Evidence map›Paper›PMID 18812596›Full record

ArticleJournal of lipid research2009

Triglyceride-rich lipoprotein lipolysis releases neutral and oxidized FFAs that induce endothelial cell inflammation.

Limin Wang, Rajan Gill, Theresa L Pedersen, Laura J Higgins, John W Newman, John C Rutledge

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
164citing papers in PubMed, 2 pooled it
5.9field-weighted citation impact, top 4% 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

164 citing papers in PubMed, 2 syntheses or guidelines pooled it, 294 citations in OpenAlex.

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  12. Targeting triglycerides for cardiovascular risk reduction.Internal and emergency medicine · 2026
    Review
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104 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Limin WangDivision of Endocrinology, Clinical Nutrition, and Vascular Medicine, University of California, Davis, Davis, CA, USA. lwang@ucdavis.edu
Rajan Gill
Theresa L Pedersen
Laura J Higgins
John W Newman
John C Rutledge
University of California, Davis · USUnited States Department of Agriculture · US

Funding

Workshop on Environmental Technology Transfer and EntrepreneurshipP42ES004699 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1987 to 2021
$50.1M
Imaging Lipoprotein-Endothelial Cell InteractionsR01HL078615 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI RUTLEDGE, JOHN CALVERT · 2004 to 2007
$2.2M
Molecular Modulation of Cardiac Na+ Channel FunctionR01HL055665 · NHLBI · VANDERBILT UNIVERSITY · PI MURRAY, KATHERINE T · 1997 to 2004
$1.7M
NHLBI NIH HHS HL-55665NHLBI NIH HHS HL-78615NHLBI NIH HHS R01 HL055665NHLBI NIH HHS R01 HL078615NIEHS NIH HHS P42 ES004699NIEHS NIH HHS P42-ES04699
6 · The paper itself

Abstract

Triglyceride-rich lipoprotein (TGRL) lipolysis products provide a pro-inflammatory stimulus that can alter endothelial barrier function. To probe the mechanism of this lipolysis-induced event, we evaluated the pro-inflammatory potential of lipid classes derived from human postprandial TGRL by lipoprotein lipase (LpL). Incubation of TGRL with LpL for 30 min increased the saturated and unsaturated FFA content of the incubation solutions significantly. Furthermore, concentrations of the hydroxylated linoleates 9-hydroxy ocatadecadienoic acid (9-HODE) and 13-HODE were elevated by LpL lipolysis, more than other measured oxylipids. The FFA fractions elicited pro-inflammatory responses inducing TNFalpha and intracellular adhesion molecule expression and reactive oxygen species (ROS) production in human aortic endothelial cells (HAECs). The FFA-mediated increase in ROS was blocked by both the cytochrome P450 2C9 inhibitor sulfaphenazole and NADPH oxidase inhibitors. Compared with linoleate, 13-HODE was found to be a more potent inducer of ROS production in HAECs, an activity that was insensitive to both NADPH oxidase and cytochrome P450 inhibitors. Therefore, although the oxidative metabolism of FFA in endothelial cells can produce inflammatory responses, TGRL lipolysis can also release preformed mediators of oxidative stress (e.g., HODEs) that may influence endothelial cell function in vivo by stimulating intracellular ROS production.

Indexed as

Cells, CulturedEndothelial CellsFatty Acids, NonesterifiedHumansInflammation MediatorsLipolysisLipoprotein LipaseLipoproteinsOxidation-ReductionPostprandial PeriodReactive Oxygen SpeciesTriglyceridesTumor Necrosis Factor-alphaFatty Acids, NonesterifiedInflammation MediatorsLipoprotein LipaseLipoproteinsReactive Oxygen SpeciesTriglyceridesTumor Necrosis Factor-alpha

Identifiers

PMID18812596
PMCPMC2636918
OpenAlexW2052172788

What Socratic 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 Socratic graph.