Evidence map›Paper›PMID 19218241›Full record

ArticleThe Journal of biological chemistry2009

Peroxisome proliferator-activated receptor {gamma} stimulation of adipocyte ApoE gene transcription mediated by the liver receptor X pathway.

Lili Yue, Theodore Mazzone

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
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  10. Article
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  15. The effect of dietary fish oil on weight gain and insulin sensitivity is dependent onFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  16. The effects of PPARγ on the regulation of the TOMM40-APOE-C1 genes cluster.Biochimica et biophysica acta. Molecular basis of disease · 2017
    Article
  17. Article
  18. Article
  19. Article
  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

2 authors at 1 institution in 1 country.

Lili YueDepartments of Medicine, Pharmacology, and Human Nutrition, University of Illinois, Chicago, Illinois 60612.
Theodore Mazzone
University of Illinois Chicago · US

Funding

Adipocyte Lipid Metabolism and ApoE ExpressionR01DK071711 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MAZZONE, THEODORE · 2006 to 2009
$1.2M
Adipocyte Lipid Metabolism and ApoE ExpressionR56DK071711 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MAZZONE, THEODORE · 2005 to 2010
$352k
NIDDK NIH HHS DK71711
6 · The paper itself

Abstract

Peroxisome proliferator-activated receptor (PPARgamma) agonists increase insulin sensitivity in humans and are useful for treating human diabetes. Treatment with these agonists leads to increased apoE expression and triglyceride accumulation in adipocytes. The importance of apoE for adipocyte triglyceride accumulation is demonstrated by observations that triglyceride accumulation is impaired in apoE knockout adipocytes treated with PPARgamma agonists. The current studies investigate the molecular mechanism for PPARgamma stimulation of the adipocyte apoE gene and demonstrate that the liver receptor X (LXR) response element within an apoE gene downstream enhancer is required for the apoE response to PPARgamma agonists. The response of the apoE gene to treatment with PPARgamma agonists was delayed beyond 12 h suggesting the involvement of an intermediary pathway. The combined addition of PPARgamma and LXR agonists did not increase apoE response beyond that observed with addition of either alone. Deletion or mutation of the LXR response element completely eliminated the adipocyte apoE gene response to a PPARgamma agonist. Chromatin immunoprecipitation analyses performed using isolated adipocytes, or adipose tissue from mice treated with PPARgamma agonists, showed increased LXR binding to the apoE gene after PPARgamma agonist treatment. Knockdown of LXR expression completely eliminated the increase in apoE message, protein, and triglyceride in response to PPARgamma stimulation. The LXR response element has been previously shown to mediate sterol responsiveness of the apoE gene, and apoE expression plays an important role in adipocyte triglyceride balance. The current observations suggest that the PPARgamma-LXR-apoE regulatory cascade could be an important molecular link for cross-talk between adipocyte triglyceride and cholesterol homeostasis.

Indexed as

Apolipoproteins E3T3-L1 CellsAdipocytesAnimalsDNA-Binding ProteinsGene Knockdown TechniquesGenes, ReporterHumansHypoglycemic AgentsLigandsLiver X ReceptorsMiceMice, Inbred C57BLMutagenesis, Site-DirectedOrphan Nuclear ReceptorsPPAR gammaApolipoproteins EciglitazoneDNA-Binding ProteinsHypoglycemic AgentsLigandsLiver X ReceptorsOrphan Nuclear ReceptorsPPAR gammaReceptors, Cytoplasmic and NuclearThiazolidinedionesTriglycerides

Identifiers

PMID19218241
PMCPMC2667732
OpenAlexW2152032545

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.