first sighs, modern medicine really has too little understanding of the human body. Many times the research is only based on the surface and is too macroscopic. As for what the microscopic world is like, we don’t know. Just like diabetes , we all know Insulin can lower blood sugar, but as a hormone, insulin acts on target cells , and we don’t know what kind of reaction occurs to lower blood sugar. This also limits the research and development of hypoglycemic drugs.
Similarly, it is well known that overnutrition and unhealthy eating habits can lead to insulin resistance and ultimately type 2 diabetes. But what kind of reaction took place to cause the target cells to develop insulin resistance and pancreatic beta cell apoptosis? What substances participated in the reaction and what targets they acted on. We don’t understand this process either. Therefore, modern medicine has not been able to completely solve diabetes.
If these molecular mechanisms are discovered, it will not be a very difficult problem to develop corresponding therapeutic drugs based on the current medical level, combined with the corresponding targets, especially with the rise of biological drugs now, there are comparisons in these aspects Big advantage.
Recently, the team of Professor Chen Wenbiao of Vanderbilt University in the United States has made a certain breakthrough in this regard. They discovered that during the development of type 2 diabetes, macrophages and neutrophils participate in the mechanism of regulating the death of pancreatic islet β cells, and will The findings were published in Cell Reports.
Previously, Professor Chen Wenbiao's team has discovered that RIPK3-mediated islet inflammatory response will lead to endoplasmic reticulum sustained stress, which in turn leads to pancreatic islet β-cell apoptosis, and found that this process is related to macrophages.
This time, Yang Binyuan, a postdoctoral fellow in Chen Wenbiao's team, further explored the involvement of macrophages and neutrophils in the process of pancreatic islet β-cell apoptosis, and finally proved that macrophage invasion can cause pancreatic islets under the condition of excessive nutrition. Tnfα-dependent Cxcl8a expression is increased in β cells. Increased Cxcl8a will recruit neutrophils to attack beta cells contacted by macrophages and cause their death.
subsequently found through mouse experiments that if uses the CXCR1/2 antagonist to block neutrophil chemotaxis , it can reduce the apoptosis of pancreatic beta cells and slow down the progression of diabetes.
However, this research still has limitations. The research was only conducted in the zebrafish model, which should be quite different from the situation in adults. However, this research result is still of great help to humans in overcoming the problem of diabetes. It provides new research ideas for avoiding the further deterioration of type 2 diabetes and treating diabetes. I believe that with the gradual deepening of research, humans will eventually defeat diabetes. .
This research also has great enlightenment for us ordinary people, that is, confirms that overnutrition plays a vital role in the pathogenesis of type 2 diabetes.. Of course, overnutrition is not just about eating too much sugar, but also includes many other nutrients, such as high triglycerides and central obesity, which can also easily cause insulin resistance, which is also related to not paying attention to the usual diet and eating too greasy food. .
Therefore, it makes sense that we often say "70% full, 30% cold". After all, type 2 diabetes is a "disease of wealth". In an era of hunger and hunger, it is unlikely to get diabetes. It is today's overnutrition and irregular diet that aggravate the possibility of diabetes.
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