Evidence map›Paper›PMID 28161804›Full record

ArticleMolecular and cellular biochemistry2017

Tryptophan depletion under conditions that imitate insulin resistance enhances fatty acid oxidation and induces endothelial dysfunction through reactive oxygen species-dependent and independent pathways.

Theodoros Eleftheriadis, Georgios Pissas, Maria Sounidaki, Georgia Antoniadi, Christos Rountas, Vassilios Liakopoulos, Loannis Stefanidis

Erratum issuedAbstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 39% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Theodoros EleftheriadisDepartment of Nephrology, Medical School, University of Thessaly, Neo Ktirio, Mezourlo Hill, 41110, Larissa, Greece. teleftheriadis@yahoo.com.ORCID http://orcid.org/0000-0001-9302-1633
Georgios PissasDepartment of Nephrology, Medical School, University of Thessaly, Neo Ktirio, Mezourlo Hill, 41110, Larissa, Greece.
Maria SounidakiDepartment of Nephrology, Medical School, University of Thessaly, Neo Ktirio, Mezourlo Hill, 41110, Larissa, Greece.
Georgia AntoniadiDepartment of Nephrology, Medical School, University of Thessaly, Neo Ktirio, Mezourlo Hill, 41110, Larissa, Greece.
Christos RountasDepartment of Interventional Radiology, Medical School, University of Thessaly, Larissa, Greece.
Vassilios LiakopoulosDepartment of Nephrology, Medical School, University of Thessaly, Neo Ktirio, Mezourlo Hill, 41110, Larissa, Greece.
Loannis StefanidisDepartment of Nephrology, Medical School, University of Thessaly, Neo Ktirio, Mezourlo Hill, 41110, Larissa, Greece.
University of Thessaly · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In atherosclerosis-associated pathologic entities characterized by malnutrition and inflammation, L-tryptophan (TRP) levels are low. Insulin resistance is an independent cardiovascular risk factor and induces endothelial dysfunction by increasing fatty acid oxidation. It is also associated with inflammation and low TRP levels. Low TRP levels have been related to worse cardiovascular outcome. This study evaluated the effect of TRP depletion on endothelial dysfunction under conditions that imitate insulin resistance. Fatty acid oxidation, harmful pathways due to increased fatty acid oxidation, and endothelial dysfunction were assessed in primary human aortic endothelial cells cultured under normal glucose, low insulin conditions in the presence or absence of TRP. TRP depletion activated general control non-derepressible 2 kinase and inhibited aryl hydrocarbon receptor. It increased fatty acid oxidation by increasing expression and activity of carnitine palmitoyltransferase 1. Elevated fatty acid oxidation increased the formation of reactive oxygen species (ROS) triggering the polyol and hexosamine pathways, and enhancing protein kinase C activity and methylglyoxal production. TRP absence inhibited nitric oxide synthase activity in a ROS-dependent way, whereas it increased the expression of ICAM-1 and VCAM-1 in a ROS independent and possibly p53-dependent manner. Thus, TRP depletion, an amino acid whose low levels have been related to worse cardiovascular outcome and to inflammatory atherosclerosis-associated pathologic entities, under conditions that imitate insulin resistance enhances fatty acid oxidation and induces endothelial dysfunction through ROS-dependent and independent pathways. These findings may offer new insights at the molecular mechanisms involved in accelerated atherosclerosis that frequently accompanies malnutrition and inflammation.

Indexed as

AortaCells, CulturedEndothelial CellsFatty AcidsHumansInsulin ResistanceLipid MetabolismModels, BiologicalOxidation-ReductionReactive Oxygen SpeciesReceptors, Aryl HydrocarbonRisk FactorsSignal TransductionTryptophanFatty AcidsReactive Oxygen SpeciesReceptors, Aryl HydrocarbonTryptophanAtherosclerosisEndothelial dysfunctionFatty acid oxidationInflammationInsulin resistanceROSTryptophan depletion

Identifiers

PMID28161804
OpenAlexW2584669306

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.