动物造模,胰岛素 z-bo 2020-09-15 371

　　Glucagon can stimulate the glucose produced by the liver to enter the blood, thereby maintaining the brain's fuel supply. Insulin can block the secretion of glucagon, counteract the effect of glucagon on the liver, and instruct the body to take up glucose from the blood. Patients with type 2 diabetes cannot respond properly to insulin, and the production of glucagon is out of control, which causes the liver to overproduce glucose and cause high blood sugar levels. Patients with type 2 diabetes often use insulin in an effort to overcome insulin resistance and lower blood sugar levels.

　　But insulin also instructs the body to produce fat, so when mice are given the high levels of insulin needed to control excess glucose, the mice will get fat.

　　By studying genetically modified mice lacking glucagon receptors, researchers at the Touchstone Diabetes Center of UT Southwestern Medical Center found that if they were given the high levels of insulin found in type 2 diabetic mice (and humans), these genetically modified mice Mice will become fat, which is not the case in other cases. This result suggests that the high levels of insulin found in people with insulin resistance and type 2 diabetes are a contributing factor to obesity and its complications.

　　Research results indicate that doctors may need to reconsider the use of intensive insulin therapy to control hyperglycemia (high blood sugar levels) in obese diabetic patients with hyperinsulinemia (insulin overproduction). In addition, research results show that inhibiting the effect of glucagon can prevent hyperinsulinemia without causing diabetes. The research team found that inhibiting glucagon in obese, insulin-resistant type 2 diabetic mice can restore blood sugar to normal levels.