Introduction Insulin resistance may be defined in pharmacological terms as a state in which normal amounts of insulin produce a subnormal biological response [ 1 ]. It is increasingly recognized that the consequences of impaired insulin action are evident in a wide spectrum of clinical disease. In 1988, Gerald Reaven [ 2 ] proposed that tissue resistance to the effects of insulin is a key factor linking glucose intolerance, hypertension, dyslipidaemia and coronary artery disease. This clustering of metabolic abnormalities is termed ‘Syndrome X’, the ‘Metabolic Syndrome’ or the ‘Insulin Resistance Syndrome’. The ‘syndrome’ has been expanded to include other risk factors for cardiovascular disease, including central obesity [ 3 ], abnormalities of thrombosis and fibrinolysis, impaired endothelium‐dependent vasodilatation [ 4 ], and low birthweight [ 5,6 ]. Recently it has been postulated that enhanced activity of the glucocorticoid hormone cortisol contributes to insulin resistance and thus manipulation of cortisol action could provide a novel therapeutic target to enhance insulin sensitivity. In this review, we describe some of the mechanisms whereby glucocorticoids influence insulin sensitivity and the evidence from human studies that glucocorticoids play a key role in the pathophysiology of insulin resistance in the population. Finally, we
Diabetes Obesity & Metabolism – Wiley
Published: Jan 1, 2003
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