Chronic hyperglycemia in Diabetes Mellitus (DM) represents the basis of the production of chronic lesions, specific for this pathology. Its negative effects are realized by the means of forcing some abnormal metabolic pathways, among which the most important ones are: 1. Enzymatic and non-enzymatic protein glycosylation; 2. Excessive activation of the polyol pathway; 3. Stimulation of free oxygen radicals' production and the decrease of the antioxidative capacity. Enzymatic and non-enzymatic protein glycosylation leads to the production of AGE (advanced glycosylation end-products); these ones, in their turn, form the atherosclerotic plate by the means of macrophages' stimulation. Other secondary modifications of protein glycosylation are: altered structure and function of proteins which compose the walls of the blood vessels and the myelin sheath; stimulation of endothelins' production; increase of glycosylated proteins' susceptibility to oxidative stress; thickening of glomerular basement membrane and of the capillary walls, modifications that lead to diabetic micro- and macroangiopathy; modifications of collagen's properties; modifications of crystaline's properties until its opacification (a phenomenon which causes diabetic retinopathy). Glycation also causes dysmetabolic cardiomyopathy, diabetic renal disease and diabetic neuropathy. Along with an excessive production of sorbitol and fructose, resulted from polyol pathway's activation, hyperglycemia leads to cellular hyperosmolarity, which favours nervous cells' affecting, in its turn, together with the decrease of nervous conduction speed and with the production of some segmentary demielinisations. These changes bring about diabetic neuropathy, including cardiovascular neuropathy too. Thus, a great number of chronic diabetic complications (such as: cataract development, diabetic neuropathy, vascular alterations which lead to atherosclerosis, retinopathy and so on) can be caused by the polyol pathway. Hyperglycemic conditions activate the process of glucose autooxidation, which causes the production of free oxygen radicals. Thus, oxidative stress can lead to macroangiopathy (by the means of the increased synthesis of TX A2 and of trombi's forming), as well as to diabetic renal disease. DM is also responsible for some changes in the blood properties; erythrocytes become more rigid because of the modifications of cellular membranes, related to protein glycosylation, including hemoglobin glycosylation too. Changes of blood platelets' functions, along with the increase of their agregability, as an answer to the changes to which vascular collagen has been submitted to, and an increased synthesis of TX A2 are also being produced. Vasodilation mediated by endothelial nitric oxide is lowered too.

Chronic hyperglycemia in Diabetes Mellitus (DM) represents the basis of the production of chronic lesions, specific for this pathology. Its negative effects are realized by the means of forcing some abnormal metabolic pathways, among which the most important ones are: 1. Enzymatic and non-enzymatic protein glycosylation; 2. Excessive activation of the polyol pathway; 3. Stimulation of free oxygen radicals' production and the decrease of the antioxidative capacity. Enzymatic and non-enzymatic protein glycosylation leads to the production of AGE (advanced glycosylation end-products); these ones, in their turn, form the atherosclerotic plate by the means of macrophages' stimulation. Other secondary modifications of protein glycosylation are: altered structure and function of proteins which compose the walls of the blood vessels and the myelin sheath; stimulation of endothelins' production; increase of glycosylated proteins' susceptibility to oxidative stress; thickening of glomerular basement membrane and of the capillary walls, modifications that lead to diabetic micro- and macroangiopathy; modifications of collagen's properties; modifications of crystaline's properties until its opacification (a phenomenon which causes diabetic retinopathy). Glycation also causes dysmetabolic cardiomyopathy, diabetic renal disease and diabetic neuropathy. Along with an excessive production of sorbitol and fructose, resulted from polyol pathway's activation, hyperglycemia leads to cellular hyperosmolarity, which favours nervous cells' affecting, in its turn, together with the decrease of nervous conduction speed and with the production of some segmentary demielinisations. These changes bring about diabetic neuropathy, including cardiovascular neuropathy too. Thus, a great number of chronic diabetic complications (such as: cataract development, diabetic neuropathy, vascular alterations which lead to atherosclerosis, retinopathy and so on) can be caused by the polyol pathway. Hyperglycemic conditions activate the process of glucose autooxidation, which causes the production of free oxygen radicals. Thus, oxidative stress can lead to macroangiopathy (by the means of the increased synthesis of TX A2 and of trombi's forming), as well as to diabetic renal disease. DM is also responsible for some changes in the blood properties; erythrocytes become more rigid because of the modifications of cellular membranes, related to protein glycosylation, including hemoglobin glycosylation too. Changes of blood platelets' functions, along with the increase of their agregability, as an answer to the changes to which vascular collagen has been submitted to, and an increased synthesis of TX A2 are also being produced. Vasodilation mediated by endothelial nitric oxide is lowered too.