The causes of Type 2 diabetes are complex. Insulin resistance is the main metabolic abnormality leading to the development of Type 2 diabetes.
The most recent research suggests that Type 2 diabetes can be seen as a consequence of a series of physiological disruptions, each of which makes the person vulnerable to subsequent disruption of normal glucose metabolism.
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Insulin resistance is common and is usually caused by obesity. There are effectively three stages in the development of Type 2 diabetes:
Insulin resistance, for which the body compensates by increasing the secretion of insulin to allow the liver and muscles to continue to function normally.
Eventually the pancreas is unable to produce enough insulin to compensate for the insulin resistance. This leads to a sequence of impaired glucose tolerance, high blood glucose after eating (postprandial hyperglycaemia) and finally, high blood glucose levels even when fasting (fasting hyperglycaemia) and worsening postprandially. These high glucose levels are toxic not only to the large and small blood vessels but also to the cells producing insulin, the so-called beta-cells of the pancreas.
This damage to the beta-cells leads to a decline in their function and eventually less insulin is produced as the disease progresses.
The raised fasting and postprandial glucose levels result in complications which affect the small and large blood vessels of the body, and this contributes to renal failure, eye complications and more importantly, accelerated atherosclerosis leading to strokes and heart disease. The artherosclerotic complications are responsible for 80% of the deaths in diabetics.
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