Figure 2.

The m6A modification and organ metabolism in T2D. Patients with T2D are in a condition of low m6A modification, which causes functional abnormalities in multiple organs throughout the body. Firstly, in adipose tissue, there is excessive lipid droplet accumulation, increased white adipose tissue and decreased browning, which causes the release of large amounts of TG from adipose tissue into the circulation, and these TG absorbed by the liver and skeletal muscle, resulting in inflammation and IR due to lipotoxicity. Furthermore, the condition also directly affects the function of islet β-cells, leading to abnormal differentiation and ER stress, all of which cause a decrease in insulin secretion In addition, low m6A modification alters the expression of hepatic glycolipid genes, leading to hepatic steatosis as well as reduced glycogen synthesis. All of these further aggravates the hyperglycemic symptoms in T2D patients. ER, endoplasmic reticulum; TG, triglycerides; IR, insulin resistance.