Genetic and environmental factors play different roles in the development of type 1 diabetes. It is not completely clear how environmental factors trigger the autoimmune response of islet B cells. In general, human L type diabetes requires a genetic background of susceptibility, that is, some environmental agents induce an autoimmune reaction of B cells in individuals with Genetic predisposition. Hypothesis: type 1 diabetes occurs when environmental factors damage B cells more than an individual’s genetically determined tolerance for B cell damage.
Environmental factors specifically or not specifically damage B cells by releasing cytokines such as interleukin-1(IL-1) or tumor necrosis factor (tnf-α) . Genetic factors play a permissive role and determine the susceptibility of B cells to initially impair the initiation of autoimmunity. In rare cases, specific B cell toxins cross the body’s immune system and cause extensive damage to B cells. More commonly, repeated B cell damage induces secondary anti B cell autoimmunity in genetically susceptible individuals, which may occur spontaneously without the involvement of environmental factors. The final common pathway of B cell death may come from the destruction of B cells by excessive oxygen free radical or NO.
The etiology of type 2 diabetes is not very clear, is now generally considered to have a strong genetic or polygenic genetic heterogeneity of disease, environmental factors such as obesity, lack of activity and aging. The main cause of the disease is the deficiency of insulin secretion, which usually precedes insulin secretion, or the deficiency of insulin secretion with or without insulin resistance. Although type 2 diabetes is genetically heterogeneous, most patients with type 2 diabetes and fasting hyperglycemia are characterized by insulin resistance, impaired insulin secretion, and increased glucose production in the liver.
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