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The Syndrome of Insulin Resistance and Its Links to Atherosclerosis

  1. Riccardo C. Bonadonna

Published Online: 15 NOV 2003

DOI: 10.1002/0470862092.d1009

International Textbook of Diabetes Mellitus

International Textbook of Diabetes Mellitus

How to Cite

Bonadonna, R. C. 2003. The Syndrome of Insulin Resistance and Its Links to Atherosclerosis. International Textbook of Diabetes Mellitus. .

Author Information

  1. University of Verona School of Medicine, Verona, Italy

Publication History

  1. Published Online: 15 NOV 2003

Abstract

Obesity, central fat distribution, altered glucose tolerance, dyslipidemia, and hypertension cluster together to a variable extent presumably because of the common pathogenetic denominator represented by insulin resistance. This cluster has been named insulin resistance syndrome, or dysmetabolic syndrome X, or metabolic syndrome, and possibly is involved in the etiology and/or pathophysiology of atherosclerosis, as also demonstrated by epidemiological studies in which hyperinsulinemia and insulin resistance are independent indicators/predictors of cardiovascular disease. This relationship may be explained by the presence of a common antecedent (“common soil” hypothesis), causing both insulin resistance and atherosclerosis, or by a direct causal role of insulin resistance/hyperinsulinemia in atherogenesis (“insulin-resistance-dependent atherosclerosis” hypothesis). At the molecular level, the common soil hypothesis may find its counterpart in the I-κB-kinase-mediated activation of the transcription factor nuclear factor κB raised by the common soil hypothesis and by the insulin-resistance-dependent atherosclerosis hypothesis remains unsolved, largely because it may be inherently difficult to gauge the biological link(s) between one “complex” phenotype (the insulin resistance syndrome) and another “hypercomplex” phenotype (the atherosclerotic plaque).

Keywords:

  • insulin;
  • insulin resistance;
  • dysmetabolic syndrome X;
  • “common soil”;
  • “thrifty genotype/phenotype”;
  • endothelium;
  • IRS-1;
  • MAP kinase;
  • PI3 kinase;
  • I-κB kinase;
  • NF-κB;
  • vascular remodeling;
  • atherosclerosis