Evidence map›Paper›PMID 29241556›Full record

ArticleCell reports2017

Hepatic Dysfunction Caused by Consumption of a High-Fat Diet.

Anthony R Soltis, Norman J Kennedy, Xiaofeng Xin, Feng Zhou, Scott B Ficarro, Yoon Sing Yap, Bryan J Matthews, Douglas A Lauffenburger, Forest M White, Jarrod A Marto and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

50 citing papers in PubMed, 109 citations in OpenAlex.

  1. Article
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  11. Article
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  13. Article
  14. Food technology and biotechnology · 2023
    Article
  15. Article
  16. Article
  17. Pharmaceutical efficacy of novel human-originFrontiers in endocrinology · 2023
    Article
  18. Article
  19. Review
  20. Article
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

12 authors at 6 institutions in 1 country.

Anthony R SoltisDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Norman J KennedyProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Xiaofeng XinDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Feng ZhouDepartment of Cancer Biology, Department of Oncologic Pathology, and Blais Proteomics Center, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02215, USA; Department of Pathology, Brigham and Women's Hospital, Boston, MA 02215, USA.
Scott B FicarroDepartment of Cancer Biology, Department of Oncologic Pathology, and Blais Proteomics Center, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02215, USA; Department of Pathology, Brigham and Women's Hospital, Boston, MA 02215, USA.
Yoon Sing YapDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Bryan J MatthewsDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Douglas A LauffenburgerDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Forest M WhiteDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Jarrod A MartoDepartment of Cancer Biology, Department of Oncologic Pathology, and Blais Proteomics Center, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02215, USA; Department of Pathology, Brigham and Women's Hospital, Boston, MA 02215, USA.
Roger J DavisProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA; Howard Hughes Medical Institute, Worcester, MA 01605, USA. Electronic address: roger.davis@umassmed.edu.
Ernest FraenkelDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. Electronic address: fraenkel-admin@mit.edu.
Massachusetts Institute of Technology · USBrigham and Women's Hospital · USDana-Farber Cancer Institute · USHarvard University · USHoward Hughes Medical Institute · USUniversity of Massachusetts Chan Medical School · US

Funding

Genomic Analysis of Network Perturbations in Human DiseaseP50HG004233 · NHGRI · DANA-FARBER CANCER INST · PI VIDAL, MARC · 2007 to 2017
$31.6M
TOXICOLOGY CORE UNITP30ES002109 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LEVINE, STUART S · 1985 to 2020
$25.6M
Transcriptional control of inhibitory synapse formationP01NS047572 · NINDS · DANA-FARBER CANCER INSTITUTE · PI STILES, CHARLES D · 2004 to 2013
$13.5M
Systems Biology of Insulin ResistanceR24DK090963 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI DAVIS, ROGER J. · 2011 to 2014
$8.4M
Epigenetic Pathology and Therapy in Huntington's DiseaseR01NS089076 · NINDS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI FRAENKEL, ERNEST, HOUSMAN, DAVID · 2015 to 2024
$4.9M
Metabolic Stress SignalingR01DK107220 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI DAVIS, ROGER J. · 2016 to 2023
$3.6M
NHGRI NIH HHS P50 HG004233NIDDK NIH HHS R01 DK107220NIDDK NIH HHS R24 DK090963NIEHS NIH HHS P30 ES002109NINDS NIH HHS P01 NS047572NINDS NIH HHS R01 NS089076
6 · The paper itself

Abstract

Obesity is a major human health crisis that promotes insulin resistance and, ultimately, type 2 diabetes. The molecular mechanisms that mediate this response occur across many highly complex biological regulatory levels that are incompletely understood. Here, we present a comprehensive molecular systems biology study of hepatic responses to high-fat feeding in mice. We interrogated diet-induced epigenomic, transcriptomic, proteomic, and metabolomic alterations using high-throughput omic methods and used a network modeling approach to integrate these diverse molecular signals. Our model indicated that disruption of hepatic architecture and enhanced hepatocyte apoptosis are among the numerous biological processes that contribute to early liver dysfunction and low-grade inflammation during the development of diet-induced metabolic syndrome. We validated these model findings with additional experiments on mouse liver sections. In total, we present an integrative systems biology study of diet-induced hepatic insulin resistance that uncovered molecular features promoting the development and maintenance of metabolic disease.

Indexed as

TranscriptomeAdipose TissueAnimalsApoptosisDiet, High-FatGene Expression ProfilingGene Expression RegulationGene Regulatory NetworksHepatocytesInsulinInsulin ResistanceLiverMaleMetabolomeMiceMice, Inbred C57BLInsulincomputational biologyhigh-fat dietinsulin resistanceintegrative modelingobesityomic datasystems biology

Identifiers

PMID29241556
PMCPMC5734865
OpenAlexW2771958146

What OpenQuestion holds

Textmetadata
LicenceTDM
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.