Evidence map›Paper›PMID 28404815›Full record

ArticleThe Journal of biological chemistry2017

The hepatokine FGF21 is crucial for peroxisome proliferator-activated receptor-α agonist-induced amelioration of metabolic disorders in obese mice.

Tsuyoshi Goto, Mariko Hirata, Yumeko Aoki, Mari Iwase, Haruya Takahashi, Minji Kim, Yongjia Li, Huei-Fen Jheng, Wataru Nomura, Nobuyuki Takahashi and 8 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Fenofibrate Protects Against Antipsychotic-Induced Hyperglycemia Through Weight Loss and FGF21 Dependent Mechanisms.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  12. Article
  13. Nutrients · 2023
    Article
  14. Review
  15. Article
  16. Review
  17. Crosstalk between CYP2E1 and PPARActa pharmaceutica Sinica. B · 2022
    Article
  18. Article
  19. Article
  20. Review
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

18 authors at 4 institutions in 2 countries.

Tsuyoshi GotoFrom the Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Uji 611-0011, Japan, tgoto@kais.kyoto-u.ac.jp.
Mariko HirataFrom the Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Uji 611-0011, Japan.
Yumeko AokiFrom the Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Uji 611-0011, Japan.
Mari IwaseFrom the Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Uji 611-0011, Japan.
Haruya TakahashiFrom the Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Uji 611-0011, Japan.
Minji KimFrom the Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Uji 611-0011, Japan.
Yongjia LiFrom the Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Uji 611-0011, Japan.
Huei-Fen JhengFrom the Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Uji 611-0011, Japan.
Wataru NomuraFrom the Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Uji 611-0011, Japan.
Nobuyuki TakahashiFrom the Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Uji 611-0011, Japan.
Chu-Sook KimDepartment of Food Science and Nutrition, University of Ulsan, Ulsan 680-749, South Korea.
Rina YuDepartment of Food Science and Nutrition, University of Ulsan, Ulsan 680-749, South Korea.
Shigeto SenoDepartment of Bioinformatic Engineering, Graduate School of Information Science and Technology, Osaka University, Suita 565-0871, Japan.
Hideo MatsudaDepartment of Bioinformatic Engineering, Graduate School of Information Science and Technology, Osaka University, Suita 565-0871, Japan.
Megumi Aizawa-AbeInstitute for Advancement of Clinical and Translational Science, Kyoto University Hospital, Kyoto 606-8507, Japan, and.
Ken EbiharaInstitute for Advancement of Clinical and Translational Science, Kyoto University Hospital, Kyoto 606-8507, Japan, and.
Nobuyuki ItohDepartment of Genetic Biochemistry, Kyoto University Graduate School of Pharmaceutical Sciences, Kyoto 606-8501, Japan.
Teruo KawadaFrom the Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Uji 611-0011, Japan.
Kyoto University · JPKyoto University Hospital · JPOsaka University · JPUniversity of Ulsan · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity causes excess fat accumulation in white adipose tissues (WAT) and also in other insulin-responsive organs such as the skeletal muscle, increasing the risk for insulin resistance, which can lead to obesity-related metabolic disorders. Peroxisome proliferator-activated receptor-α (PPARα) is a master regulator of fatty acid oxidation whose activator is known to improve hyperlipidemia. However, the molecular mechanisms underlying PPARα activator-mediated reduction in adiposity and improvement of metabolic disorders are largely unknown. In this study we investigated the effects of PPARα agonist (fenofibrate) on glucose metabolism dysfunction in obese mice. Fenofibrate treatment reduced adiposity and attenuated obesity-induced dysfunctions of glucose metabolism in obese mice fed a high-fat diet. However, fenofibrate treatment did not improve glucose metabolism in lipodystrophic A-Zip/F1 mice, suggesting that adipose tissue is important for the fenofibrate-mediated amelioration of glucose metabolism, although skeletal muscle actions could not be completely excluded. Moreover, we investigated the role of the hepatokine fibroblast growth factor 21 (FGF21), which regulates energy metabolism in adipose tissue. In WAT of WT mice, but not of FGF21-deficient mice, fenofibrate enhanced the expression of genes related to brown adipocyte functions, such as

Indexed as

Adipocytes, BrownAdipose TissueAnimalsEnergy MetabolismFenofibrateFibroblast Growth FactorsGlucoseHyperlipidemiasMiceObesityPPAR alphaFenofibratefibroblast growth factor 21Fibroblast Growth FactorsGlucosePPAR alphaadipocytebeige cellsbrowningfibratesfibroblast growth factor (FGF)insulin resistanceobesityperoxisome proliferator-activated receptor (PPAR)UCP1

Identifiers

PMID28404815
PMCPMC5454100
OpenAlexW2606430072

What OpenQuestion holds

Textmetadata
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.