Wang TN, Hu XG, Chen GX. Uses of knockout, knockdown, and transgenic models in the studies of glucose transporter 4. World J Meta-Anal 2022; 10(1): 1-11 [DOI: 10.13105/wjma.v10.i1.1]
Corresponding Author of This Article
Guo-Xun Chen, PhD, Associate Professor, Research Scientist, Department of Nutrition, The University of Tennessee, Room 229, Jessie Harris Building 1215 West Cumberland Avenue, Knoxville, TN 37996, United States. gchen6@utk.edu
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Minireviews
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 Meta-Anal. Feb 28, 2022; 10(1): 1-11 Published online Feb 28, 2022. doi: 10.13105/wjma.v10.i1.1
Uses of knockout, knockdown, and transgenic models in the studies of glucose transporter 4
Tian-Nan Wang, Xin-Ge Hu, Guo-Xun Chen
Tian-Nan Wang, Xin-Ge Hu, Guo-Xun Chen, Department of Nutrition, The University of Tennessee, Knoxville, TN 37996, United States
Author contributions: Chen GX was responsible for the design of the topics; Wang TN and Hu XG were responsible for PubMed search and information collection; Wang TN, Hu XG and Chen GX were responsible for writing.
Conflict-of-interest statement: All authors confirmed that there is no conflict-of-interest to be reported.
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: Guo-Xun Chen, PhD, Associate Professor, Research Scientist, Department of Nutrition, The University of Tennessee, Room 229, Jessie Harris Building 1215 West Cumberland Avenue, Knoxville, TN 37996, United States. gchen6@utk.edu
Received: November 21, 2021 Peer-review started: November 21, 2021 First decision: December 10, 2021 Revised: December 10, 2021 Accepted: February 23, 2022 Article in press: February 23, 2022 Published online: February 28, 2022 Processing time: 99 Days and 7.6 Hours
Core Tip
Core Tip: The whole body glucose transporter 4 (GLUT4)-null mice have growth retardation, but normal glucose tolerance and basal glucose turnover rates. The muscle-specific GLUT4 knockout mice have normal body weight and fat pad weight at least before 6 mo of age, whereas the adipose-GLUT4 knockout mice have glucose intolerance. The adipose and muscle GLUT4 double knockout mice develop hyperglycemia in the fasting state, suggesting the role of GLUT4 in fasting state. Compared to the control mice, wholebody GLUT4 transgenic mice have similar growth rate before 10 wk of age, lower blood glucose in the fasting, and lower insulin level in the fed state. The adipose tissue specific GLUT4 overexpression increases body weight, glucose transport rate and adipose tissue weight. Data from both transgenic overexpression and tissue specific knockout of GLUT4 indicate that GLUT4 probably plays a role in the glucose uptake in the fasting state.
