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The Effects of Asprosin on Exercise-Intervention in Metabolic Diseases
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...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9311488/ https://www.ncbi.nlm.nih.gov/pubmed/35899030 http://dx.doi.org/10.3389/fphys.2022.907358 |
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author | Liu, Lifei Liu, Yuhao Huang, Mei Zhang, Miao Zhu, Chenyu Chen, Xi Bennett, Samuel Xu, Jiake Zou, Jun |
author_facet | Liu, Lifei Liu, Yuhao Huang, Mei Zhang, Miao Zhu, Chenyu Chen, Xi Bennett, Samuel Xu, Jiake Zou, Jun |
author_sort | Liu, Lifei |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-9311488 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-93114882022-07-26 The Effects of Asprosin on Exercise-Intervention in Metabolic Diseases Liu, Lifei Liu, Yuhao Huang, Mei Zhang, Miao Zhu, Chenyu Chen, Xi Bennett, Samuel Xu, Jiake Zou, Jun Front Physiol Physiology 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. Frontiers Media S.A. 2022-07-11 /pmc/articles/PMC9311488/ /pubmed/35899030 http://dx.doi.org/10.3389/fphys.2022.907358 Text en Copyright © 2022 Liu, Liu, Huang, Zhang, Zhu, Chen, Bennett, Xu and Zou. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Physiology Liu, Lifei Liu, Yuhao Huang, Mei Zhang, Miao Zhu, Chenyu Chen, Xi Bennett, Samuel Xu, Jiake Zou, Jun The Effects of Asprosin on Exercise-Intervention in Metabolic Diseases |
title | The Effects of Asprosin on Exercise-Intervention in Metabolic Diseases |
title_full | The Effects of Asprosin on Exercise-Intervention in Metabolic Diseases |
title_fullStr | The Effects of Asprosin on Exercise-Intervention in Metabolic Diseases |
title_full_unstemmed | The Effects of Asprosin on Exercise-Intervention in Metabolic Diseases |
title_short | The Effects of Asprosin on Exercise-Intervention in Metabolic Diseases |
title_sort | effects of asprosin on exercise-intervention in metabolic diseases |
topic | Physiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9311488/ https://www.ncbi.nlm.nih.gov/pubmed/35899030 http://dx.doi.org/10.3389/fphys.2022.907358 |
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