Evidence map›Paper›PMID 22899824›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2012

PGC-1α overexpression results in increased hepatic fatty acid oxidation with reduced triacylglycerol accumulation and secretion.

E Matthew Morris, Grace M E Meers, Frank W Booth, Kevin L Fritsche, Christopher D Hardin, John P Thyfault, Jamal A Ibdah

Abstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

113 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Article
  4. Loss of ovarian function and estrogen therapy remodel the brain's synaptic and metabolic proteome.American journal of physiology. Regulatory, integrative and comparative physiology · 2026
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  12. Loss of hepatocyte-specific RECK exacerbates metabolic dysfunction-associated steatohepatitis.American journal of physiology. Endocrinology and metabolism · 2025
    Article
  13. Article
  14. Loss of ovarian function prevents exercise-induced activation of hepatic mitophagic flux.American journal of physiology. Endocrinology and metabolism · 2025
    Article
  15. Article
  16. Scaffold implantationAnnals of surgical treatment and research · 2025
    Article
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  20. Antioxidants (Basel, Switzerland) · 2024
    Article

53 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

7 authors.

E Matthew MorrisDepartment of Internal Medicine-Gastroenterology, University of Missouri, Columbia, Missouri, USA.
Grace M E Meers
Frank W Booth
Kevin L Fritsche
Christopher D Hardin
John P Thyfault
Jamal A Ibdah

Funding

Exercise &Health: Integration from Molecule to PatientT32AR048523 · NIAMS · UNIVERSITY OF MISSOURI-COLUMBIA · PI TERJUNG, RONALD L · 2003 to 2013
$2.5M
Aerobic fitness, mitochondrial dysfunction, and fatty liver diseaseR01DK088940 · NIDDK · UNIVERSITY OF MISSOURI-COLUMBIA · PI THYFAULT, JOHN P · 2011 to 2015
$1.5M
NIAMS NIH HHS 5T32 AR-48523-8NIAMS NIH HHS T32 AR048523NIDDK NIH HHS DK-068210NIDDK NIH HHS DK-088940NIDDK NIH HHS R01 DK088940
6 · The paper itself

Abstract

Studies have shown that decreased mitochondrial content and function are associated with hepatic steatosis. We examined whether peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) overexpression and a subsequent increase in mitochondrial content and function in rat primary hepatocytes (in vitro) and Sprague-Dawley rats (in vivo) would comprehensively alter mitochondrial lipid metabolism, including complete (CO(2)) and incomplete (acid-soluble metabolites) fatty acid oxidation (FAO), tricarboxylic acid cycle flux, and triacylglycerol (TAG) storage and export. PGC-1α overexpression in primary hepatocytes produced an increase in markers of mitochondrial content and function (citrate synthase, mitochondrial DNA, and electron transport system complex proteins) and an increase in FAO, which was accompanied by reduced TAG storage and TAG secretion compared with control. Also, the PGC-1α-overexpressing hepatocytes were protected from excess TAG accumulation following overnight lipid treatment. PGC-1α overexpression in hepatocytes lowered expression of genes critical to VLDL assembly and secretion (apolipoprotein B and microsomal triglyceride transfer protein). Adenoviral transduction of rats with PGC-1α resulted in a liver-specific increase in PGC-1α expression and produced an in vivo liver phenotype of increased FAO via increased mitochondrial function that also resulted in reduced hepatic TAG storage and decreased plasma TAG levels. In conclusion, overexpression of hepatic PGC-1α and subsequent increases in FAO through elevated mitochondrial content and/or function result in reduced TAG storage and secretion in the in vitro and in vivo milieu.

Indexed as

AnimalsApolipoproteins BFatty AcidsHepatocytesLipid MetabolismLiverMitochondriaOxidation-ReductionPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRatsRats, Sprague-DawleyRNA-Binding ProteinsTranscription FactorsTriglyceridesApolipoproteins BFatty AcidsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, ratRNA-Binding ProteinsTranscription FactorsTriglycerides

Identifiers

PMID22899824
PMCPMC3469696

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.