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

ABSTRACT: KCNH6 has been proven to affect glucose metabolism and insulin secretion both in humans and mice. Further study revealed that Kcnh6 knockout (KO) mice showed impaired glucose tolerance. However, the precise function of KCNH6 in the liver remains unknown. Mitochondria have been suggested to maintain intracellular Ca²⁺ homeostasis; ROS generation and defective mitochondria can cause glucose metabolism disorders, including type 2 diabetes (T2D). Here, we found that Kcnh6 attenuated glucose metabolism disorders by decreasing PEPCK and G6pase abundance and induced Glut2 and IRS2 expression. Overexpression of Kcnh6 increased hepatic glucose uptake and glycogen synthesis. Kcnh6 attenuated intracellular and mitochondrial calcium levels in primary hepatocytes and reduced intracellular RO

SUBMITTER: Zhang YC 

PROVIDER: S-EPMC9547380 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature