Evidence map›Paper›PMID 16906479›Full record

ArticleDiabetologia2006

PPARgamma agonism increases rat adipose tissue lipolysis, expression of glyceride lipases, and the response of lipolysis to hormonal control.

W T Festuccia, M Laplante, M Berthiaume, Y Gélinas, Y Deshaies

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In one paragraph

Article in Diabetologia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

57 citing papers in PubMed, 140 citations in OpenAlex.

  1. Article
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  5. Review
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  7. Article
  8. Novel Effect ofMolecules (Basel, Switzerland) · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. PPARs-Orchestrated Metabolic Homeostasis in the Adipose Tissue.International journal of molecular sciences · 2021
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Trace Elements, PPARs, and Metabolic Syndrome.International journal of molecular sciences · 2020
    Review
  18. Anti-Lipolysis Induced by Insulin in Diverse Pathophysiologic Conditions of Adipose Tissue.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020
    Review
  19. Article
  20. Journal of obesity · 2018
    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

5 authors at 1 institution in 1 country.

W T FestucciaLaval Hospital Research Center, Faculty of Medicine, Laval University, Quebec, G1V 4G5, Canada.
M Laplante
M Berthiaume
Y Gélinas
Y Deshaies
Université Laval · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisThe aim of this study was to investigate the effect and mechanisms of action of in vivo peroxisome proliferator-activated receptor gamma (PPARgamma) activation on white adipose tissue (WAT) lipolysis and NEFA metabolism. MATERIALS AND

methodsStudy rats were treated for 7 days with 15 mg/kg of rosiglitazone per day; control rats were not treated. After a 6-h fast, lipolysis and levels of mRNA for lipases were assessed in explants from various adipose depots.

resultsRosiglitazone markedly increased basal and noradrenaline (norepinephrine)-stimulated glycerol and NEFA release from WAT explants, and amplified their inhibition by insulin. Primary adipocytes isolated from PPARgamma agonist-treated rats were also more responsive to noradrenaline stimulation expressed per cell, ruling out a contribution of an altered number of mature adipocytes in explants. Rosiglitazone concomitantly increased levels of mRNA transcripts for adipose triglyceride lipase (ATGL) and monoglyceride lipase (MGL) in subcutaneous and visceral WAT, and mRNA for hormone-sensitive lipase (HSL) in subcutaneous WAT. Lipase expression increased within 12 h of in vitro exposure of naïve explants to rosiglitazone, suggesting direct transcriptional activation. In parallel, chronic in vivo treatment with rosiglitazone lowered plasma NEFAs and in WAT its expected stimulatory action on glycerol and NEFA recycling, and on the expression of genes involved in NEFA uptake and retention by WAT, such processes counteracting net NEFA export. CONCLUSIONS/

interpretationThese findings demonstrate that, in the face of its plasma NEFA-lowering action, PPARgamma agonism stimulates WAT lipolysis, an effect that is compensated by lipid-retaining pathways. The results further suggest that PPARgamma agonism stimulates lipolysis by increasing the lipolytic potential, including the expression levels of the genes encoding adipose triglyceride lipase and monoglyceride lipase.

Indexed as

Adipose TissueAnimalsBucladesineEnergy IntakeFatty Acid-Binding ProteinsFatty Acids, NonesterifiedLipaseLipolysisMalePPAR gammaRatsRats, Sprague-DawleyRNARNA, MessengerRosiglitazoneThiazolidinedionesBucladesineFatty Acid-Binding ProteinsFatty Acids, NonesterifiedLipasePPAR gammaRNARNA, MessengerRosiglitazoneThiazolidinediones

Identifiers

PMID16906479
OpenAlexW2057577150

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.