Evidence map›Paper›PMID 30168806›Full record

ReviewThe Journal of clinical investigation2018

Mitochondrial role in the neonatal predisposition to developing nonalcoholic fatty liver disease.

Peter R Baker, Jacob E Friedman

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Non-Alcoholic Fatty Liver Disease: Metabolic, Genetic, Epigenetic and Environmental Risk Factors.International journal of environmental research and public health · 2021
    Review
  17. Article
  18. Observational
  19. Review
  20. Developmental effects ofTrends in developmental biology · 2021
    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

2 authors at 2 institutions in 2 countries.

Peter R BakerSection of Clinical Genetics and Metabolism, Department of Pediatrics.
Jacob E FriedmanSection of Neonatology, Department of Pediatrics.
Laboratory of Molecular Genetics · PLPediatrics and Genetics · US

Funding

PILOT STUDY--SUBSTRATE METABOLISM IN EXTREMELY LOW BIRTH WEIGHT INFANTSP30DK048520 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI Edward L Melanson · 1995 to 2026
$32.6M
The Impact of Maternal Health and Diet on Development of Fetal Metabolic SystemsR24DK090964 · NIDDK · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI AAGAARD, KJERSTI MARIE, FRIEDMAN, JACOB E · 2010 to 2019
$15.8M
Training in Basic and Translational Child Health ResearchK12HD068372 · NICHD · UNIVERSITY OF COLORADO DENVER · PI DANIELS, STEPHEN R · 2011 to 2020
$3.7M
NICHD NIH HHS K12 HD068372NIDDK NIH HHS P30 DK048520NIDDK NIH HHS R24 DK090964
6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) is a global epidemic in obese children and adults, and the onset might have fetal origins. A growing body of evidence supports the role of developmental programming, whereby the maternal environment affects fetal and infant development, altering the risk profile for disease later in life. Human and nonhuman primate studies of maternal obesity demonstrate that risk factors for pediatric obesity and NAFLD begin in utero. The pathologic mechanisms for NAFLD are multifactorial but have centered on altered mitochondrial function/dysfunction that might precede insulin resistance. Compared with the adult liver, the fetal liver has fewer mitochondria, low activity of the fatty acid metabolic enzyme carnitine palmitoyl-CoA transferase-1, and little or no gluconeogenesis. Exposure to excess maternal fuels during fetal life uniquely alters hepatic fatty acid oxidation, tricarboxylic acid cycle activity, de novo lipogenesis, and mitochondrial health. These events promote increased oxidative stress and excess triglyceride storage, and, together with altered immune function and epigenetic changes, they prime the fetal liver for NAFLD and might drive the risk for nonalcoholic steatohepatitis in the next generation.

Indexed as

AnimalsApoptosisChildDisease SusceptibilityEpigenesis, GeneticFemaleFetal DevelopmentFetusHumansInfant, NewbornInsulin ResistanceLipid MetabolismMaternal-Fetal ExchangeMitochondria, LiverNon-alcoholic Fatty Liver DiseaseObesity

Identifiers

PMID30168806
PMCPMC6118579
OpenAlexW2889527760

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.