Glucose kinetics and exercise tolerance in mice lacking the GLUT4 glucose transporter

• DOI: 10.1113/jphysiol.2007.132902
• Publication Date: 2007-05-11T01:04:05Z
• Authors: Patrick T. Fueger; Candice Y. Li; Julio E. Ayala; Jane Shearer; Deanna P. Bracy; Maureen J. Charron; Jeffrey N. Rottman; David H. Wasserman
• Keywords: GLUT4; Basal (medicine)

The absence of GLUT4 severely impairs basal glucose uptake in vivo , but does not alter homeostasis or circulating insulin. Glucose isolated contracting skeletal muscle (MGU) is also impaired by the GLUT4, and onset fatigue hastened. Whether body can compensate preserve during exercise, as it state, unknown. One aim was to test effectiveness glucoregulatory compensation for vivo. used further define role hexokinase (HK) II, which catalyses phosphorylation after transported cell. HK II increases MGU well exercise endurance. In expression will affect MGU. A second whether, retains its ability increase Wild‐type (WT), null (GLUT4 −/− ), overexpressing Tg ) mice were studied using a catheterized mouse model that allows blood sampling isotope infusions treadmill exercise. capacity working take up partially offset an exaggerated glucagon: insulin ratio, increased liver production, hyperglycaemia, greater capillary density order delivery exercising . Hearts exhibited compensatory paradoxical uptake. Exercise tolerance reduced compared WT. As expected, same However, overexpression retained conclusion, unlike state where preserved, hyperglycaemia results due robust stimulation release face severe impairments Finally, studies show improves tolerance, independent effects on