糖尿病,肥胖 z-bo 2020-09-17 327

　　Researchers at the Harvard School of Public Health (HSPH) have discovered a new mechanism for triggering type 2 diabetes and hope that this mechanism can be used to prevent or treat type 2 diabetes. The researchers pointed out that this mechanism mainly exists in previously undiscovered molecular pathways. This can cause liver cell damage in obese patients and may lead to insulin resistance and diabetes.

　　The main author of the article, Dean of the Harvard School of Genetics? khanS.Hotamisligil said: partly. Our findings explain a new mechanism, pointing out that metabolic stress can cause changes in the structure of liver cells that perform these functions.

　　The global obesity epidemic is related to the increase in type 2 diabetes. This is caused by the inefficient use of insulin in the body. Obese people are prone to develop inflammation of adipose tissue, which in turn reduces the sensitivity of fat cells to insulin, which can lead to type II diabetes.

　　Insulin production in type II diabetic patients is insufficient. The form of diabetes is usually related to obesity. The disease is caused by stress on beta cells. This pressure is due to the increased demand for insulin-producing cells and the higher levels of fat and sugar in the blood. Previous research has shown that in diabetes, immune system proteins (called cytokines) can be released into the environment around beta cells, causing stress.

　　In this article, the researchers used electron microscopy and other imaging techniques to analyze thousands of cells in the liver tissue of obese and lean mice. The contact point, the point of contact between the mitochondria and the endoplasmic reticulum (ER), was first discovered. With obesity, the number of MAM increases significantly. Under normal circumstances, these contact points are also necessary components for the two organelles to complete their functions, but in this article, the increase in contact points will cause calcium ions to migrate from the ER to the mitochondria. It turns out that too much stress triggers mitochondria. The researchers also adopted an important proof-of-principle method that uses synthetic molecules to reduce the physical distance between the ER and the mitochondria of cells and liver tissue. It was found that this intervention impaired mitochondrial function and made mice more susceptible to disease. A high-fat diet can cause insulin resistance and diabetes. The researchers also proved that interfering with the interaction between ER and mitochondria and calcium ion transport can significantly improve the metabolic state of obese diabetic mice, which is a potential therapeutic target. .. Hotamisrigil said: "This shows that the formation of MAM in obese patients is not good news. It may damage the function of multicellular organelles and increase cellular stress." In addition, "Nature Medicine" published another new discovery last week. When fed to obese and diabetic mice, certain cytokine IL-22 can protect beta cells from stress. Completely restore blood sugar control. According to research, oxidative stress prevents proteins (such as insulin) from being assembled into the correct structure of the right cell organ (follicle), which is very important for diabetes. Follicle pressure reduces insulin production, reminds the immune system, and may even induce β-cell suicide. At the beginning of these processes, IL-22 can stop these processes by preventing oxidative stress. This shows that it is effective for various stress inducing factors. It removes reactive oxygen species by turning off genes encoding stress-causing proteins and turning on genes encoding antioxidant proteins. In other words, IL-22 is a powerful natural antioxidant for beta cells.