Evidence map›Paper›PMID 31036368›Full record

ArticleJournal of pediatric surgery2019

Omega-3 fatty acids are protective in hepatic ischemia reperfusion injury in the absence of GPR120 signaling.

Meredith A Baker, Prathima Nandivada, Paul D Mitchell, Gillian L Fell, Amy Pan, Bennet S Cho, Denis J De La Flor, Lorenzo Anez-Bustillos, Duy T Dao, Vania Nosé and 1 more

Open access · greenAbstract read
In one paragraph

Article in Journal of pediatric surgery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Meredith A BakerVascular Biology Program and Department of Surgery, Boston Children's Hospital.
Prathima NandivadaVascular Biology Program and Department of Surgery, Boston Children's Hospital.
Paul D MitchellInstitutional Centers for Clinical and Translational Research, Boston Children's Hospital.
Gillian L FellVascular Biology Program and Department of Surgery, Boston Children's Hospital.
Amy PanVascular Biology Program and Department of Surgery, Boston Children's Hospital.
Bennet S ChoVascular Biology Program and Department of Surgery, Boston Children's Hospital.
Denis J De La FlorVascular Biology Program and Department of Surgery, Boston Children's Hospital.
Lorenzo Anez-BustillosVascular Biology Program and Department of Surgery, Boston Children's Hospital.
Duy T DaoVascular Biology Program and Department of Surgery, Boston Children's Hospital.
Vania NoséDepartment of Pathology, Massachusetts General Hospital.
Mark PuderVascular Biology Program and Department of Surgery, Boston Children's Hospital. Electronic address: mark.puder@childrens.harvard.edu.
Boston Children's Hospital · USMassachusetts General Hospital · US

Funding

HARVARD-LONGWOOD RESEARCH TRAINING IN VASCULAR SURGERYT32HL007734 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI FERRAN, CHRISTIANE, LOGERFO, FRANK W · 1993 to 2023
$10.5M
Harvard-Longwood Short-Term Research Training in Vascular SurgeryT35HL110843 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI CHRISTIANE FERRAN, FRANK W LOGERFO · 2013 to 2026
$609k
Generation and use of lipid emulsions to understand mechanisms of and optimally manage parenteral nutrition associated liver diseaseF32DK104525 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI FELL, GILLIAN LYNAPP · 2014 to 2016
$163k
NHLBI NIH HHS T32 HL007734NHLBI NIH HHS T35 HL110843NIDDK NIH HHS F32 DK104525NIDDK NIH HHS L40 DK106831
6 · The paper itself

Abstract

backgroundA single dose of IV fish oil (FO) before hepatic ischemia reperfusion injury (HIRI) increases hepatocyte proliferation and reduces necrosis in wild type (WT) mice. It has been suggested that the GPR120 receptor on Kupffer cells mediates FO's ability to reduce HIRI. The purpose of this study was to determine whether GPR120 is required for FO to reduce HIRI.

methodsSixty-four (n = 8/group) adult male WT (C57BL/6) and GPR120 knockout (KO) mice received IV FO (1 g/kg) or saline 1 h prior to HIRI or sham operation. Mice were euthanized 24 h postoperatively for analysis of hepatic histology, NFκB activity, and serum alanine transaminase (ALT) levels.

resultsFO pretreated livers had less necrosis after HIRI than saline pretreated livers in both WT (mean ± SEM 25.9 ± 7.3% less, P = 0.007) and KO (36.6 ± 7.3% less, P < 0.0001) mice. There was no significant difference in percent necrosis between WT-FO and KO-FO groups. Sham groups demonstrated minimal necrosis (0-1.9%). Mean [95% CI] ALT after HIRI was significantly higher (P = 0.04) in WT-Saline mice (1604 U/L [751-3427]) compared to WT-FO (321 U/L [150-686]) but was not significantly higher in KO-Saline mice compared to KO-FO. There were no differences in ALT between WT-FO and KO-FO mice who underwent HIRI or between groups who underwent sham surgery. There were no differences in NFκB or IKKβ activation among groups as measured by Western blot analysis.

conclusionsIV FO pretreatment was able to reduce HIRI in GPR120 KO mice, suggesting the hepatoprotective effects of FO are not mediated by GPR120 alone.

Indexed as

Alanine TransaminaseAnimalsCell ProliferationFatty Acids, Omega-3HepatocytesLiverMaleMice, Inbred C57BLMice, KnockoutNecrosisNF-kappa B p50 SubunitReceptors, G-Protein-CoupledReperfusion InjurySignal TransductionAlanine TransaminaseFatty Acids, Omega-3FFAR4 protein, mouseNF-kappa B p50 SubunitNfkb1 protein, mouseReceptors, G-Protein-CoupledFish oilFree fatty acid receptor 4GPR120IschemiaLiverReperfusion

Identifiers

PMID31036368
PMCPMC6790164
OpenAlexW2939566739

What OpenQuestion holds

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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.