Evidence map›Paper›PMID 16210703›Full record

ArticleThe American journal of clinical nutrition2005

Arterial endothelial dysfunction in baboons fed a high-cholesterol, high-fat diet.

Qiang Shi, Jane F Vandeberg, Catherine Jett, Karen Rice, Michelle M Leland, Leslie Talley, Rampratap S Kushwaha, David L Rainwater, John L Vandeberg, Xing Li Wang

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of clinical nutrition, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 37 citations in OpenAlex.

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  11. Genetic regulation of endothelial inflammatory responses in baboons.Arteriosclerosis, thrombosis, and vascular biology · 2010
    Article
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  16. [Not Available].Pathophysiology : the official journal of the International Society for Pathophysiology · 2008
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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

10 authors at 2 institutions in 1 country.

Qiang ShiDepartment of Genetics and the Southwest National Primate Research Center, the Southwest Foundation for Biomedical Research, San Antonio, Texas, USA.
Jane F Vandeberg
Catherine Jett
Karen Rice
Michelle M Leland
Leslie Talley
Rampratap S Kushwaha
David L Rainwater
John L Vandeberg
Xing Li Wang
Baylor College of Medicine · USTexas Biomedical Research Institute · US

Funding

WNV REPLIVAX VACCINE IN NON-HUMAN PRIMATESP51RR013986 · NCRR · TEXAS BIOMEDICAL RESEARCH INSTITUTE · PI GAUDUIN, MARIE-CLAIRE ELISABETH · 1999 to 2011
$79.1M
VETERINARY SERVICES--COREP01HL028972 · NHLBI · TEXAS BIOMEDICAL RESEARCH INSTITUTE · PI VANDEBERG, JOHN L · 1985 to 2012
$42.0M
NO, Genotype Dependent &Environment Specific RegulationR01HL066053 · NHLBI · SOUTHWEST FOUNDATION FOR BIOMEDICAL RES · PI WANG, XING LI L · 2001 to 2004
$1.5M
NCRR NIH HHS P51 RR013986NCRR NIH HHS P51 RR013986-060207NCRR NIH HHS P51 RR13986NHLBI NIH HHS P01 HL028972NHLBI NIH HHS P01 HL28972NHLBI NIH HHS R01 HL066053NHLBI NIH HHS R01 HL066053-03NHLBI NIH HHS R01 HL66053
6 · The paper itself

Abstract

backgroundEndothelial dysfunction signals the initiation and progression of atherosclerosis. Elevated LDL-cholesterol concentrations have been suggested to induce endothelial dysfunction, but direct in vivo evidence for the relation is still lacking.

objectiveWe examined the hypothesis that a high-cholesterol, high-fat (HCHF) diet can directly cause endothelial dysfunction in vivo.

designWe measured inflammatory and endothelial dysfunctional markers in circulating blood and directly in endothelial cells, which were collected by femoral artery biopsies, in 10 baboons before and after a 7-wk HCHF dietary challenge.

resultsWe found that the HCHF diet induced a high inflammatory status, as indicated by increased concentrations of interleukin 6, tumor necrosis factor alpha (TNF-alpha), and monocyte chemoattractant protein 1. Although the concentrations of endothelial dysfunctional markers, such as soluble vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1, were not increased by the HCHF diet, membrane-bound VCAM-1 and membrane-bound E-selectin on endothelial cells were highly increased after 7 wk of the HCHF diet (P < 0.01). In contrast, the concentrations of endothelial nitric oxide synthase in endothelial cells were significantly reduced by the 7-wk HCHF diet (P < 0.01). Furthermore, the dietary challenge attenuated endothelial cell responses to TNF-alpha, lipopolysaccharide, native LDL cholesterol, and oxidized LDL-cholesterol stimulation.

conclusionsOur results show that an HCHF diet can directly induce inflammation and endothelial dysfunction. Prior in vivo exposure to an HCHF diet attenuates the in vitro responses of endothelial cells to atherogenic risk factors. This preconditioning phenomenon may have significant clinical relevance.

Indexed as

AnimalsBiomarkersBiopsyChemokine CCL2Cholesterol, DietaryDietary FatsDisease Models, AnimalEndothelium, VascularE-SelectinFemaleFemoral ArteryInflammationInflammation MediatorsInterleukin-6LipidsMaleBiomarkersChemokine CCL2Cholesterol, DietaryDietary FatsE-SelectinInflammation MediatorsInterleukin-6LipidsNitric Oxide SynthaseTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1

Identifiers

PMID16210703
PMCPMC1283143
OpenAlexW2161827120

What OpenQuestion holds

Textmetadata
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.