Abstract
Glucose homeostasis relies on adequate and coordinated stimulation of insulin secretion from beta cells, insulin-stimulated glucose uptake in the periphery (primarily muscle and also fat) and insulin-stimulated suppression of hepatic glucose output. Insulin resistance is characterized as a failure or attenuation of insulin action in response to normal or elevated levels of insulin. Though the presence of insulin resistance does not imply a certainty for progression to type 2 diabetes, insulin resistance in combination with a cluster of physiological abnormalities, including central obesity, impaired glucose tolerance and a number of risk factors for cardiovascular disease (hypertension, atherosclerosis, dyslipidemia) comprises “syndrome X” or “insulin-resistance syndrome” and plays a critical role in the pathogenesis of type 2 diabetes (Reaven, 1995). Initially, insulin resistance is compensated by an increased production of insulin. Progressive beta cell failure combined with defects in insulin action eventually result in the hyperglycemic condition of type 2 diabetes.
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