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Research Article Free access | 10.1172/JCI119636

Elevated circulating free fatty acid levels impair endothelium-dependent vasodilation.

H O Steinberg, M Tarshoby, R Monestel, G Hook, J Cronin, A Johnson, B Bayazeed, and A D Baron

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

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

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

Find articles by Tarshoby, M. in: PubMed | Google Scholar

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

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

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

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

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

Find articles by Cronin, J. in: PubMed | Google Scholar

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

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

Published September 1, 1997 - More info

Published in Volume 100, Issue 5 on September 1, 1997
J Clin Invest. 1997;100(5):1230–1239. https://doi.org/10.1172/JCI119636.
© 1997 The American Society for Clinical Investigation
Published September 1, 1997 - Version history
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Abstract

We have recently shown that insulin-resistant obese subjects exhibit impaired endothelial function. Here, we test the hypothesis that elevation of circulating FFA to levels seen in insulin-resistant subjects can impair endothelial function. We studied leg blood flow responses to graded intrafemoral artery infusions of the endothelium-dependent vasodilator methacholine chloride (Mch) or the endothelium-independent vasodilator sodium nitroprusside during the infusion of saline and after raising systemic circulating FFA levels exogenously via a low- or high-dose infusion of Intralipid plus heparin or endogenously by an infusion of somatostatin (SRIF) to produce insulinopenia in groups of lean healthy humans. After 2 h of infusion of Intralipid plus heparin, FFA levels increased from 562+/-95 to 1,303+/-188 micromol, and from 350+/-35 to 3,850+/-371 micromol (P < 0.001) vs. saline for both low- and high-dose groups, respectively. Mch-induced vasodilation relative to baseline was reduced by approximately 20% in response to the raised FFA levels in both groups (P < 0.05, saline vs. FFA, ANOVA). In contrast, similar FFA elevation did not change leg blood flow responses to sodium nitroprusside. During the 2-h SRIF infusion, insulin levels fell, and FFA levels rose from 474+/-22 to 1,042+/-116 micromol (P < 0.01); Mch-induced vasodilation was reduced by approximately 20% (P < 0.02, saline vs. SRIF, ANOVA). Replacement of basal insulin levels during SRIF resulted in a fall of FFA levels from 545+/-47 to 228+/-61 micromol, and prevented the impairment of Mch-induced vasodilation seen with SRIF alone. In conclusion, (a) elevated circulating FFA levels cause endothelial dysfunction, and (b) impaired endothelial function in insulin-resistant humans may be secondary to the elevated FFA concentrations observed in these patients.

Version history
  • Version 1 (September 1, 1997): No description

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