Evidence map›Paper›PMID 27504979›Full record

ArticlePloS one2016

Glucagon Like Peptide-1 Promotes Adipocyte Differentiation via the Wnt4 Mediated Sequestering of Beta-Catenin.

Rui Liu, Na Li, Yi Lin, Mei Wang, Yongde Peng, Keidren Lewi, Qinghua Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Signaling pathways in obesity: mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2022
    Review
  8. Article
  9. Article
  10. Site-Dependent Lineage Preference of Adipose Stem Cells.Frontiers in cell and developmental biology · 2020
    Article
  11. Article
  12. Article
  13. 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

7 authors at 4 institutions in 2 countries.

Rui LiuDepartment of Endocrinology, Huashan Hospital, Fudan University, Shanghai 200040, China.
Na LiDepartment of Endocrinology, Shanghai First People's Hospital, Shanghai Jiao TongUniversity, Shanghai 200080, China.
Yi LinDepartment of Endocrinology, Shanghai First People's Hospital, Shanghai Jiao TongUniversity, Shanghai 200080, China.
Mei WangDepartment of Endocrinology, Shanghai First People's Hospital, Shanghai Jiao TongUniversity, Shanghai 200080, China.
Yongde PengDepartment of Endocrinology, Shanghai First People's Hospital, Shanghai Jiao TongUniversity, Shanghai 200080, China.
Keidren LewiDivision of Endocrinology and Metabolism, Keenan Research Centre for Biomedical Science of St. Michael's Hospital, Departments of Physiology and Medicine, University of Toronto, Toronto, M5B 1W8, Canada.
Qinghua WangDepartment of Endocrinology, Huashan Hospital, Fudan University, Shanghai 200040, China.
Shanghai Jiao Tong University · CNFudan University · CNHuashan Hospital · CNUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucagon-like peptide-1 (GLP-1) plays a role in the regulation of adipogenesis; however, the precise underlying molecular mechanism has not been fully defined. Wnt was recently identified as an important regulator of adipogenesis. This study aimed to investigate the involvement of the Wnt signaling pathway in the effects of GLP-1 on adipocyte differentiation. 3T3-L1 cells were induced to differentiate. The changes in the expression levels of adipogenic transcription factors and Wnts and the phosphorylation level and subcellular localization of β-catenin were quantified after GLP-1 treatment. GLP-1 stimulated adipocyte differentiation and lipid accumulation, which were accompanied by the expression of adipocyte marker genes. The expression of Wnt4 was upregulated in the process of adipocyte differentiation, which was further enhanced by treatment with GLP-1. β-catenin, an important mediator of the Wnt pathway, was immediately dephosphorylated and translocated from cytoplasm to nucleus when differentiation was induced. In the presence of GLP-1, however, β-catenin was redirected to the cell plasma membrane leading to its decreased accumulation in the nucleus. Knockdown of Wnt4 blocked the effect of GLP-1 on the cellular localization of β-catenin and expression level of adipogenic transcription factors. Our findings showed that GLP-1 promoted adipogenesis through the modulation of the Wnt4/β-catenin signaling pathway, suggesting that the GLP-1-Wntβ-catenin system might be a new target for the treatment of metabolic disease.

Indexed as

3T3-L1 CellsAdipocytesAnimalsbeta CateninCell DifferentiationCell MembraneCell ProliferationGene Expression RegulationGlucagon-Like Peptide 1MiceProtein TransportWnt4 ProteinWnt Signaling Pathwaybeta CateninGlucagon-Like Peptide 1Wnt4 Protein

Identifiers

PMID27504979
PMCPMC4978386
OpenAlexW2498576294

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.