Review
Copyright ©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Biol Chem. Sep 27, 2021; 12(5): 70-86
Published online Sep 27, 2021. doi: 10.4331/wjbc.v12.i5.70
Culprits or consequences: Understanding the metabolic dysregulation of muscle in diabetes
Colleen L O'Reilly, Selina Uranga, James D Fluckey
Colleen L O'Reilly, Selina Uranga, James D Fluckey, Health and Kinesiology, Texas A&M University, TX 77843, United States
Author contributions: O’Reilly CL wrote the majority of the review; Uranga S contributed to the writing, designed and produced the figures; Fluckey JD contributed to the writing and edited the manuscript.
Conflict-of-interest statement: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: James D Fluckey, PhD, Professor, Health and Kinesiology, Texas A&M University, TAMU 4243, College Station, TX 77843, United States. jfluckey@tamu.edu
Received: March 31, 2021
Peer-review started: March 31, 2021
First decision: June 7, 2021
Revised: June 21, 2021
Accepted: August 3, 2021
Article in press: August 3, 2021
Published online: September 27, 2021
Processing time: 174 Days and 9.5 Hours
Core Tip

Core Tip: The prevalence of type 2 diabetes (T2D) continues to rise despite the amount of research dedicated to finding the culprits of this debilitating disease. Within skeletal muscle there is a clear link to metabolic dysregulation during the progression of T2D but the determination of culprits vs consequences of the disease has been elusive. Emerging evidence in skeletal muscle implicates influential cross talk between the mammalian target of rapamycin (mTOR) complexes (mTORC1 and mTORC2) during insulin stimulated glucose uptake. This review highlights interactions between protein and glucose regulatory pathways and the implications this may have for the control of glucoregulatory function in skeletal muscle.