Evidence map›Paper›PMID 32079203›Full record

ArticleBiomolecules2020

Regulation of Adipsin Expression by Endoplasmic Reticulum Stress in Adipocytes.

Ka-Young Ryu, Eon Ju Jeon, Jaechan Leem, Jae-Hyung Park, Hochan Cho

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Investigating the Pathogenesis and Treatment of Type 2 Diabetes from the Perspective of Adipose Tissue.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
    Review
  3. Article
  4. Tetra methyl bisphenol F: another potential obesogen.International journal of obesity (2005) · 2024
    Article
  5. Article
  6. Review
  7. Article
  8. ORMDL in metabolic health and disease.Pharmacology & therapeutics · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. 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

5 authors at 2 institutions in 1 country.

Ka-Young RyuDepartment of Physiology, Keimyung University School of Medicine, Daegu 42601, Korea.
Eon Ju JeonDepartment of Internal Medicine, School of Medicine, Catholic University of Daegu, Daegu 42472, Korea.ORCID 0000-0002-8858-5343
Jaechan LeemDepartment of Immunology, School of Medicine, Catholic University of Daegu, Daegu 42472, Korea.ORCID 0000-0003-2329-4374
Jae-Hyung ParkDepartment of Physiology, Keimyung University School of Medicine, Daegu 42601, Korea.ORCID 0000-0002-3549-5977
Hochan ChoDepartment of Internal Medicine, Keimyung University School of Medicine, Daegu 42601, Korea.
Keimyung University · KRDaegu Catholic University · KR

Funding

Korea Health Industry Development Institute HI14C1324National Research Foundation of Korea NRF-2015R1D1A1A01057395National Research Foundation of Korea NRF-2017R1C1B5076755National Research Foundation of Korea NRF-2017R1D1A1B03035278
6 · The paper itself

Abstract

Adpsin is an adipokine that stimulates insulin secretion from β-cells and improves glucose tolerance. Its expression has been found to be markedly reduced in obese animals. However, it remains unclear what factors lead to downregulation of adipsin in the context of obesity. Endoplasmic reticulum (ER) stress response is activated in various tissues under obesity-related conditions and can induce transcriptional reprogramming. Therefore, we aimed to investigate the relationship between adipsin expression and ER stress in adipose tissues during obesity. We observed that obese mice exhibited decreased levels of adipsin in adipose tissues and serum and increased ER stress markers in adipose tissues compared to lean mice. We also found that ER stress suppressed adipsin expression via adipocytes-intrinsic mechanisms. Moreover, the ER stress-mediated downregulation of adipsin was at least partially attributed to decreased expression of peroxisome proliferator-activated receptor γ (PPARγ), a key transcription factor in the regulation of adipocyte function. Finally, treatment with chemical chaperones recovered the ER stress-mediated downregulation of adipsin and PPARγ in vivo and in vitro. Our findings suggest that activated ER stress in adipose tissues is an important cause of the suppression of adipsin expression in the context of obesity.

Indexed as

Down-RegulationEndoplasmic Reticulum Stress3T3-L1 CellsAdipocytesAdipose TissueAnimalsCells, CulturedComplement Factor DMaleMiceMice, Inbred C57BLObesityPPAR gammaComplement Factor Dcomplement factor D, mousePPAR gammaadipocytesadipsindiabetes mellitusendoplasmic reticulum stressobesity

Identifiers

PMID32079203
PMCPMC7072197
OpenAlexW3005551465

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.