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In the present study, we tested the hypothesis that acute oral administration of tauroursodeoxycholic acid (TUDCA, 1500\u00a0mg), a chemical chaperone known to alleviate ER stress, would prevent hyperglycaemia-induced endothelial dysfunction. In 12 young healthy subjects (seven men, five women), brachial artery flow-mediated dilation (FMD) was assessed at baseline, and at 60 and 120\u00a0min after an oral glucose challenge. Subjects were tested on two separate visits in a single-blind randomized cross-over design: after oral ingestion of TUDCA or placebo capsules. FMD was reduced from baseline during hyperglycaemia under the placebo condition (\u221232% at 60\u00a0min and \u221228% at 120\u00a0min post oral glucose load; P&amp;lt;0.05 from baseline) but not under the TUDCA condition (\u22124% at 60\u00a0min and +0.3% at 120\u00a0min post oral glucose load; P&amp;gt;0.05 from baseline). Postprandial plasma glucose and insulin were not altered by TUDCA ingestion. Plasma oxidative stress markers 3-nitrotyrosine and thiobarbituric acid reactive substance (TBARS) remained unaltered throughout the oral glucose challenge in both conditions. These results suggest that hyperglycaemia-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 hyperglycaemia.<\/jats:p>","DOI":"10.1042\/cs20160501","type":"journal-article","created":{"date-parts":[[2016,8,8]],"date-time":"2016-08-08T21:23:53Z","timestamp":1470691433000},"page":"1881-1888","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":42,"title":["Administration of tauroursodeoxycholic acid prevents endothelial dysfunction caused by an oral glucose load"],"prefix":"10.1042","volume":"130","author":[{"given":"Lauren\u00a0K.","family":"Walsh","sequence":"first","affiliation":[{"name":"Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO 65211, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert\u00a0M.","family":"Restaino","sequence":"additional","affiliation":[{"name":"Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO 65212, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martha","family":"Neuringer","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University, Portland, OR 97239, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Camila","family":"Manrique","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Missouri, Columbia, MO 65212, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jaume","family":"Padilla","sequence":"additional","affiliation":[{"name":"Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO 65211, U.S.A."},{"name":"Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65201, U.S.A."},{"name":"Department of Child Health, University of Missouri, Columbia, MO 65212, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2016,9,22]]},"reference":[{"key":"2021113010475118900_B1","doi-asserted-by":"publisher","first-page":"165","DOI":"10.1002\/path.3960","article-title":"Chronic inhibition of endoplasmic reticulum stress and inflammation prevents ischaemia-induced vascular pathology in type\u00a0II diabetic mice","volume":"227","author":"Amin","year":"2012","journal-title":"J. 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