New Study Shows Bear Bile or TUDCA Improves Endothelial Function

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Clin Sci (Lond). 2016 Aug 8

Administration of tauroursodeoxycholic acid [bear bile concentrate] prevents endothelial dysfunction caused by an oral glucose load.

Walsh LK1, Restaino RM2, Neuringer M3, Manrique C4, Padilla J5.

1Nutrition and Exercise Physiology, University of Missouri, 204 Gwynn Hall, Columbia, Missouri, 65211, United States.
2Medical Pharmacology and Physiology, Univeristy of Missouri, Columbia, Missouri, 65211, United States.
3Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Portland, Oregon, United States.
4Internal Medicine, University of Missouri, Columbia, Missouri, United States.
5Biomedical Sciences, University of Missouri, 1600 E. Rollins, E102 Vet Med Bldg, Columbia, Missouri, 65211, United States padillaja@missouri.edu.

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.

Conclusion
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.

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 Glob Adv Health Med. 2014 May;3(3):58-69

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