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Accepted Manuscript

Administration of tauroursodeoxycholic acid prevents endothelial dysfunction caused by an oral glucose load

Lauren K Walsh, Robert M Restaino, Martha Neuringer, Camila Manrique, Jaume Padilla
Clinical Science Aug 08, 2016, CS20160501; DOI: 10.1042/CS20160501
Lauren K Walsh
Nutrition and Exercise Physiology, University of Missouri, 204 Gwynn Hall, Columbia, Missouri, 65211, United States
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Robert M Restaino
Medical Pharmacology and Physiology, Univeristy of Missouri, Columbia, Missouri, 65211, United States
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Martha Neuringer
Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Portland, Oregon, United States
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Camila Manrique
Internal Medicine, University of Missouri, Columbia, Missouri, United States
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Jaume Padilla
Biomedical Sciences, University of Missouri, 1600 E. Rollins, E102 Vet Med Bldg, Columbia, Missouri, 65211, United States
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  • For correspondence: padillaja@missouri.edu
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Abstract

Postprandial hyperglycemia leads to a transient impairment in endothelial function; however, the mechanisms remain largely unknown. Previous work in cell culture models demonstrate that high glucose results in endoplasmic reticulum (ER) stress and, in animal studies, ER stress has been implicated as a cause of endothelial dysfunction. Herein we tested the hypothesis that acute oral administration of tauroursodeoxycholic acid (TUDCA, 1500mg), a chemical chaperone known to alleviate ER stress, would prevent hyperglycemia-induced endothelial dysfunction. In 12 young healthy subjects (seven men, five women), brachial artery flow-mediated dilation (FMD) was assessed at baseline, 1 hour, and 2 hours post an oral glucose challenge. Subjects were tested on two separate visits in a single-blind randomized crossover design: after oral ingestion of TUDCA or placebo capsules. FMD was reduced from baseline during hyperglycemia under the placebo condition (-32% at 1 hr and -28% at 2 hr post oral glucose load; p0.05 from baseline). Postprandial plasma glucose and insulin were not altered by TUDCA ingestion. Plasma oxidative stress markers 3-nitrotyrosine and TBARs remained unaltered throughout the oral glucose challenge in both conditions. These results suggest that hyperglycemia-induced endothelial dysfunction can be mitigated by oral administration of TUDCA, thus supporting the hypothesis that ER stress may contribute to endothelial dysfunction during postprandial hyperglycemia.

  • Postprandial Hyperglycemia
  • TUDCA
  • endothelial function
  • ©2016 The Author(s)

This is an Accepted Manuscript; not the final Version of Record. Archiving permitted only in line with the archiving policy of Portland Press Limited. All other rights reserved.

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Administration of tauroursodeoxycholic acid prevents endothelial dysfunction caused by an oral glucose load
Lauren K Walsh, Robert M Restaino, Martha Neuringer, Camila Manrique, Jaume Padilla
Clinical Science Aug 2016, CS20160501; DOI: 10.1042/CS20160501
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Administration of tauroursodeoxycholic acid prevents endothelial dysfunction caused by an oral glucose load
Lauren K Walsh, Robert M Restaino, Martha Neuringer, Camila Manrique, Jaume Padilla
Clinical Science Aug 2016, CS20160501; DOI: 10.1042/CS20160501

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Keywords

Postprandial Hyperglycemia
TUDCA
endothelial function

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