BCAA level (P<0.01), but decreased the p-AMPK expression (P<0.01). CONCLUSION: Adiponectin notably improves the BCAA catabolism of HepG2 cells through upregulating p-AMPK expression.
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