Fig. 2: Cr³⁺ attenuates ATP synthase activity and activates AMPK through binding to ATP5B catalytic site.

a Dose-dependent inhibition of ATP synthase activity by Cr³⁺ treatment in HepG2 cells under hyperglycaemia condition. ATP5B inhibitor Octyl-α-ketoglutarate (O-KG) is used as a control. n = 3; mean ± SEM. Two-sided Student’s t test. b Time-dependent inhibition of ATP synthase activity by Cr³⁺ treatment in HepG2 cells under hyperglycaemia condition. n = 3; mean ± SEM. Two-sided Student’s t test. c AMP/ATP ratios in HepG2 cells under different conditions. n = 6; mean ± SEM. Two-sided Student’s t test. d Dose-dependent and (e) Time-dependent activation of AMPK and ACC by Cr³⁺ in HepG2 cells under hyperglycaemia condition. n = 3; mean ± SEM. f The effect of ATP5B gene silencing on Cr³⁺-mediated AMPK and ACC activation in HepG2 cells. n = 3; mean ± SEM. Two-sided Student’s t test. g The substitution of Mg²⁺ in ATP5B by Cr³⁺ as determined by ICP-MS. n = 3; mean ± SEM. h The metal contents in Cr-ATP5B upon supplementation of various amounts of Mg²⁺. n = 3; mean ± SEM. i The Cr³⁺ binding capability of wild-type (WT) ATP5B and various mutants as determined by ICP-MS. n = 3; mean ± SEM. Two-sided Student’s t test. GAPDH is used as a control. Source data are provided as a Source Data file.