Diabetes mellitus represents 10-15% of diabetes cases. It occurs most often in a non-obese before the age of 30.
Mechanisms
The role of autoimmunity in the onset of type one diabetes is certain. Often found antibodies to islets of Langerhans, antibodies that attack the pancreas cells producing insulin autoimmune reaction is triggered by environmental factors such as poorly understood toxic, viruses, etc.... Moreover, the type one diabetes is eventually associated with other autoimmune diseases (Hashimoto's thyroiditis, Graves' disease, idiopathic myxedema, Addison's disease, pernicious anemia, vitiligo, celiac disease, etc....).
There is a genetic predisposition to type 1 diabetes linked to HLA genes located on the short arm of chromosome 6.
The natural history of type 1 diabetes can be represented as follows: in genetically predisposed subjects, the beta cells within the pancreas are attacked by external factors during the prediabetic stage. This phase can last for years. The functions of insulin secretion are altered so gradually and quietly, and glucose tolerance wanes. These anomalies are probably reversible, at least in some cases. The type 1 diabetes eventually proved to be suddenly in favor of an external factor, is gradually reduced, to below the critical level (20%), the number of functional beta cell's Langerhans.
Hyperglycemia resulting from a defect of insulin plays an aggravating role: it exhausts the remaining ß-cells and resulting in decreased peripheral sensitivity to insulin action.
We can therefore obtain remissions as a result of immunosuppressive therapy (cyclosporine) at the beginning of clinical type 1 diabetes or consequently, of strict glycemic normalization. Prevention may be probably. In the future, the initiation of immunosuppressive therapy at the prediabetic stage - when the number of beta cells destroyed is limited - make prevention possible.
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