Evidence map›Paper›PMID 28723961›Full record

ArticlePloS one2017

Dysfunctional GPR40/FFAR1 signaling exacerbates pain behavior in mice.

Kazuo Nakamoto, Fuka Aizawa, Kei Miyagi, Takuya Yamashita, Mitsumasa Mankura, Yutaka Koyama, Fumiyo Kasuya, Akira Hirasawa, Takashi Kurihara, Atsuro Miyata and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  8. Article
  9. Pharmacology of Free Fatty Acid Receptors and Their Allosteric Modulators.International journal of molecular sciences · 2021
    Review
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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

11 authors at 5 institutions in 1 country.

Kazuo NakamotoDepartment of Clinical Pharmacy, School of Pharmaceutical Sciences, Kobe Gakuin University, Chuo-ku, Kobe, Japan.
Fuka AizawaDepartment of Clinical Pharmacy, School of Pharmaceutical Sciences, Kobe Gakuin University, Chuo-ku, Kobe, Japan.
Kei MiyagiDepartment of Clinical Pharmacy, School of Pharmaceutical Sciences, Kobe Gakuin University, Chuo-ku, Kobe, Japan.
Takuya YamashitaBiochemical Toxicology Laboratory, Faculty of Pharmaceutical Sciences, Kobe Gakuin University, Chuo-ku, Kobe, Japan.
Mitsumasa MankuraFaculty of Food Culture, Kurashiki Sakuyo University, Kurashiki, Okayama, Japan.
Yutaka KoyamaLaboratory of Pharmacology, Faculty of Pharmacy, Osaka Ohtani University, Tondabayashi, Osaka, Japan.
Fumiyo KasuyaBiochemical Toxicology Laboratory, Faculty of Pharmaceutical Sciences, Kobe Gakuin University, Chuo-ku, Kobe, Japan.
Akira HirasawaDepartment of Genomic Drug Discovery Science, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan.
Takashi KuriharaDepartment of Pharmacology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Atsuro MiyataDepartment of Pharmacology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Shogo TokuyamaDepartment of Clinical Pharmacy, School of Pharmaceutical Sciences, Kobe Gakuin University, Chuo-ku, Kobe, Japan.
Kobe Gakuin University · JPKagoshima University · JPKurashiki Sakuyo University · JPKyoto Pharmaceutical University · JPOsaka Ohtani University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously showed that activation of G protein-coupled receptor 40/free fatty acid receptor 1 (GPR40/FFAR1) signaling modulates descending inhibition of pain. In this study, we investigated the involvement of fatty acid-GPR40/FFAR1 signaling in the transition from acute to chronic pain. We used GPR40/FFAR1-knockout (GPR40KO) mice and wild-type (WT) mice. A plantar incision was performed, and mechanical allodynia and thermal hyperalgesia were evaluated with a von Frey filament test and plantar test, respectively. Immunohistochemistry was used to localize GPR40/FFAR1, and the levels of free fatty acids in the hypothalamus were analyzed with liquid chromatography-tandem mass spectrometry. The repeated administration of GW1100, a GPR40/FFAR1 antagonist, exacerbated the incision-induced mechanical allodynia and significantly increased the levels of phosphorylated extracellular signal-regulated kinase in the spinal cord after low-threshold touch stimulation in the mice compared to vehicle-treated mice. The levels of long-chain free fatty acids, such as docosahexaenoic acid, oleic acid, and palmitate, which are GPR40/FFAR1 agonists, were significantly increased in the hypothalamus two days after the surgery compared to levels in the sham group. Furthermore, the incision-induced mechanical allodynia was exacerbated in the GPR40KO mice compared to the WT mice, while the response in the plantar test was not changed. These findings suggested that dysfunction of the GPR40/FFAR1 signaling pathway altered the endogenous pain control system and that this dysfunction might be associated with the development of chronic pain.

Indexed as

AnimalsBehavior, AnimalBenzoatesDocosahexaenoic AcidsHyperalgesiaHypothalamusMiceMice, KnockoutOleic AcidPain MeasurementPalmitic AcidPhosphorylationPyrimidinesReceptors, G-Protein-CoupledSignal TransductionBenzoatesDocosahexaenoic AcidsFfar1 protein, mouseGW1100Oleic AcidPalmitic AcidPyrimidinesReceptors, G-Protein-Coupled

Identifiers

PMID28723961
PMCPMC5516985
OpenAlexW2739246125

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LicenceCC BY
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Registered trials

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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.