Evidence map›Paper›PMID 27089991›Full record

ArticleScientific reports2016

Gpr97 is dispensable for metabolic syndrome but is involved in macrophage inflammation in high-fat diet-induced obesity in mice.

Jueping Shi, Xiaoyu Zhang, Shaoying Wang, Jinjin Wang, Bing Du, Zhugang Wang, Mingyao Liu, Wenzheng Jiang, Min Qian, Hua Ren

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. 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
1.9field-weighted citation impact, top 14% 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, 30 citations in OpenAlex.

  1. Adhesion G protein-coupled receptors.Pharmacological reviews · 2026
    Review
  2. Article
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  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. The Roles of Orphan G Protein-Coupled Receptors in Autoimmune Diseases.Clinical reviews in allergy & immunology · 2021
    Review
  11. Article
  12. Article
  13. Gpr97 Exacerbates AKI by Mediating Sema3A Signaling.Journal of the American Society of Nephrology : JASN · 2018
    Article
  14. Adhesion GPCRs in Kidney Development and Disease.Frontiers in cell and developmental biology · 2018
    Review
  15. The Adhesion G Protein-Coupled Receptor GPR97/Frontiers in immunology · 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

10 authors at 2 institutions in 1 country.

Jueping ShiShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China.
Xiaoyu ZhangShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China.
Shaoying WangShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China.
Jinjin WangShanghai Research Center for Model Organisms, Shanghai, China.
Bing DuShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China.
Zhugang WangShanghai Research Center for Model Organisms, Shanghai, China.
Mingyao LiuShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China.
Wenzheng JiangShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China.
Min QianShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China.
Hua RenShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China.
East China Normal University · CNShanghai Model Organisms (China) · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Local inflammation in tissues is one of primary causes in development of metabolic disorder in obesity. The accumulation of macrophages in some tissues can induce inflammatory reactions in obesity. Gpr97 is highly expressed in some immunocytes, but its potential role in inflammatory regulation has not been revealed clearly. In our research, we investigated Gpr97 in regulating macrophage inflammation and metabolic dysfunction in the high-fat diet (HFD)-induced obese mice. The major metabolic phenotyping were not different after Gpr97 knockout in HFD-fed mice. Similar pathological alterations in adipose tissue, liver, and kidney were observed in Gpr97(-/-) HFD mice compared with WT-HFD mice. In white adipose tissue, loss of Gpr97 reduced the ratio of M1-macrophages and increased the M2-macrophage ratio, which was opposite to that seen in the wild-type HFD mice. More macrophages invaded in the liver and kidney after Gpr97 knockout in HFD mice. Furthermore, the levels of TNF-α were higher in the liver and kidney of Gpr97(-/-) HFD mice compared to those in wild-type HFD mice. The data indicate that Gpr97 might be required for local inflammation development in obesity-relative tissues, but does not play a role in metabolic disorder in HFD-induced obesity.

Indexed as

Adipose Tissue, WhiteAnimalsDiet, High-FatInflammationKidneyLiverMacrophagesMaleMetabolic SyndromeMiceMice, Inbred C57BLObesityReceptors, G-Protein-CoupledTumor Necrosis Factor-alphaAdgrg3 protein, mouseReceptors, G-Protein-CoupledTumor Necrosis Factor-alpha

Identifiers

PMID27089991
PMCPMC4835759
OpenAlexW2339928875

What OpenQuestion holds

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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.