Texas diabetes and endocrinology such as immune system disorders to a certain degree, which eventually leads to the killing of insulin-secreting β cells in the pancreas and becoming fewer and fewer. What has not been completely clear so far is that neither genetic factors nor behavioral factors, whether for diabetes type I or type II, can not explain why some people get diabetes while others do not get the disease under all conditions.
I have long been regarded as two different diseases. Diabetes type I has a great relationship with heredity and is an autoimmune disease; while diabetes type II is a metabolic disorder, which is closely related to obesity and a lifestyle with little exercise. “They are two fundamentally different diseases,” said Ronald Kahn, a professor of internal medicine at Harvard Medical School and a senior researcher at the Joslin Diabetes Research Center. “Although these two diseases cause the same metabolic defects and long-term complications, they There are very different pathologies and pathogenesis.”
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However, researchers are revealing more and more commonalities between type I and type II diabetes, many of which are beyond the previous understanding of them. Diabetes type I and type II have similar pathogenesis such as immune system disorders to a certain degree, which eventually leads to the killing of insulin-secreting β cells in the pancreas and becoming fewer and fewer. What has not been completely clear so far is that neither genetic factors nor behavioral factors, whether for diabetes type I or type II, can not explain why some people get diabetes while others do not get the disease under all conditions.
Although there are some common risk factors,
these two diseases do have their own independent conditions. Scientists have studied the influence of many genetic factors, epigenetic factors and environmental factors on each type of diabetes. They are trying to find the exact cause of the two diseases in order to effectively prevent them.
Diabetes Type I: Is there a family history?
Diabetes type I is an autoimmune disease, and its main pathological change is that the immune system kills its own pancreatic β-cells that produce insulin. It has a clear genetic disease feature—family history. In addition, it is now known that 60% of the genetic risk factors for diabetes type I come from several specific auto-compatible antigen (HLA) gene variants. The proteins expressed by these variant genes can present antigens to immune cells and participate It has an immune attack on its own beta cells. Therefore, a detailed understanding of HLA can help reveal the origin of diabetes type I.
In the past five years
Texas diabetes and endocrinology George Eisenbarth and immunologist John Kappler of the Klerrad Medical School in Denmark have discovered a complex of three proteins through close cooperation. They believe that this protein complex is diabetes type I. The key to disease. This complex includes antigen-presenting HLA particles, the presented antigen, and a T cell receptor capable of recognizing the above-mentioned HLA particle and the presented antigen binding body.
T cells are the central link in all autoimmune diseases,
including diabetes type I. Under normal circumstances, cytotoxic T cells can only eliminate infected cells; and those T cells that react to the body’s own molecules are eliminated before they mature, which gives the immune system what is called autoimmune tolerance. But this process found errors in patients with texas diabetes and endocrinology type I: the main function is to recognize the T lymphocytes of their own pancreatic β cells into the circulation, attack and damage the pancreatic β cells.
How these T lymphocytes, which should be cleared by the body,
escape and mature is still unclear. Several factors may be involved in this process, such as mutations in the insulin gene, changes in diet and intestinal flora. Eisenbarth has been involved in a lot of work exploring the pancreatic beta cell antigens recognized by T lymphocytes. In addition to insulin itself, currently known autoantigens are ZnT8, GAD65 and IA-2. Eesenbarth said: “By tracking antibodies against these self-antigens, we can now predict diabetes; if a patient has antibodies against two of the above four antigens, it is almost certain that he will develop texas diabetes and endocrinology in the future.”
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At present, another new technology can further explore the early onset of diabetes in humans and mice. Researchers at Harvard Medical School and Massachusetts General Hospital used MRI nanoparticle imaging technology to observe pancreatic insulitis, which is the earliest manifestation of pancreatic tissue inflammation in diabetes. At the same time, they also used this technology in experiments with non-obese diabetic mice, a type I animal model of diabetes. They used MRI imaging technology to observe the pancreas of mice, using nano-scale particles in the pancreas as markers. Even if there are only 6 to 10 weeks old mice, they can accurately distinguish which mouse will have type I diabetes. Harvard Medical School immunologist Diane Mathis said: “We now have a way to determine whether a mouse will have diabetes in the future at a very early stage, and compare the differences between these mice at the molecular level.” This comparative study at the molecular level It also brought them unexpected gains. They discovered some molecular and cellular components that were never known before. Mice with these components rarely get diabetes.
Because not every individual with a genetic susceptibility to diabetes type I has diabetes, there must be some motivating factors. There is evidence that viral infections-most likely enteroviruses (such as Coxsackie virus)-cause the immune system to make mistakes, but there are currently two theories about the relationship between viral infections and diabetes. One theory is that infections by viruses and other microorganisms increase immune tolerance and help prevent diabetes type I. Matthias Herrath, director of the Diabetes Type I Research Center at the La Jolla Institute of Allergy and Immunity in California, believes that if childhood infections are rare, then the immune system will “unemployment and become boring” for a long time, and it is these microorganisms and other pathogens that make the immune system immune. The system “cheers up” again. Another theory holds the opposite view. After the virus is infected, its antigens are exposed to pancreatic beta cells, which induces the immune system to attack these cells.
In order to determine whether a virus or other environmental factors induce diabetes type I, a study called DAISY was launched in 1993. The study included a total of 30,000 newborns, and the inclusion criteria included those whose parents or siblings had type I diabetes, and those with genetic risk factors for diabetes in the general population. Researchers collected blood samples of these children and recorded all aspects of their diet, health, and life through interviews with their parents. As of February 2007, 61 people have been confirmed to have type 1 diabetes. DAISY researchers have identified several autoantigens and genes related to diabetes type I in 15 years of follow-up studies, and discovered the relationship between diet and the onset or delay of diabetes, and it is clear that the use of immunization vaccines in children has no relationship with diabetes. The researchers also said that although a small prospective study showed that enterovirus infection and diabetes type I are not related, this conclusion still needs more large-scale studies to support.
Diabetes Type II: The cause is complicated!
It is also difficult to find the cause of diabetes type II. The onset of type II diabetes stems from two main pathologies. One is that muscle tissue and adipose tissue cannot store or use sugar normally and effectively under the action of insulin, and the other is that the pancreas cannot secrete more insulin to combat the aforementioned abnormalities. The resulting increase in blood sugar.
In addition, although the statistical associations between diabetes type II and obesity and the lifestyle of too little exercise have been confirmed, researchers are still debating how these factors cause insulin resistance, or, further, whether these factors actually cause insulin Resistance leads to diabetes type II, because after all, 75% of 80% of obese people do not have type II diabetes.
Another point is that, like diabetes type I,
diabetes type II seems to have a family history, indicating that genetic factors play a non-negligible role in diabetes type II. However, the data from the GWAS study is still very vague. So far, GWAS has identified more than forty genes associated with diabetes type II, most of which are related to the function of β cells, but all these data only explain less than 10% of genetic risk factors.