Type 1 diabetes onset mechanism.
As previously mentioned, the main factors closely related to the onset of type 1 diabetes include genetic factors, viral infections, autoimmunity, and certain chemical toxins. However, the detailed mechanism of triggering the onset of type 1 diabetes is not fully understood. Most scholars now believe that genetic factors are the internal cause, while other factors are external causes, and these two types of factors interact to cause type 1 diabetes.
Recently, many scholars suggest that on the basis of genetic susceptibility, certain external factors induce autoimmune reactions, leading to the destruction of islet β cells and thus causing diabetes. However, it is controversial whether external factors such as viral infections, chemical toxins, and nutritional factors are antigen-specific or non-specific in triggering autoimmunity. Increasing evidence suggests that under the influence of non-specific environmental factors, excessive production of cytokines leads to the imbalance of β cell protective and destructive factors, causing β cell damage.
This in turn triggers a secondary humoral immune response, resulting in the production of anti-islet cell antibodies. This exacerbates the destruction of β cells. When the destruction of β cells exceeds 90%, the clinical manifestation can be characterized as type 1 diabetes.
Type 2 diabetes onset mechanism.
Similar to the pathogenesis of type 1 diabetes, although the detailed mechanisms of type 1 diabetes are not fully understood, it mainly includes two aspects: 1) genetic factors, currently believed to be a polygenic inheritance-related disease, with genetic characteristics even similar to cancer, such as insulin resistance; 2) environmental factors, such as malnutrition, lack of physical activity, obesity, and social psychological stress. Currently, it is believed that the hyperglycemic state of type 2 diabetes is caused by receptor and post-receptor defects.
