KCNH6 Enhanced Hepatic Glucose Metabolism through Mitochondrial Ca²⁺ Regulation and Oxidative Stress Inhibition

Figure 6

KCNH6 ameliorated hepatic glucose metabolism disorders in reversal KO mice. (a) Lentiviruses with GFP (LV-Ctrl) or Kcnh6 (LV-Kcnh6) were injected into 12-week-old male KO mice via the tail vein ( TU/g body weight). (a) Restoration of KCNH6 expression reversed the glucose metabolism disorder in KO mice ( for the WT group; for the KO group). (b) mRNA levels of PEPCK and G6pase in the livers of mice detected by qRT-PCR (). (c) Levels of PEPCK and G6pase detected by western blotting (). (d) Fluo-4 AM staining for detecting changes in calcium ion levels in the cytoplasm of primary liver cells of KO mice ( for the WT group; for the KO group). (e) Calcium ion levels of mitochondria in the KO mouse liver as detected by Rhod-2-AM staining ( for the WT group; for the KO group). (f) Protein levels of the JNK signaling pathway as detected by western blotting (). (g) Western blotting was performed for measuring of the protein levels of genes related to the p38MAPK signaling pathway in the LV-Ctrl and LV-Kcnh6 mice (). , , and vs. the LV-Ctrl group; mice in each group. Statistical comparisons were calculated using the (b–g) Mann–Whitney test and (a) unpaired-sample -test.

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