Evidence map›Paper›PMID 27503949›Full record

Trial reportClinical science (London, England : 1979)2016

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

Open access · bronzeAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Clinical science (London, England : 1979), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Review
  6. Article
  7. Neuraminidase inhibition improves endothelial function in diabetic mice.American journal of physiology. Heart and circulatory physiology · 2023
    Article
  8. Impact of sex and diet-induced weight loss on vascular insulin sensitivity in type 2 diabetes.American journal of physiology. Regulatory, integrative and comparative physiology · 2023
    Article
  9. Article
  10. Article
  11. Endothelial HSP72 is not reduced in type 2 diabetes nor is it a key determinant of endothelial insulin sensitivity.American journal of physiology. Regulatory, integrative and comparative physiology · 2022
    Article
  12. Article
  13. Review
  14. Effect of endoplasmic reticulum stress on endothelial ischemia-reperfusion injury in humans.American journal of physiology. Regulatory, integrative and comparative physiology · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Lauren K WalshDepartment of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO 65211, U.S.A.
Robert M RestainoDepartment of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO 65212, U.S.A.
Martha NeuringerDepartment of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University, Portland, OR 97239, U.S.A.
Camila ManriqueDepartment of Internal Medicine, University of Missouri, Columbia, MO 65212, U.S.A.
Jaume PadillaDepartment of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO 65211, U.S.A. Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65201, U.S.A. Department of Child Health, University of Missouri, Columbia, MO 65212, U.S.A. padillaja@missouri.edu.
University of Missouri · USOregon National Primate Research Center · USUniversity of Missouri Health System · US

Funding

Mineralocorticoid and estrogen receptor alpha signaling in the pathogenesis of vascular stiffness in insulin resistant femalesK08HL129074 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI MANRIQUE ACEVEDO, CAMILA MARGARITA · 2015 to 2019
$802k
Vascular Insulin Resistance in Obesity: Role of Endoplasmic Reticulum StressK01HL125503 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI PADILLA, JAUME · 2015 to 2018
$564k
Targeting endoplasmic reticulum stress to correct vascular insulin resistance and glycemic dysregulation in diabetesR21DK105368 · NIDDK · UNIVERSITY OF MISSOURI-COLUMBIA · PI PADILLA, JAUME · 2015 to 2016
$422k
NHLBI NIH HHS K01 HL125503NHLBI NIH HHS K08 HL129074NIDDK NIH HHS R21 DK105368
6 · The paper itself

Abstract

Postprandial hyperglycaemia 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. In the present study, we tested the hypothesis that acute oral administration of tauroursodeoxycholic acid (TUDCA, 1500 mg), 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 min 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 (-32% at 60 min and -28% at 120 min post oral glucose load; P<0.05 from baseline) but not under the TUDCA condition (-4% at 60 min and +0.3% at 120 min post oral glucose load; P>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.

Indexed as

AdultBlood GlucoseCardiovascular DiseasesEndoplasmic Reticulum StressEndothelium, VascularFemaleHumansHyperglycemiaInsulinMaleOxidative StressPostprandial PeriodTaurochenodeoxycholic AcidThiobarbituric Acid Reactive SubstancesTyrosineYoung Adult3-nitrotyrosineBlood GlucoseInsulinTaurochenodeoxycholic AcidThiobarbituric Acid Reactive SubstancesTyrosineursodoxicoltaurineendothelial functionER stresspostprandial hyperglycaemiatauroursodeoxycholic acid (TUDCA)

Identifiers

PMID27503949
PMCPMC5507333
OpenAlexW2511079692

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.