Evidence map›Paper›PMID 35899030›Full record

ReviewFrontiers in physiology2022

The Effects of Asprosin on Exercise-Intervention in Metabolic Diseases.

Lifei Liu, Yuhao Liu, Mei Huang, Miao Zhang, Chenyu Zhu, Xi Chen, Samuel Bennett, Jiake Xu, Jun Zou

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Adipokine in Metabolic Liver Disease: Adipo-Brain-Liver Cross talk.International journal of endocrinology · 2026
    Review
  6. Article
  7. Article
  8. Article
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  11. Bone-muscle crosstalk under physiological and pathological conditions.Cellular and molecular life sciences : CMLS · 2024
    Review
  12. Review
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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

9 authors at 5 institutions in 2 countries.

Lifei LiuSchool of Kinesiology, Shanghai University of Sport, Shanghai, China.
Yuhao LiuDepartment of Orthopaedic, The First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, China.
Mei HuangSchool of Kinesiology, Shanghai University of Sport, Shanghai, China.
Miao ZhangSchool of Kinesiology, Shanghai University of Sport, Shanghai, China.
Chenyu ZhuSchool of Kinesiology, Shanghai University of Sport, Shanghai, China.
Xi ChenSchool of Sports Science, Wenzhou Medical University, Wenzhou, China.
Samuel BennettSchool of Biomedical Sciences, University of Western Australia, Perth, WA, Australia.
Jiake XuSchool of Biomedical Sciences, University of Western Australia, Perth, WA, Australia.
Jun ZouSchool of Kinesiology, Shanghai University of Sport, Shanghai, China.
Shanghai University of Sport · CNUniversity of Western Australia · AUFirst Affiliated Hospital of Guangzhou University of Chinese Medicine · CNLiaoning Provincial People's Hospital · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrillin is the major constituent of extracellular microfibrils, which are distributed throughout connective tissues. Asprosin is derived from the C-terminal region of the FBN1 gene, which encodes profibrillin that undergoes cleavage by furin protein. In response to fasting with low dietary glucose, asprosin is released as a secreted factor from white adipose tissue, and is transported to the liver for the mediation of glucose release into the blood circulation. Through binding to OLFR734, an olfactory G-protein-coupled receptor in liver cells, asprosin induces a glucogenic effect to regulate glucose homeostasis. Bioinformatics analyses revealed that the FBN1 gene is abundantly expressed in human skeletal muscle-derived mesoangioblasts, osteoblast-like cells, and mesenchymal stem cells, indicating that the musculoskeletal system might play a role in the regulation of asprosin expression. Interestingly, recent studies suggest that asprosin is regulated by exercise. This timely review discusses the role of asprosin in metabolism, its receptor signalling, as well as the exercise regulation of asprosin. Collectively, asprosin may have a vital regulatory effect on the improvement of metabolic disorders such as diabetes mellitus and obesity via exercise.

Indexed as

asprosinexercisemetabolism diseaseobesitypcosT2DM

Identifiers

PMID35899030
PMCPMC9311488
OpenAlexW4285008190

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.