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Research Article Free access | 10.1172/JCI118709

Obesity/insulin resistance is associated with endothelial dysfunction. Implications for the syndrome of insulin resistance

Helmut O. Steinberg, Haitham Chaker, Rosalind Leaming, Ann Johnson, Ginger Brechtel, and Alain D. Baron

Department of Medicine, Indiana University Medical Center, Indianapolis, Indiana 46202, USA.

Find articles by Steinberg, H. in: JCI | PubMed | Google Scholar

Department of Medicine, Indiana University Medical Center, Indianapolis, Indiana 46202, USA.

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Department of Medicine, Indiana University Medical Center, Indianapolis, Indiana 46202, USA.

Find articles by Leaming, R. in: JCI | PubMed | Google Scholar

Department of Medicine, Indiana University Medical Center, Indianapolis, Indiana 46202, USA.

Find articles by Johnson, A. in: JCI | PubMed | Google Scholar

Department of Medicine, Indiana University Medical Center, Indianapolis, Indiana 46202, USA.

Find articles by Brechtel, G. in: JCI | PubMed | Google Scholar

Department of Medicine, Indiana University Medical Center, Indianapolis, Indiana 46202, USA.

Find articles by Baron, A. in: JCI | PubMed | Google Scholar

Published June 1, 1996 - More info

Published in Volume 97, Issue 11 on June 1, 1996
J Clin Invest. 1996;97(11):2601–2610. https://doi.org/10.1172/JCI118709.
© 1996 The American Society for Clinical Investigation
Published June 1, 1996 - Version history
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Abstract

To test the hypothesis that obesity/insulin resistance impairs both endothelium-dependent vasodilation and insulin-mediated augmentation of endothelium-dependent vasodilation, we studied leg blood flow (LBF) responses to graded intrafemoral artery infusions of methacholine chloride (MCh) or sodium nitroprusside (SNP) during saline infusion and euglycemic hyperinsulinemia in lean insulin-sensitive controls (C), in obese insulin-resistant subjects (OB), and in subjects with non-insulin-dependent diabetes mellitus (NIDDM). MCh induced increments in LBF were approximately 40% and 55% lower in OB and NIDDM, respectively, as compared with C (P < 0.05). Euglycemic hyperinsulinemia augmented the LBF response to MCh by - 50% in C (P < 0.05 vs saline) but not in OB and NIDDM. SNP caused comparable increments in LBF in all groups. Regression analysis revealed a significant inverse correlation between the maximal LBF change in response to MCh and body fat content. Thus, obesity/insulin resistance is associated with (a) blunted endothelium-dependent, but normal endothelium-independent vasodilation and (b) failure of euglycemic hyperinsulinemia to augment endothelium-dependent vasodilation. Therefore, obese/insulin-resistant subjects are characterized by endothelial dysfunction and endothelial resistance to insulin's effect on enhancement of endothelium-dependent vasodilation. This endothelial dysfunction could contribute to the increased risk of atherosclerosis in obese insulin-resistant subjects.

Version history
  • Version 1 (June 1, 1996): Updated with full author names.

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