Evidence map›Paper›PMID 23155420›Full record

ArticlePloS one2012

Cross regulation of sirtuin 1, AMPK, and PPARγ in conjugated linoleic acid treated adipocytes.

Shan Jiang, Wei Wang, Jess Miner, Michael Fromm

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.2field-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

22 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Pharmacological Approaches to Decelerate Aging: A Promising Path.Oxidative medicine and cellular longevity · 2022
    Review
  6. Review
  7. Critical Role for AMPK in Metabolic Disease-Induced Chronic Kidney Disease.International journal of molecular sciences · 2020
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Self-regulation of the inflammatory response by peroxisome proliferator-activated receptors.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Review
  13. Article
  14. Sirt7 promotes adipogenesis in the mouse by inhibiting autocatalytic activation of Sirt1.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

4 authors at 2 institutions in 1 country.

Shan JiangDepartment of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America.
Wei Wang
Jess Miner
Michael Fromm
University of Nebraska–Lincoln · USThe University of Texas Southwestern Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Trans-10, cis-12 conjugated linoleic acid (t10c12 CLA) reduces triglyceride (TG) levels in adipocytes through multiple pathways, with AMP-activated protein kinase (AMPK) generally facilitating, and peroxisome proliferator-activated receptor γ (PPARγ) generally opposing these reductions. Sirtuin 1 (SIRT1), a histone/protein deacetylase that affects energy homeostasis, often functions coordinately with AMPK, and is capable of binding to PPARγ, thereby inhibiting its activity. This study investigated the role of SIRT1 in the response of 3T3-L1 adipocytes to t10c12 CLA by testing the following hypotheses: 1) SIRT1 is functionally required for robust TG reduction; and 2) SIRT1, AMPK, and PPARγ cross regulate each other. These experiments were performed by using activators, inhibitors, or siRNA knockdowns that affected these pathways in t10c12 CLA-treated 3T3-L1 adipocytes. Inhibition of SIRT1 amounts or activity using siRNA, sirtinol, nicotinamide, or etomoxir attenuated the amount of TG loss, while SIRT1 activator SRT1720 increased the TG loss. SRT1720 increased AMPK activity while sirtuin-specific inhibitors decreased AMPK activity. Reciprocally, an AMPK inhibitor reduced SIRT1 activity. Treatment with t10c12 CLA increased PPARγ phosphorylation in an AMPK-dependent manner and increased the amount of PPARγ bound to SIRT1. Reciprocally, a PPARγ agonist attenuated AMPK and SIRT1 activity levels. These results indicated SIRT1 increased TG loss and that cross regulation between SIRT1, AMPK, and PPARγ occurred in 3T3-L1 adipocytes treated with t10c12 CLA.

Indexed as

3T3-L1 CellsAdenylate KinaseAdipocytesAnimalsChemokine CCL2Cyclooxygenase 2Fatty AcidsLinoleic Acids, ConjugatedMiceNF-kappa BPPAR gammaSirtuin 1Adenylate KinaseCcl2 protein, mouseChemokine CCL2Cyclooxygenase 2Fatty AcidsLinoleic Acids, ConjugatedNF-kappa BPPAR gammaSirtuin 1

Identifiers

PMID23155420
PMCPMC3498327
OpenAlexW2157873672

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.