Abstract
The restoration of normoglycemia ensures the control of diabetic symptoms and reduction in microangiopathic complications in type 1 and type 2 diabetes. However, there is no conclusive evidence that intensive glycemic control alone will prevent macrovascular disease, the commonest cause of morbidity and mortality in type 2 diabetes. As atherosclerosis is an inflammatory condition, it is relevant that the two common insulin resistant states of obesity and type 2 diabetes have significant inflammatory processes, which promote atherosclerosis. It is also relevant that glucose has been shown to have profound effects on the endothelial cell, the leukocyte and the platelet. These effects include the induction of acute oxidative and inflammatory stress and a prothrombotic and pro-apoptotic effect following glucose intake. In contrast insulin has been shown to exert several biological effects at physiologically relevant concentrations, in relation to the endothelial cell, the platelet and leucocyte function, which may be cardioprotective and potentially anti-atherosclerotic. These findings are of great interest as it is possible that the prevention of macrovascular complications in type 2 diabetes may require the use of those glucose lowering drugs which have additional anti-inflammatory effects in addition to the control of comorbid conditions (hypertension and dyslipidemia) associated with this disease. Results of future clinical trials are awaited to confirm the benefits of this approach in the primary and secondary prevention of macrovascular complications in type 2 diabetes.
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