Human insulin resistance: the role of glucocorticoids

Human insulin resistance: the role of glucocorticoids 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 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Diabetes Obesity & Metabolism Wiley

Human insulin resistance: the role of glucocorticoids

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Publisher
Wiley
Copyright
Copyright © 2003 Wiley Subscription Services, Inc., A Wiley Company
ISSN
1462-8902
eISSN
1463-1326
DOI
10.1046/j.1463-1326.2003.00221.x
Publisher site
See Article on Publisher Site

Abstract

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

Journal

Diabetes Obesity & MetabolismWiley

Published: Jan 1, 2003

References

  • Thinness at birth and insulin resistance in adult life
    Phillips, Phillips; Barker, Barker; Hales, Hales; Hirst, Hirst; Osmond, Osmond
  • Regulation of phosphoenolpyruvate carboxykinase (GTP) gene expression
    Hanson, Hanson; Reshef, Reshef
  • Size at birth and adrenocortical function in childhood
    Clark, Clark; Hindmarsh, Hindmarsh; Shiell, Shiell; Law, Law; Honour, Honour; Barker, Barker

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