Journal
APPLIED PHYSIOLOGY NUTRITION AND METABOLISM-PHYSIOLOGIE APPLIQUEE NUTRITION ET METABOLISME
Volume 34, Issue 3, Pages 481-487Publisher
NATL RESEARCH COUNCIL CANADA-N R C RESEARCH PRESS
DOI: 10.1139/H09-047
Keywords
GLUT4; glucose uptake; muscle; exocytosis; endocytosis; intrinsic activity
Categories
Ask authors/readers for more resources
Glucose uptake into skeletal muscle is primarily mediated by glucose transporter 4 (GLUT4). The number of GLUT4 polypeptides at the surface of muscle cells rises rapidly in response to insulin, contraction, depolarization, or energy deprivation. However, distinct mechanisms underlie the gain in surface GLUT4 in each case. Insulin promotes its exocytosis to the membrane, regulating vesicle movement, tethering, docking, and fusion. In contrast, muscle contraction, depolarization, and energy demand reduce GLUT4 endocytosis. The signals involved in each case also differ. Insulin utilizes Akt, Rabs, and selective actin remodelling, whereas depolarization and energy deprivation engage AMP-activated protein kinase and Ca(2+)-dependent signals. GLUT4 internalizes via 2 major routes that involve dynamin, but only one requires clathrin. The clathrin-independent route is slowed down by energy deprivation, and is regulated by AMP-activated protein kinase. In addition to regulation of the exocytic and endocytic movement of GLUT4, glucose uptake is also modulated through changes in the transporter's intrinsic activity. The glycolytic enzymes glyceraldehyde-3-dehydrogenase and hexokinase II contribute to such regulation, through differential binding to GLUT4.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available