G6PC1 and Hyperglycemia: In our work, IR promoted the upregulation of inactivated FOXO1 expression, which further promoted PEPCK and G6Pase expression, then upregulated the relative transcriptional level of glucose transporter 2 (GLUT2), which is responsible for the transport of glucose from the liver to the blood, leading to aggravated gluconeogenesis and enhanced MBCDs-induced hyperglycemia in mice.