Evidence map›Paper›PMID 26067236›Full record

ArticleeLife2015

The genetic architecture of NAFLD among inbred strains of mice.

Simon T Hui, Brian W Parks, Elin Org, Frode Norheim, Nam Che, Calvin Pan, Lawrence W Castellani, Sarada Charugundla, Darwin L Dirks, Nikolaos Psychogios and 5 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
8.1field-weighted citation impact, top 2% 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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

  1. Pooled it
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  15. Gene Regulatory Networks in Coronary Artery Disease.Current atherosclerosis reports · 2023
    Review
  16. Review
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14 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

15 authors at 4 institutions in 2 countries.

Simon T HuiDepartment of Medicine/Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, United States.
Brian W ParksDepartment of Medicine/Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, United States.
Elin OrgDepartment of Medicine/Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, United States.
Frode NorheimDepartment of Nutrition, Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Oslo, Norway.
Nam CheDepartment of Medicine/Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, United States.
Calvin PanDepartment of Medicine/Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, United States.
Lawrence W CastellaniDepartment of Medicine/Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, United States.
Sarada CharugundlaDepartment of Medicine/Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, United States.
Darwin L DirksDepartment of Medicine/Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, United States.
Nikolaos PsychogiosCardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, United States.
Isaac NeuhausDepartment of Computational Genomics, Bristol-Myers Squibb, Princeton, United States.
Robert E GersztenCardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, United States.
Todd KirchgessnerDepartment of Cardiovascular Drug Discovery, Bristol-Myers Squibb, Princeton, United States.
Peter S GargalovicDepartment of Computational Genomics, Bristol-Myers Squibb, Princeton, United States.
Aldons J LusisDepartment of Medicine/Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, United States.
University of California, Los Angeles · USBristol-Myers Squibb (United States) · USMassachusetts General Hospital · USUniversity of Oslo · NO

Funding

Systems genomics of metabolic syndrome traitsP01HL028481 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 1985 to 2019
$50.2M
Systems Genetics of Type 1 Diabetes ComplicationsDP3DK094311 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 2011 to 2011
$4.3M
Neuroendocrinology, Sex Differences, and ReproductionT32HD007228 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARNOLD, ARTHUR P · 1985 to 2015
$3.9M
NHLBI NIH HHS HL028481NHLBI NIH HHS P01 HL028481NICHD NIH HHS T32-HD07228NIDDK NIH HHS DK094311
6 · The paper itself

Abstract

To identify genetic and environmental factors contributing to the pathogenesis of non-alcoholic fatty liver disease, we examined liver steatosis and related clinical and molecular traits in more than 100 unique inbred mouse strains, which were fed a diet rich in fat and carbohydrates. A >30-fold variation in hepatic TG accumulation was observed among the strains. Genome-wide association studies revealed three loci associated with hepatic TG accumulation. Utilizing transcriptomic data from the liver and adipose tissue, we identified several high-confidence candidate genes for hepatic steatosis, including Gde1, a glycerophosphodiester phosphodiesterase not previously implicated in triglyceride metabolism. We confirmed the role of Gde1 by in vivo hepatic over-expression and shRNA knockdown studies. We hypothesize that Gde1 expression increases TG production by contributing to the production of glycerol-3-phosphate. Our multi-level data, including transcript levels, metabolite levels, and gut microbiota composition, provide a framework for understanding genetic and environmental interactions underlying hepatic steatosis.

Indexed as

Genome-Wide Association StudyAdipose TissueAnimalsGene ExpressionGene Expression ProfilingGene Knockdown TechniquesLiverMice, Inbred StrainsNon-alcoholic Fatty Liver DiseasePhosphoric Diester HydrolasesRodent DiseasesTriglyceridesglycerophosphodiester phosphodiesterasePhosphoric Diester HydrolasesTriglycerideschromosomesevolutionary biologygenesgenome-wide associationgenomicshepatic steatosismetabolomemicrobiomemousetranscriptome

Identifiers

PMID26067236
PMCPMC4493743
OpenAlexW2120244696

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.