Evidence map›Paper›PMID 23238934›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2013

Impact of L-FABP and glucose on polyunsaturated fatty acid induction of PPARα-regulated β-oxidative enzymes.

Anca D Petrescu, Huan Huang, Gregory G Martin, Avery L McIntosh, Stephen M Storey, Danilo Landrock, Ann B Kier, Friedhelm Schroeder

Abstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. The Use of Organoid Cultures in Advancing Nutrition Research.Advances in nutrition (Bethesda, Md.) · 2025
    Review
  3. Article
  4. Article
  5. Mechanisms underlying reduced weight gain in intestinal fatty acid-binding protein (IFABP) null mice.American journal of physiology. Gastrointestinal and liver physiology · 2020
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Impact of dietary phytol on lipid metabolism in SCP2/SCPX/L-FABP null mice.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2017
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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 1 institution in 1 country.

Anca D PetrescuDepartment of Physiology and Pharmacology, Texas A&M University, TVMC, College Station, TX 77843, USA.
Huan Huang
Gregory G Martin
Avery L McIntosh
Stephen M Storey
Danilo Landrock
Ann B Kier
Friedhelm Schroeder
Texas A&M University · US

Funding

FATTY ACID BINDING PROTEINS-LIGAND SPECIFICITYR01DK041402 · NIDDK · UNIVERSITY OF CINCINNATI · PI SCHROEDER, FRIEDHELM · 1989 to 2010
$4.4M
NIDDK NIH HHS DK41402
6 · The paper itself

Abstract

Liver fatty acid binding protein (L-FABP) is the major soluble protein that binds very-long-chain n-3 polyunsaturated fatty acids (n-3 PUFAs) in hepatocytes. However, nothing is known about L-FABP's role in n-3 PUFA-mediated peroxisome proliferator activated receptor-α (PPARα) transcription of proteins involved in long-chain fatty acid (LCFA) β-oxidation. This issue was addressed in cultured primary hepatocytes from wild-type, L-FABP-null, and PPARα-null mice with these major findings: 1) PUFA-mediated increase in the expression of PPARα-regulated LCFA β-oxidative enzymes, LCFA/LCFA-CoA binding proteins (L-FABP, ACBP), and PPARα itself was L-FABP dependent; 2) PPARα transcription, robustly potentiated by high glucose but not maltose, a sugar not taken up, correlated with higher protein levels of these LCFA β-oxidative enzymes and with increased LCFA β-oxidation; and 3) high glucose altered the potency of n-3 relative to n-6 PUFA. This was not due to a direct effect of glucose on PPARα transcriptional activity nor indirectly through de novo fatty acid synthesis from glucose. Synergism was also not due to glucose impacting other signaling pathways, since it was observed only in hepatocytes expressing both L-FABP and PPARα. Ablation of L-FABP or PPARα as well as treatment with MK886 (PPARα inhibitor) abolished/reduced PUFA-mediated PPARα transcription of these genes, especially at high glucose. Finally, the PUFA-enhanced L-FABP distribution into nuclei with high glucose augmentation of the L-FABP/PPARα interaction reveals not only the importance of L-FABP for PUFA induction of PPARα target genes in fatty acid β-oxidation but also the significance of a high glucose enhancement effect in diabetes.

Indexed as

Acyl-CoA OxidaseAnimalsBlotting, WesternCarnitine O-PalmitoyltransferaseCell NucleusCells, CulturedFatty Acid-Binding ProteinsFatty AcidsFatty Acids, UnsaturatedGlucoseHepatocytesMaltoseMiceMice, Inbred C57BLMicroscopy, ConfocalOsmolar ConcentrationAcyl-CoA OxidaseCarnitine O-PalmitoyltransferaseFatty Acid-Binding ProteinsFatty AcidsFatty Acids, UnsaturatedGlucoseMaltosePPAR alphaStearic Acids

Identifiers

PMID23238934
PMCPMC3566512
OpenAlexW2119196942

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.