Evidence map›Paper›PMID 23747828›Full record

ArticleBiochimica et biophysica acta2013

High glucose potentiates L-FABP mediated fibrate induction of PPARα in mouse hepatocytes.

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

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  8. ΔJournal of lipid research · 2018
    Article
  9. Article
  10. Article
  11. 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
  12. Article
  13. Review
  14. Article
  15. Impact of SCP-2/SCP-x gene ablation and dietary cholesterol on hepatic lipid accumulation.American journal of physiology. Gastrointestinal and liver physiology · 2015
    Article
  16. Article
  17. Human FABP1 T94A variant impacts fatty acid metabolism and PPAR-α activation in cultured human female hepatocytes.American journal of physiology. Gastrointestinal and liver physiology · 2014
    Article
  18. Article
  19. Article
  20. 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

8 authors at 1 institution in 1 country.

Anca D PetrescuDepartment of Physiology and Pharmacology, Texas A&M University, TVMC, College Station, TX 77843-4466, USA.
Avery L McIntosh
Stephen M Storey
Huan Huang
Gregory G Martin
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 DK41402NIDDK NIH HHS R01 DK041402
6 · The paper itself

Abstract

Although liver fatty acid binding protein (L-FABP) binds fibrates and PPARα in vitro and enhances fibrate induction of PPARα in transformed cells, the functional significance of these findings is unclear, especially in normal hepatocytes. Studies with cultured primary mouse hepatocytes show that: 1) At physiological (6mM) glucose, fibrates (bezafibrate, fenofibrate) only weakly activated PPARα transcription of genes in LCFA β-oxidation; 2) High (11-20mM) glucose, but not maltose (osmotic control), significantly potentiated fibrate-induction of mRNA of these and other PPARα target genes to increase LCFA β-oxidation. These effects were associated with fibrate-mediated redistribution of L-FABP into nuclei-an effect prolonged by high glucose-but not with increased de novo fatty acid synthesis from glucose; 3) Potentiation of bezafibrate action by high glucose required an intact L-FABP/PPARα signaling pathway as shown with L-FABP null, PPARα null, PPARα inhibitor-treated WT, or PPARα-specific fenofibrate-treated WT hepatocytes. High glucose alone in the absence of fibrate was ineffective. Thus, high glucose potentiation of PPARα occurred through FABP/PPARα rather than indirectly through other PPARs or glucose induced signaling pathways. These data indicated L-FABP's importance in fibrate-induction of hepatic PPARα LCFA β-oxidative genes, especially in the context of high glucose levels.

Indexed as

AnimalsBezafibrateCell NucleusFatty Acid-Binding ProteinsFatty AcidsFenofibrateGlucoseHepatocytesHypolipidemic AgentsMiceMice, Mutant StrainsOxidation-ReductionPPAR alphaSignal TransductionSweetening AgentsBezafibrateFabp1 protein, mouseFatty Acid-Binding ProteinsFatty AcidsFenofibrateGlucoseHypolipidemic AgentsPPAR alphaSweetening Agents

Identifiers

PMID23747828
PMCPMC3730521
OpenAlexW1999359190

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.