动物实验,I型糖尿病,阻断胰腺神经信号 z-bo 2020-10-08 305

　　In a new study published in the journal Science Advances, researchers at the La Jolla Institute for Immunology (LJI) reported that the nervous system may promote the death of pancreatic beta cells. New findings in a mouse model indicate that blocking nerve signals from the pancreas can prevent patients from developing type 1 diabetes. The lead author of the study, LJI Professor Matthias von Herrath, pointed out that "the role of neurons can prevent this process." The von Herrath laboratory has long been trying to determine the cause of type 1 diabetes. Although the disease has environmental and genetic risk factors, the onset of type 1 diabetes appears to be random. For many years, researchers have been searching for the cause of β-cell death. One theory is that these cell deaths are either due to differences in the surrounding blood supply, or they are destroyed by an immune attack caused by a virus. To test this theory, the researchers used a mouse model that can artificially induce β-cell death. They use surgery or neurotoxins or pharmacological methods to "create neurasthenia", thereby blocking most of the pancreatic sympathetic nerve signals. The researchers then used imaging equipment to track the pattern of mouse beta cell death.

　　The research team found that compared with untreated mice or mice given only β-blockers, blocking nerve signals protected mice from β-cell death. "These antipsychotics have been found to have a major impact on the development of diabetes."

　　The importance of this new discovery goes far beyond the explanation of cell death in type 1 diabetes. As you know, certain autoimmune diseases have similar cell death events. For example, vitreous inflammation and arthritis.

　　VonHerrath believes that breakthroughs in neuroimmunology have broad significance in explaining why the human body reverses organs in many autoimmune diseases. Looking ahead, the author hopes to study the cellular mechanisms between the nervous system and the development of type 1 diabetes.

　　In the latest study published in the journal Science Advances, researchers at the La Jolla Institute for Immunology (LJI) reported that the nervous system is the pancreas. He said this may promote the death of beta cells. Their new findings in a mouse model show that blocking nerve signals from the pancreas can prevent patients from developing type 1 diabetes. The lead author of the study, LJI Professor Matthias von Herrath, pointed out that "the role of neurons can prevent this process." The von Herrath laboratory has long been trying to determine the cause of type 1 diabetes. Although the disease has environmental and genetic risk factors, the onset of type 1 diabetes appears to be random. For many years, researchers have been searching for the cause of β-cell death. One theory is that these cell deaths are either due to differences in the surrounding blood supply, or they are destroyed by an immune attack caused by a virus. To test this theory, the researchers used a mouse model that can artificially induce β-cell death. They use surgery or neurotoxins or pharmacological methods to "create neurasthenia", thereby blocking most of the pancreatic sympathetic nerve signals. The researchers then used imaging equipment to track the pattern of mouse beta cell death.

　　The research team found that compared with untreated mice and mice given only beta blockers, blocking nerve signals can protect mice from beta cell death. "These antipsychotics have been found to have a major impact on the development of diabetes."

　　The importance of this new discovery goes far beyond the explanation of cell death in type 1 diabetes. As you know, certain autoimmune diseases have similar cell death events. For example, vitreous inflammation and arthritis.

　　VonHerrath believes that breakthroughs in neuroimmunology have broad significance in explaining why the human body reverses organs in many autoimmune diseases. In the future, the author hopes to study the cellular mechanisms between the nervous system and the development of type 1 diabetes.