Evidence map›Paper›PMID 30042157›Full record

ArticleJournal of lipid research2018

Mitochondrial dysfunction-related lipid changes occur in nonalcoholic fatty liver disease progression.

Kang-Yu Peng, Matthew J Watt, Sander Rensen, Jan Willem Greve, Kevin Huynh, Kaushala S Jayawardana, Peter J Meikle, Ruth C R Meex

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers.

0numbers the graph read from it
0cells of the map it votes in
132citing papers in PubMed
14.4field-weighted citation impact, top 1% 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

132 citing papers in PubMed, 218 citations in OpenAlex.

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72 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

8 authors at 4 institutions in 2 countries.

Kang-Yu PengBaker Heart and Diabetes Institute, Melbourne, Victoria, Australia.
Matthew J WattDepartment of Physiology, Faculty of Medicine, Dentistry, and Health Sciences, University of Melbourne, Melbourne, Victoria, Australia.
Sander RensenDepartments of Surgery Maastricht University Medical Centre, Maastricht, The Netherlands.
Jan Willem GreveDepartment of Surgery, Zuyderland Medical Center Heerlen, Heerlen, The Netherlands.
Kevin HuynhBaker Heart and Diabetes Institute, Melbourne, Victoria, Australia.
Kaushala S JayawardanaBaker Heart and Diabetes Institute, Melbourne, Victoria, Australia.
Peter J MeikleBaker Heart and Diabetes Institute, Melbourne, Victoria, Australia ruth.meex@maastrichtuniversity.nl peter.meikle@baker.edu.au.
Ruth C R MeexHuman Biology, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Centre, Maastricht, The Netherlands ruth.meex@maastrichtuniversity.nl peter.meikle@baker.edu.au.
Baker Heart and Diabetes Institute · AUUniversity of Melbourne · AUMaastricht University Medical Centre · NLZuyderland Medisch Centrum · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) comprises fat-accumulating conditions within hepatocytes that can cause severe liver damage and metabolic comorbidities. Studies suggest that mitochondrial dysfunction contributes to its development and progression and that the hepatic lipidome changes extensively in obesity and in NAFLD. To gain insight into the relationship between lipid metabolism and disease progression through different stages of NAFLD, we performed lipidomic analysis of plasma and liver biopsy samples from obese patients with nonalcoholic fatty liver (NAFL) or nonalcoholic steatohepatitis (NASH) and from those without NAFLD. Congruent with earlier studies, hepatic lipid levels overall increased with NAFLD. Lipid species that differed with NAFLD severity were related to mitochondrial dysfunction; specifically, hepatic cardiolipin and ubiquinone accumulated in NAFL, and levels of acylcarnitine increased with NASH. We propose that increased levels of cardiolipin and ubiquinone may help to preserve mitochondrial function in early NAFLD, but that mitochondrial function eventually fails with progression to NASH, leading to increased acylcarnitine. We also found a negative association between hepatic odd-chain phosphatidylcholine and NAFLD, which may result from mitochondrial dysfunction-related impairment of branched-chain amino acid catabolism. Overall, these data suggest a close link between accumulation of specific hepatic lipid species, mitochondrial dysfunction, and the progression of NAFLD.

Indexed as

Disease ProgressionLipid MetabolismAdultCohort StudiesFemaleHumansLiverMaleMiddle AgedMitochondriaNon-alcoholic Fatty Liver Diseaselipidomicsliver metabolismmitochondriaobesity

Identifiers

PMID30042157
PMCPMC6168306
OpenAlexW2884907724

What OpenQuestion holds

Textmetadata
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.