Evidence map›Paper›PMID 26676813›Full record

ReviewSeminars in liver disease2015

Insights from Genome-Wide Association Analyses of Nonalcoholic Fatty Liver Disease.

Bratati Kahali, Brian Halligan, Elizabeth K Speliotes

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in liver disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
3.1field-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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Mechanism and therapeutic strategy of hepaticWorld journal of gastroenterology · 2022
    Article
  9. Review
  10. Article
  11. Article
  12. Glycogenosis is common in nonalcoholic fatty liver disease and is independently associated with ballooning, but lower steatosis and lower fibrosis.Liver international : official journal of the International Association for the Study of the Liver · 2021
    Article
  13. Article
  14. Review
  15. Review
  16. Observational
  17. Article
  18. Article
  19. Article
  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

3 authors at 1 institution in 1 country.

Bratati KahaliDivision of Gastroenterology, Department of Internal Medicine, Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Michigan.
Brian HalliganDivision of Gastroenterology, Department of Internal Medicine, Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Michigan.
Elizabeth K SpeliotesDivision of Gastroenterology, Department of Internal Medicine, Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Michigan.
University of Michigan–Ann Arbor · US

Funding

University of Michigan Center for Gastrointestinal ResearchP30DK034933 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI OMARY, BISHR · 1986 to 2021
$22.5M
Identification and functional impact of NAFLD associated genetic variantsR01DK106621 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SPELIOTES, ELIZABETH K · 2015 to 2019
$3.3M
NIDDK NIH HHS P30 DK034933NIDDK NIH HHS R01 DK106621NIDDK NIH HHS R01DK106621-01
6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) is caused by hepatic steatosis, which can progress to nonalcoholic steatohepatitis, fibrosis/cirrhosis, and hepatocellular carcinoma in the absence of excessive alcohol consumption. Nonalcoholic fatty liver disease will become the number one cause of liver disease worldwide by 2020. Nonalcoholic fatty liver disease is correlated albeit imperfectly with obesity and other metabolic diseases such as diabetes, hyperlipidemia, and cardiovascular disease, but exactly how having one of these diseases contributes to the development of other metabolic diseases is only now being elucidated. Development of NAFLD and related metabolic diseases is genetically influenced in the population, and recent genome-wide association studies (GWASs) have discovered genetic variants that associate with these diseases. These GWAS-associated variants cannot only help us to identify individuals at high risk of developing NAFLD, but also to better understand its pathophysiology so that we can develop more effective treatments for this disease and related metabolic diseases in the future.

Indexed as

AcyltransferasesAdaptor Proteins, Signal TransducingCarcinoma, HepatocellularGenetic Predisposition to DiseaseGenome-Wide Association StudyGraft RejectionGraft SurvivalHumansInsulin ResistanceIntracellular Signaling Peptides and ProteinsLipaseLiver NeoplasmsLiver TransplantationLysophospholipaseMembrane ProteinsNon-alcoholic Fatty Liver DiseaseAcyltransferasesAdaptor Proteins, Signal TransducingGCKR protein, humanIntracellular Signaling Peptides and ProteinsLipaseLYPLAL1 protein, humanLysophospholipaseMembrane ProteinsPhospholipases A2, Calcium-IndependentPNPLA3 protein, humanPPP1R3B protein, humanProtein Phosphatase 1Protein Serine-Threonine KinasesTM6SF2 protein, humanTRIB1 protein, human

Identifiers

PMID26676813
PMCPMC4941959
OpenAlexW2258693492

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.