Molecular mechanisms of diabetic complications.

The main molecular process responsible for the development of diabetic complications is the activation of intracellular protein kinase C by long-term hyperglycemia. In ordinary somatic cells (e.g., endothelial or retinal cells) this activation disturbs the metabolism of these cells, whereas a transition into an "excited state" of effector cells such as monocytes or polymorphonuclear leukocytes causes an avalanche-like increase of various pathological processes damaging the body. In relatively compensated diabetes mellitus, when the duration of hyperglycemia is not long and levels of hyperglycemia are not too high, the intensity of the above-mentioned processes is low. However, due to the long time course of reparative processes, some damages which appear in short periods of decompensation can accumulate in the body, finally causing the clinical manifestation of vascular complications of diabetes mellitus.