Figure 1.

Diagram illustrates the mechanisms of insulin resistance. Normally, after a meal, pancreatic β cells secrete insulin in response to meal-induced increase in blood glucose. First, insulin promotes muscle tissue to assimilate blood glucose and convert it into muscle glycogen and protein. Additionally, insulin also promotes hepatocytes to absorb blood glucose and converts it into liver glycogen. Meanwhile, insulin can inhibit glycogenolysis and gluconeogenesis to reduce postprandial blood glucose in liver tissues. Moreover, insulin can stimulate adipose cells to assimilate blood glucose and convert it into fat. Under starvation conditions, the secretion of insulin will be inhibited, and the hypoglycemic activity of insulin on liver, muscle, and adipose is also suppressed. Under insulin-resistant conditions, lipolysis is promoted in adipose tissue, thereby releasing excess fatty acids into the blood and then transporting them to the liver and skeletal muscle tissue. Then, fatty acids can activate PKC, which may markedly impair insulin signal pathway to cause hepatic and skeletal muscle insulin resistance. IR, insulin resistance; DNL, de novo lipogenesis; DAG, diacylglycerol; IRS, insulin receptor substrate; PKC, protein kinase C; ChREBP, carbohydrate responsive element-binding protein; ACC, acetyl-CoA carboxylase; GLUT, glucose transporter.