Evidence map›Paper›PMID 32413335›Full record

ArticleCell metabolism2020

Positive Reinforcing Mechanisms between GPR120 and PPARγ Modulate Insulin Sensitivity.

Vivian A Paschoal, Evelyn Walenta, Saswata Talukdar, Ariane R Pessentheiner, Olivia Osborn, Nasun Hah, Tyler J Chi, George L Tye, Aaron M Armando, Ronald M Evans and 4 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 66 citations in OpenAlex.

  1. GαNature communications · 2026
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  6. DHA ModulatesInternational journal of molecular sciences · 2025
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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

14 authors at 5 institutions in 1 country.

Vivian A PaschoalTouchstone Diabetes Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Division of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Evelyn WalentaDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Saswata TalukdarDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA; Merck & Co., Inc., SSF, 630 Gateway Boulevard, South San Francisco, CA 94080, USA.
Ariane R PessentheinerDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Olivia OsbornDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Nasun HahGene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Tyler J ChiDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
George L TyeDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA; Case Western Reserve University School of Medicine, 2109 Adelbert Road, Cleveland, OH 44106, USA.
Aaron M ArmandoDepartment of Pharmacology, University of California, San Diego, La Jolla, CA 92093, USA.
Ronald M EvansGene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037, USA; Howard Hughes Medical Institute, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Nai-Wen ChiDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA; VA San Diego Healthcare System, San Diego, CA, USA.
Oswald QuehenbergerDepartment of Pharmacology, University of California, San Diego, La Jolla, CA 92093, USA.
Jerrold M OlefskyDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA. Electronic address: jolefsky@health.ucsd.edu.
Da Young OhTouchstone Diabetes Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Division of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA. Electronic address: dayoung.oh@utsouthwestern.edu.
University of California, San Diego · USHoward Hughes Medical Institute · USMerck & Co., Inc., Rahway, NJ, USA (United States) · USSalk Institute for Biological Studies · USThe University of Texas Southwestern Medical Center · US

Funding

Viral Vector Core (VVC)P30CA014195 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Ye Zheng · 1985 to 2026
$82.8M
Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PETER J TONTONOZ · 2003 to 2026
$40.4M
Project# 4: INTERACTIONS OF ANCHORING PROTEINS WITH THEIR TARGETSP01DK054441 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TAYLOR, SUSAN S. · 1999 to 2017
$27.3M
U of Calif, San Diego Neuroscience Microscopy ImagingP30NS047101 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLEESON, JOSEPH G, ZHENG, BINHAI · 2003 to 2022
$9.0M
Feed-forward regulation between GPR120 and PPAR gamma - Revision - 1R01DK108773 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI OH, DAYOUNG · 2017 to 2021
$2.2M
Howard Hughes Medical InstituteNCI NIH HHS P30 CA014195NIDDK NIH HHS P01 DK054441NIDDK NIH HHS P30 DK063491NIDDK NIH HHS R01 DK108773NINDS NIH HHS P30 NS047101
6 · The paper itself

Abstract

G protein-coupled receptor 120 (GPR120) and PPARγ agonists each have insulin sensitizing effects. But whether these two pathways functionally interact and can be leveraged together to markedly improve insulin resistance has not been explored. Here, we show that treatment with the PPARγ agonist rosiglitazone (Rosi) plus the GPR120 agonist Compound A leads to additive effects to improve glucose tolerance and insulin sensitivity, but at lower doses of Rosi, thus avoiding its known side effects. Mechanistically, we show that GPR120 is a PPARγ target gene in adipocytes, while GPR120 augments PPARγ activity by inducing the endogenous ligand 15d-PGJ2 and by blocking ERK-mediated inhibition of PPARγ. Further, we used macrophage- (MKO) or adipocyte-specific GPR120 KO (AKO) mice to show that GRP120 has anti-inflammatory effects via macrophages while working with PPARγ in adipocytes to increase insulin sensitivity. These results raise the prospect of a safer way to increase insulin sensitization in the clinic.

Indexed as

3T3-L1 CellsAcetatesAdipocytesAnimalsCells, CulturedFemaleInsulinMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicPPAR gammaReceptors, G-Protein-CoupledRosiglitazoneTyramine2-(4-acetoxyphenyl)-2-chloro-N-methylethylamineAcetatesFFAR4 protein, mouseInsulinPPAR gammaReceptors, G-Protein-CoupledRosiglitazoneTyramine15d-PGJ2combination therapyCompound AGPR120insulin resistancePPARγthiazolidinedionetype 2 diabetes

Identifiers

PMID32413335
PMCPMC7337476
OpenAlexW3024758623

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.