Evidence map›Paper›PMID 32647011›Full record

ArticleThe Journal of biological chemistry2020

The key royal jelly component 10-hydroxy-2-decenoic acid protects against bone loss by inhibiting NF-κB signaling downstream of FFAR4.

Yosuke Tsuchiya, Mikihito Hayashi, Katashi Nagamatsu, Takehito Ono, Masaki Kamakura, Takanori Iwata, Tomoki Nakashima

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

Article in The Journal of biological chemistry, 2020. 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
2.1field-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, 37 citations in OpenAlex.

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  8. Royal Jelly: Biological Action and Health Benefits.International journal of molecular sciences · 2024
    Review
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  11. Article
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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

7 authors at 2 institutions in 1 country.

Yosuke TsuchiyaDepartment of Cell Signaling, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan; Department of Periodontology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Mikihito HayashiDepartment of Cell Signaling, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan; Japan Agency for Medical Research and Development, Precursory Research for Innovative Medical Care (PRIME), Tokyo, Japan.
Katashi NagamatsuR&D Division, MORIKAWA KENKODO CO., LTD., Kumamoto, Japan.
Takehito OnoDepartment of Cell Signaling, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan; Japan Agency for Medical Research and Development, Core Research for Evolutional Science and Technology (AMED-CREST), Tokyo, Japan.
Masaki KamakuraDepartment of Biotechnology, Faculty of Engineering, Toyama Prefectural University, Toyama, Japan.
Takanori IwataDepartment of Periodontology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Tomoki NakashimaDepartment of Cell Signaling, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan; Japan Agency for Medical Research and Development, Core Research for Evolutional Science and Technology (AMED-CREST), Tokyo, Japan. Electronic address: naka.csi@tmd.ac.jp.
Tokyo Medical and Dental University · JPToyama Prefectural University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The supplementation of royal jelly (RJ) is known to provide a variety of health benefits, including anti-inflammatory and anti-obesity effects. RJ treatment also reportedly protects against bone loss, but no single factor in RJ has yet been identified as an anti-osteoporosis agent. Here we fractionated RJ and identified 10-hydroxy-2-decenoic acid (10H2DA) as a key component involved in inhibiting osteoclastogenesis based on mass spectrometric analysis. We further demonstrated free fatty acid receptor 4 (FFAR4) as directly interacting with 10H2DA; binding of 10H2DA to FFAR4 on osteoclasts inhibited receptor activator of nuclear factor-κB (NF-κB) ligand (RANKL)-induced activation of NF-κB signaling, thereby attenuating the induction of nuclear factor of activated T cells (NFAT) c1, a key transcription factor for osteoclastogenesis. Oral administration of 10H2DA attenuated bone resorption in ovariectomized mice. These results suggest a potential therapeutic approach of targeting osteoclast differentiation by the supplementation of RJ, and specifically 10H2DA, in cases of pathological bone loss such as occur in postmenopausal osteoporosis.

Indexed as

AnimalsCell DifferentiationDisease Models, AnimalFatty AcidsFatty Acids, MonounsaturatedFemaleMiceNFATC Transcription FactorsNF-kappa BOsteoclastsOsteoporosisRANK LigandReceptors, G-Protein-CoupledRoyal JellySignal Transduction10-hydroxy-2-decenoic acidFatty AcidsFatty Acids, MonounsaturatedFFAR4 protein, mouseNfatc1 protein, mouseNFATC Transcription FactorsNF-kappa BRANK LigandReceptors, G-Protein-CoupledRoyal JellyTnfsf11 protein, mouse10-hydroxy-2-decenoic acidbonefatty acidfree fatty acid receptor 4 (FFAR4)NF-κB (NF-κB)osteoclastosteoporosisroyal jelly

Identifiers

PMID32647011
PMCPMC7443481
OpenAlexW3041581889

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.