Evidence map›Paper›PMID 27976696›Full record

ArticleScientific reports2016

Phospholipase D1 deficiency in mice causes nonalcoholic fatty liver disease via an autophagy defect.

Jang Ho Hur, Shi-Young Park, Claudia Dall'Armi, Jae Sung Lee, Gilbert Di Paolo, Hui-Young Lee, Mee-Sup Yoon, Do Sik Min, Cheol Soo Choi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
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  13. The immunity-related GTPase M rs13361189 variant does not increase the risk for prevalent or incident steatosis; results from the Framingham Heart Study.Liver international : official journal of the International Association for the Study of the Liver · 2019
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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

9 authors at 4 institutions in 2 countries.

Jang Ho HurDepartment of Molecular Medicine, Lee Gil Ya Cancer and Diabetes Institute, Gachon University School of Medicine, Incheon 406-840, Korea.
Shi-Young ParkDepartment of Molecular Medicine, Lee Gil Ya Cancer and Diabetes Institute, Gachon University School of Medicine, Incheon 406-840, Korea.
Claudia Dall'ArmiDepartment of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032, United States of America.
Jae Sung LeeDepartment of Molecular Medicine, Lee Gil Ya Cancer and Diabetes Institute, Gachon University School of Medicine, Incheon 406-840, Korea.
Gilbert Di PaoloDepartment of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032, United States of America.
Hui-Young LeeDepartment of Molecular Medicine, Lee Gil Ya Cancer and Diabetes Institute, Gachon University School of Medicine, Incheon 406-840, Korea.
Mee-Sup YoonDepartment of Molecular Medicine, Lee Gil Ya Cancer and Diabetes Institute, Gachon University School of Medicine, Incheon 406-840, Korea.
Do Sik MinDepartment of Molecular Biology, College of Natural Science, Pusan National University, Busan 609-735, Korea.
Cheol Soo ChoiDepartment of Molecular Medicine, Lee Gil Ya Cancer and Diabetes Institute, Gachon University School of Medicine, Incheon 406-840, Korea.
Gachon University · KRColumbia University Irving Medical Center · USGachon University Gil Medical Center · KRPusan National University · KR

Funding

Satellite Diagnostic and Treatment Clinic CoreP50AG008702 · NIA · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI DE JAGER, PHILIP L · 1989 to 2019
$46.3M
Role of phospholipids in membrane traffic at the synapseR01NS056049 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LIEM, RONALD K. · 2006 to 2016
$3.7M
Control of liver autophagy by phosphatidic acid signalingR21AG045020 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI DI PAOLO, GILBERT · 2013 to 2014
$440k
NIA NIH HHS P50 AG008702NIA NIH HHS R21 AG045020NINDS NIH HHS R01 NS056049
6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) is characterized by the accumulation of triglycerides (TG) as lipid droplets in the liver. Although lipid-metabolizing enzymes are considered important in NAFLD, the involvement of phospholipase D1 (PLD1) has not yet been studied. Here, we show that the genetic ablation of PLD1 in mice induces NAFLD due to an autophagy defect. PLD1 expression was decreased in high-fat diet-induced NAFLD. Subsequently, PLD1 deficiency led to an increase in hepatic TGs and liver weight. Autophagic flux was blocked in Pld1

Indexed as

AutophagyAnimalsBenzimidazolesCells, CulturedChromatography, High Pressure LiquidDiet, High-FatGenetic VectorsHepatocytesLipid MetabolismLipid PeroxidationLiverLysosomesMiceMice, KnockoutMicroscopy, ConfocalMicrotubule-Associated ProteinsBenzimidazolesMap1lc3b protein, mouseMicrotubule-Associated ProteinsN-(1-(4-(5-chloro-2-oxo-2,3-dihydro-1H-benzo(d)imidazol-1-yl)piperidin-1-yl)propan-2-yl)-2-naphthamidePhosphatidic AcidsPhospholipase Dphospholipase D1PiperidinesTriglycerides

Identifiers

PMID27976696
PMCPMC5156943
OpenAlexW2565738757

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.