Published online Feb 28, 2022. doi: 10.13105/wjma.v10.i1.1
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: 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.
