A DETAILED REVIEW ON MECHANISMS INVOLVED IN CHRONIC STAGES OF TYPE II DIABETIC COMPLICATIONS 

ABSTRACT

Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels. In most instances, type 2 diabetes is a dual-defect disease characterized by insulin resistance and impaired β-cell function. High blood glucose levels can lead to disease-related long-term complications in case of diabetic cardiomyopathy. There are data indicating that ROS formation is a direct consequence of hyperglycaemia. More recent studies have suggested that increased (free fatty acids) FFA levels may also result in ROS formation. In turn ROS production and oxidative stress as well as activate stress-sensitive pathways. One of cheap trx these major pathways is activation of NADPH oxidase complex which further worsen both insulin action and secretion, thereby accelerating the progression to overt type 2 diabetes. NADPH oxidase activity is regulated by factors such as cytokines (TNF-α, IL-1), growth factors (EGF, VEGF) and hormones (e.g. insulin). In addition, shear stress, flow cessation, thrombin, serotonin, endothelin-1, angiotensin-II (Ang–II), histamine, bradykinin, lysophosphatidic acid, phorbol 12 myristate 13-acetate (PMA), prostaglandin F₂α (PGF2α) and sphingosine 1-phosphate are known to have an influence on NADPH oxidase activity . Since the development of diabetic nephropathy is faster in patients with bad metabolic control hyperglycemia has been suggested to cause the renal changes by metabolism of glucose and Non-enzymatic reaction of glucose. The present review focused on, molecular mechanisms which cause major Diabetic complications in type 2 diabetes.

Key words: EGF: Endothelial growth factor, IL: Interleukin, NADPH: Nicotinamide adenine dinucleotide phosphate, ROS: Reactive oxygen species, TNF: Tumor necrosis factor, VEGF: Vascular endothelial Growth factor.