Insulin-dependent diabetes represents 10-15% of all diabetes cases. It occurs most often in a non-obese subject before the age of 25.
the role of autoimmunity in the onset of type 1 diabetes is certain. We often find anti-islets of Langerhans antibodies, antibodies that attack the pancreatic cells producing insulin. The autoimmune reaction is triggered by environmental factors (Toxic product, viruses…) Moreover; the Type 1 diabetes is often 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-related HLA genes on chromosome 6.
The history of type 1 diabetes can be depicted as follows: in genetically predisposed individuals, the beta cells of the pancreas are attacked by external factors during the pre-diabetic phase. This phase can last for several years. The functions of insulin secretion are then altered gradually and unobtrusively and glucose tolerance weakens. These abnormalities are probably reversible, at least in some cases. The type 1 diabetes can occur suddenly due to an external factor or by gradually reducing up to below the critical level (20%) of the number of Langerhans cells beta functional.
The resulting hyperglycemia failure of insulin plays an aggravating role: it exhausts the remaining beta cells resulting in decreased peripheral sensitivity to the action of insulin.
We can therefore obtain remissions thanks to immunosuppressive therapy (cyclosporine) in clinical onset of type 1 diabetes or thanks to strict glycemic normalization. Prevention may be possible. In the future, the initiation of immunosuppressive therapy at the pre-diabetic stage (when the number of destroyed beta cells is still limited) will make prevention possible.