PATHOGENESIS OF NON-INSULIN-DEPENDENT (TYPE-2) DIABETES-MELLITUS

Two major mechanisms, peripheral insulin resistance and impaired insulin secretion participate concomitantly but to a variable extent to the pathogenesis of non-insulin-dependent diabetes, whose heterogeneity, suspected for a long time, is now confirmed by the recent discoveries of the molecular biology. Mutations of several genes governing key-steps of the recognition of the glucose signal, insulin secretion or its peripheral effect have been found in some particular cases, but presently not at a large scale among non insulin-dependent diabetic patients. The tendency to worsening of the metabolic disturbances with the time, even under adequate therapy, can be explained by the vicious circle of glucose toxicity, but other mechanisms like amylin, responsible of the deposition of amyloid in the islets, may play a role. So, despite the acquisition of many new knowledges, the pathogenesis of non-insulin-dependent diabetes keeps nowadays a part of its mystery.