脑细胞PPARγ,动物实验 z-bo 2020-08-18 600

　　The researchers found that when a small part of the brain cells of mice PPARγ (a nuclear receptor) are blocked, the mice's diet will be reduced and fat tolerance will be higher. Professor Sabrina Diano said that these mice eat fat and carbohydrates, but not fat, which indicates that PPARγ, the neuronal nuclear receptor that produces POMC, can regulate body obesity in mice without causing obesity.

　　POMC neurons are located in the hypothalamus, these can regulate food intake. When these neurons are activated, the body becomes full and food intake is hindered. The receptor PPARγ regulates the activation of POMC neurons. In this article, the researchers investigated whether transgenic mice lacking the receptor PPARγ can be used to suppress obesity associated with a high-fat, high-sugar diet. Diano said that he found that blocking the receptor PPARγ in mouse hypothalamic cells can increase the level of free radical formation in POMC neurons and enhance POMC activity. This research has very practical significance for the treatment of diabetes.

　　PPARγ is the target of the insulin sensitizer thiazolidinedione (TZD), which can lower blood sugar levels. However, patients have been using it for a long time. The medicine has gained weight. This study developed a treatment for type II diabetes targeting PPARγ receptors, because the weight gain of diabetic patients treated with TZD may be due to the effects of the drug on the brain. May not penetrate. Now that the TZD compound is complete, you can maintain effective levels without being affected by the side effects of TZD (weight gain). The next step is to test the above theory in a mouse model of diabetes.