TY - JOUR
T1 - Muscling in on GLUT4 kinetics
AU - Stöckli, Jacqueline
AU - Fazakerley, Daniel J
AU - Coster, Adelle C F
AU - Holman, Geoffrey D
AU - James, David E
N1 - Addendum to: Fazakerley DJ, Holman GD, Marley A, James DE, Stöckli J, Coster AC Kinetic evidence for unique regulation of GLUT4 trafficking by insulin and AMP-activated protein kinase activators in L6 myotubesJ Biol Chem201028516531660 doi: 10.1074/jbc.M109.051185.
PY - 2010
Y1 - 2010
N2 - Insulin triggers glucose uptake into muscle and adipose tissue by stimulating the translocation of the glucose transporter GLUT4 from intracellular vesicles to the plasma membrane (PM). Insulin leads to a rapid increase in GLUT4 at the PM from ~5% to 40-50%. This effect is time and dose-dependent, reaching a new steady state after 30 min of insulin stimulation. Previous kinetic analyses in adipocytes has revealed that this is regulated by two mechanisms – increasing the amount of GLUT4 in the endosomal recycling system and increasing the exocytosis rate constant. Fazakerley et al1 focuses on GLUT4 kinetics in the L6 skeletal muscle cell line. Despite displaying a similar redistribution of GLUT4 to the cell surface with insulin to that seen in adipocytes, the mechanism for this effect in L6 cells was completely different. Insulin had a modest effect to increase the amount of GLUT4 in the recycling system with the dominant effect being on reduction of the endocytosis rate constant. Similar findings were observed with AMPK agonists. These studies indicate that different cell types are capable of achieving the same cell biological endpoint but using completely distinct mechanisms.
AB - Insulin triggers glucose uptake into muscle and adipose tissue by stimulating the translocation of the glucose transporter GLUT4 from intracellular vesicles to the plasma membrane (PM). Insulin leads to a rapid increase in GLUT4 at the PM from ~5% to 40-50%. This effect is time and dose-dependent, reaching a new steady state after 30 min of insulin stimulation. Previous kinetic analyses in adipocytes has revealed that this is regulated by two mechanisms – increasing the amount of GLUT4 in the endosomal recycling system and increasing the exocytosis rate constant. Fazakerley et al1 focuses on GLUT4 kinetics in the L6 skeletal muscle cell line. Despite displaying a similar redistribution of GLUT4 to the cell surface with insulin to that seen in adipocytes, the mechanism for this effect in L6 cells was completely different. Insulin had a modest effect to increase the amount of GLUT4 in the recycling system with the dominant effect being on reduction of the endocytosis rate constant. Similar findings were observed with AMPK agonists. These studies indicate that different cell types are capable of achieving the same cell biological endpoint but using completely distinct mechanisms.
UR - http://www.scopus.com/inward/record.url?scp=80054764437&partnerID=8YFLogxK
UR - http://www.landesbioscience.com/journals/cib/article/11457
UR - http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2918772
UR - http://dx.doi.org/10.4161/cib.3.3.11457
U2 - 10.4161/cib.3.3.11457
DO - 10.4161/cib.3.3.11457
M3 - Article
SN - 1942-0889
VL - 3
SP - 260
EP - 262
JO - Communicative & Integrative Biology
JF - Communicative & Integrative Biology
IS - 3
ER -