Chronic complications in diabetes mellitus.
Diabetes mellitus is one of the most prevalent diseases among adult population in Japan. The persistent hyperglycemia is responsible for the appearance of various organ and tissue damage in diabetic subjects. Eyes, kidneys and peripheral nerves are frequently damaged due to diabetes-specific alteration in microvessels. Furthermore, large vessels are also damaged causing severe diseases such as myocardial infarction, cerebral infarction and gangrene. The pathogenesis of these alterations in small and large vessels has been extensively studied and various metabolic abnormalities induced by hyperglycemia are proposed to play a major role in the development of these diabetic vascular complications. Among those metabolic abnormalities, the activation of the diacyl glycerol-protein kinase C pathway has been proposed to play a pivotal role in the pathogenesis of not only microvascular complications but also macrovascular complications. The beneficial effect of a protein kinase C inhibitor on renal, retinal and atherosclerotic lesions in diabetic animal models may support this notion. The results of several large-scale clinical trials have confirmed the efficacy of glycemic control as well as blood pressure control in the management of diabetic complications. It is a prerequisite, therefore, to obtain near-normal glycemic and blood pressure control in order to prevent the appearance of diabetic complications and also suppress their progression. In this aspect nutritional consideration may be an important way to improve the quality of these managements.
Third Department of Medicine, Shiga University of Medical Science, Otsu, Japan. kikkawa@belle.shiga-med.ac.jp.
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D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D002908:Chronic Disease; D016207:Cytokines / Q000502:physiology; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000188:drug therapy; D003928:Diabetic Nephropathies / Q000378:metabolism; D004789:Enzyme Activation; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000188:drug therapy; D007564:Japan; D018384:Oxidative Stress; D011493:Protein Kinase C / Q000378:metabolism
D001786:Blood Glucose; D016207:Cytokines; D017127:Glycation End Products, Advanced; D011493:Protein Kinase C