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• W1587243391 abstract "Diabetes mellitus, a chronic progressive metabolic disorder of glucose homeostasis, is a major cause of morbidity and mortality. It is broadly categorized into type 1 and type 2, each with distinctly different pathogenesis. Diabetes mellitus is extremely prevalent, with type 2 making up nearly 90% of the cases and the incidence continues to increase at an alarming rate, in parallel with aging and the increasing prevalence of obesity worldwide. Although the pathogenesis of these two major categories is different, they share similar long-term complications as a result of inadequate glycemic control. It is well established that poor glycemic control is the major causative factor in the development of microvascular complications, affecting primarily the kidney, eyes, and peripheral nerves. Recent data suggest that hyperglycemia also plays a critical role in the development of macrovascular complications. To date, a complete normalization of glucose metabolic disturbances in diabetes remains an elusive goal. Even excellent glycemic control evades a large number of affected subjects. However, advances in our understanding of the pathogenesis of the disorder at cellular and molecular levels over the past several decades had led to significant improvements in treatment outcomes. Insulin resistance is highly prevalent, and particularly so in Western societies. It can be found in a number of metabolic disorders, including the metabolic syndrome, impaired glucose tolerance, and in its extreme form, type 2 diabetes. In the current paradigm, insulin resistance plays a central role in the predisposition of an individual to the development of type 2 diabetes. Initially, compensatory overproduction of insulin by pancreatic β-cells enables an individual to sustain normal blood glucose levels. Over time, progressive β-cell dysfunction and loss of cell mass leads to relative insulin deficiency and diabetes ensues. Obesity not only directly causes insulin resistance, but also contributes to the progressive failure of β-cells through a number of mechanisms, including free fatty acid–induced β-cell apoptosis. Such maladaptive responses are also associated with an increased ectopic deposition of fat to nonadipose tissues, in turn, aggravating the preexisting insulin resistance. The development of clinical diabetes is a result of combined genetic susceptibility and environmental stressors. With only a handful of exceptions, diabetes is a polygenic disorder. Identification of candidate genes may provide a more refined framework for either better understanding of the pathophysiological processes and/or for identifying novel targets for pharmacological interventions." @default.
• W1587243391 created "2016-06-24" @default.
• W1587243391 creator A5059130197 @default.
• W1587243391 date "2006-09-15" @default.
• W1587243391 modified "2023-09-24" @default.
• W1587243391 title "Insulin Resistance, Diabetes and its Complications" @default.
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