Evidence map›Paper›PMID 20585248›Full record

ReviewCurrent opinion in endocrinology, diabetes, and obesity2010

Mitochondrial dysfunction in obesity.

Juan C Bournat, Chester W Brown

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Current opinion in endocrinology, diabetes, and obesity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 227 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
227citing papers in PubMed, 2 pooled it
8.7field-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

227 citing papers in PubMed, 2 syntheses or guidelines pooled it, 472 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Trial
  6. Trial
  7. Trial
  8. Observational
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Purslane (Preventive nutrition and food science · 2026
    Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Article

167 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

2 authors at 1 institution in 1 country.

Juan C BournataDepartments of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA.
Chester W Brown
Baylor College of Medicine · US

Funding

Roles of GDF3 in the differentiation and function of the adipocyteR01DK073572 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI BROWN, CHESTER W · 2007 to 2011
$1.7M
PILOT STUDY--BAYLOR CHILD HEALTH RESEARCH CENTERP30HD027823 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI FEIGIN, RALPH DAVID · 1990 to 2001
$515k
The roles of Gfd3 in adipogenesis and adipocyte functionR03HD049138 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI BROWN, CHESTER W · 2006 to 2007
$148k
TGF-B SUPERFAMILY AND MOUSE DEVELOPMENTK08HD001156 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI BROWN, CHESTER W · 1996 to 2000
$81k
NICHD NIH HHS HD01156NICHD NIH HHS HD27823NICHD NIH HHS R03 HD049138NIDDK NIH HHS DK073572NIDDK NIH HHS R01 DK073572
6 · The paper itself

Abstract

purpose of reviewThe review highlights recent findings regarding the functions of mitochondria in adipocytes, providing an understanding of their central roles in regulating substrate metabolism, energy expenditure, disposal of reactive oxygen species (ROS), and in the pathophysiology of obesity and insulin resistance, as well as roles in the mechanisms that affect adipogenesis and mature adipocyte function. RECENT

findingsNutrient excess leads to mitochondrial dysfunction, which in turn leads to obesity-related pathologies, in part due to the harmful effects of ROS. The recent recognition of 'ectopic' brown adipose in humans suggests that this tissue may play an underappreciated role in the control of energy expenditure. Transcription factors, PGC-1alpha and PRDM16, which regulate brown adipogenesis, and members of the TGF-beta superfamily that modulate this process may be important new targets for antiobesity drugs. SUMMARY: Mitochondria play central roles in ATP production, energy expenditure, and disposal of ROS. Excessive energy substrates lead to mitochondrial dysfunction with consequential effects on lipid and glucose metabolism. Adipocytes help to maintain the appropriate balance between energy storage and expenditure and maintaining this balance requires normal mitochondrial function. Many adipokines, including members of the TGF-beta superfamily, and transcriptional coactivators, PGC-1alpha and PRDM16, are important regulators of this process.

Indexed as

AdipogenesisAdipokinesAdipose TissueAnimalsDNA-Binding ProteinsEnergy MetabolismGlucoseHeat-Shock ProteinsHumansInsulin ResistanceIon ChannelsLipid MetabolismMiceMitochondrial DiseasesMitochondrial ProteinsObesityAdipokinesDNA-Binding ProteinsGlucoseHeat-Shock ProteinsIon ChannelsMitochondrial ProteinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanPRDM16 protein, humanReactive Oxygen SpeciesTranscription FactorsTransforming Growth Factor betaUncoupling Protein 1

Identifiers

PMID20585248
PMCPMC5001554
OpenAlexW2313583633

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.