Luo W, Zhou Y, Wang LY, Ai L. Interactions between myoblasts and macrophages under high glucose milieus result in inflammatory response and impaired insulin sensitivity. World J Diabetes 2024; 15(7): 1589-1602 [PMID: 39099815 DOI: 10.4239/wjd.v15.i7.1589]
Corresponding Author of This Article
Lei Ai, PhD, Associate Research Scientist, Department of Sports Physiology Research, Jiangsu Research Institute of Sports Science, No. 169 Xianlin Avenue, Nanjing 210033, Jiangsu Province, China. ailei_982@163.com
Research Domain of This Article
Cell Biology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Diabetes. Jul 15, 2024; 15(7): 1589-1602 Published online Jul 15, 2024. doi: 10.4239/wjd.v15.i7.1589
Interactions between myoblasts and macrophages under high glucose milieus result in inflammatory response and impaired insulin sensitivity
Wei Luo, Yue Zhou, Li-Ying Wang, Lei Ai
Wei Luo, Department of Sports and Health Sciences, Nanjing Sport Institute, Nanjing 210014, Jiangsu Province, China
Yue Zhou, Li-Ying Wang, Department of Exercise Physiology, Beijing Sport University, Beijing 100084, China
Lei Ai, Department of Sports Physiology Research, Jiangsu Research Institute of Sports Science, Nanjing 210033, Jiangsu Province, China
Author contributions: Ai L, Luo W and Zhou Y designed the research study; Luo W, Zhou Y, Wang LY and Ai L performed the research; Luo W, Ai L and Wang LY analyzed the data and wrote the manuscript; All authors have read and approve the final manuscript.
Supported byNational Natural Science Foundation of China, No. 32200944; “Qing Lan” Project of Jiangsu Province; and the Jiangsu Research Institute of Sports Science Foundation, No. BM-2023-03.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee of Nanjing Sport Institute (Protocol No. GZRDW-2022-02).
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: The data are available on reasonable request at ailei_982@163.com.
ARRIVE guidelines statement: The authors have read the ARRIVE Guidelines, and the manuscript was prepared and revised according to the ARRIVE Guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Lei Ai, PhD, Associate Research Scientist, Department of Sports Physiology Research, Jiangsu Research Institute of Sports Science, No. 169 Xianlin Avenue, Nanjing 210033, Jiangsu Province, China. ailei_982@163.com
Received: February 22, 2024 Revised: April 28, 2024 Accepted: May 20, 2024 Published online: July 15, 2024 Processing time: 136 Days and 18.6 Hours
Core Tip
Core Tip: This study demonstrated interactions between myoblasts and macrophages under high glucose (HG) milieus induced pro-inflammatory M1 polarization of macrophages to exacerbate inflammatory response. Subsequently, chronic inflammation induced by HG-related M1 macrophages damaged myogenesis and insulin sensitivity in myoblasts. Ultimately, interactions between myoblasts and macrophages resulted in skeletal muscle insulin resistance (IR), which supported macrophage may serve as a promising therapeutic target for skeletal muscle atrophy and IR. This is the first research about the mediation of macrophages to HG-related myogenic inhibition and IR in myoblasts, which provide new insights into the prevention and treatment of skeletal muscle atrophy and IR.
