Glucose restriction enhances oxidative fiber formation: A multi-omic signal network involving AMPK and CaMK2

Bibliographic Details
Title: Glucose restriction enhances oxidative fiber formation: A multi-omic signal network involving AMPK and CaMK2
Authors: Kaiyi Zhang, Ning Xie, Huaqiong Ye, Jiakun Miao, Boce Xia, Yu Yang, Huanqi Peng, Shuang Xu, Tianwen Wu, Cong Tao, Jinxue Ruan, Yanfang Wang, Shulin Yang
Source: iScience, Vol 27, Iss 1, Pp 108590- (2024)
Publisher Information: Elsevier, 2024.
Publication Year: 2024
Collection: LCC:Science
Subject Terms: Comp, Metabolomics, Omics, Genomics, Proteomics, Science
More Details: Summary: Skeletal muscle is a highly plastic organ that adapts to different metabolic states or functional demands. This study explored the impact of permanent glucose restriction (GR) on skeletal muscle composition and metabolism. Using Glut4m mice with defective glucose transporter 4, we conducted multi-omics analyses at different ages and after low-intensity treadmill training. The oxidative fibers were significantly increased in Glut4m muscles. Mechanistically, GR activated AMPK pathway, promoting mitochondrial function and beneficial myokine expression, and facilitated slow fiber formation via CaMK2 pathway. Phosphorylation-activated Perm1 may synergize AMPK and CaMK2 signaling. Besides, MAPK and CDK kinases were also implicated in skeletal muscle protein phosphorylation during GR response. This study provides a comprehensive signaling network demonstrating how GR influences muscle fiber types and metabolic patterns. These insights offer valuable data for understanding oxidative fiber formation mechanisms and identifying clinical targets for metabolic diseases.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2589-0042
Relation: http://www.sciencedirect.com/science/article/pii/S2589004223026676; https://doaj.org/toc/2589-0042
DOI: 10.1016/j.isci.2023.108590
Access URL: https://doaj.org/article/41701b2e26f24b90b443040f37adc36b
Accession Number: edsdoj.41701b2e26f24b90b443040f37adc36b
Database: Directory of Open Access Journals
More Details
ISSN:25890042
DOI:10.1016/j.isci.2023.108590
Published in:iScience
Language:English