الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Complications of diabetes as a result of oxidant stress affect multiple systems throughout the body, but the involvement of the cardiovascular system may be one of the most severe in light of the impact upon the cardiac and vascular function that can result in rapid morbidity and mortality for individuals. Given these concerns, the signaling pathways of the mammalian target of rapamycin (mTOR) offer exciting prospects for the development of novel therapies for the micro-vascular complications of diabetes
Microvascular complications of diabetes such as retinopathy, nephropathy, and neuropathy develop in 30–50% of patients with diabetes. These complications lead to blindness, renal failure, and foot ulceration.
There are two forms of diabetes. Type 1 diabetes (also known as insulin-dependent or juvenile diabetes) is caused by absolute insulin insufficiency due to autoimmune destruction of insulin-producing beta cells of the pancreas. Type 2 diabetes (insulin-independent or adult-onset diabetes) is initiated by insulin resistance (IR) in muscle, liver, and adipose tissues. Initially, an increase in insulin secretion by pancreatic beta cells compensates for IR. If/when beta cells fail, then glucose levels increase. When either fasting glucose levels or oral glucose tolerance test reach 126 and 200 mg/l, respectively, then diabetes is diagnosed. Although glucose control with intensive insulin therapy decreases the incidence of complications, diabetes remains a major cause of new-onset blindness, end-stage renal disease, and lower leg amputation.
There are two puzzling observations. First, complications can precede the onset of type 2 diabetes. Second, intensive insulin therapy may initially worsen the progression of retinopathy in both types 1 and type 2.