Evidence map›Paper›PMID 28990936›Full record

ArticleThe Journal of clinical investigation2017

Olfactory receptor 544 reduces adiposity by steering fuel preference toward fats.

Chunyan Wu, Su Hyeon Hwang, Yaoyao Jia, Joobong Choi, Yeon-Ji Kim, Dahee Choi, Duleepa Pathiraja, In-Geol Choi, Seung-Hoi Koo, Sung-Joon Lee

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Olfactory receptors and human diseases.Cell and tissue research · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. MOR23 deficiency exacerbates hepatic steatosis in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  18. NAD activates olfactory receptor 1386 to regulate type I interferon responses inProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  19. Article
  20. Review

2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Chunyan WuDepartment of Biotechnology and.
Su Hyeon HwangDepartment of Biotechnology and.
Yaoyao JiaDepartment of Biotechnology and.
Joobong ChoiDepartment of Biotechnology and.
Yeon-Ji KimDepartment of Biotechnology and.
Dahee ChoiDivision of Life Sciences, School of Life Sciences and Biotechnology for BK21 PLUS, Korea University, Seoul, Republic of Korea.
Duleepa PathirajaDepartment of Biotechnology and.
In-Geol ChoiDepartment of Biotechnology and.
Seung-Hoi KooDivision of Life Sciences, School of Life Sciences and Biotechnology for BK21 PLUS, Korea University, Seoul, Republic of Korea.
Sung-Joon LeeDepartment of Biotechnology and.
Korea University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Olfactory receptors (ORs) are present in tissues outside the olfactory system; however, the function of these receptors remains relatively unknown. Here, we determined that olfactory receptor 544 (Olfr544) is highly expressed in the liver and adipose tissue of mice and regulates cellular energy metabolism and obesity. Azelaic acid (AzA), an Olfr544 ligand, specifically induced PKA-dependent lipolysis in adipocytes and promoted fatty acid oxidation (FAO) and ketogenesis in liver, thus shifting the fuel preference to fats. After 6 weeks of administration, mice fed a high-fat diet (HFD) exhibited a marked reduction in adiposity. AzA treatment induced expression of PPAR-α and genes required for FAO in the liver and induced the expression of PPAR-γ coactivator 1-α (Ppargc1a) and uncoupling protein-1 (Ucp1) genes in brown adipose tissue (BAT). Moreover, treatment with AzA increased insulin sensitivity and ketone body levels. This led to a reduction in the respiratory quotient and an increase in the FAO rate, as indicated by indirect calorimetry. AzA treatment had similar antiobesogenic effects in HFD-fed ob/ob mice. Importantly, AzA-associated metabolic changes were completely abrogated in HFD-fed Olfr544-/- mice. To our knowledge, this is the first report to show that Olfr544 orchestrates the metabolic interplay between the liver and adipose tissue, mobilizing stored fats from adipose tissue and shifting the fuel preference to fats in the liver and BAT.

Indexed as

AdiposityLipolysis3T3-L1 CellsAdipose Tissue, BrownAnimalsCyclic AMP-Dependent Protein KinasesDiet, High-FatEnergy MetabolismGlucose IntoleranceInsulin ResistanceLiverMiceMice, Inbred C57BLMice, KnockoutObesityPPAR alphaCyclic AMP-Dependent Protein KinasesOr55b4 protein, mousePPAR alphaReceptors, Odorant

Identifiers

PMID28990936
PMCPMC5663348
OpenAlexW2761680756

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.