Muscling in on GLUT4 kinetics

Jacqueline Stöckli, Daniel J Fazakerley, Adelle C F Coster, Geoffrey D Holman, David E James

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

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.
Original languageEnglish
Pages (from-to)260-262
Number of pages3
JournalCommunicative & Integrative Biology
Volume3
Issue number3
DOIs
Publication statusPublished - 2010

Fingerprint

insulin
Insulin
kinetics
adipocytes
Adipocytes
recycling
plasma membrane
Cell Membrane
cells
glucose transporters
AMP-Activated Protein Kinases
Facilitative Glucose Transport Proteins
exocytosis
Exocytosis
Recycling
endocytosis
Endocytosis
endpoints
muscle tissues
myocytes

Cite this

Stöckli, J., Fazakerley, D. J., Coster, A. C. F., Holman, G. D., & James, D. E. (2010). Muscling in on GLUT4 kinetics. Communicative & Integrative Biology, 3(3), 260-262. https://doi.org/10.4161/cib.3.3.11457

Muscling in on GLUT4 kinetics. / Stöckli, Jacqueline; Fazakerley, Daniel J; Coster, Adelle C F; Holman, Geoffrey D; James, David E.

In: Communicative & Integrative Biology, Vol. 3, No. 3, 2010, p. 260-262.

Research output: Contribution to journalArticle

Stöckli, J, Fazakerley, DJ, Coster, ACF, Holman, GD & James, DE 2010, 'Muscling in on GLUT4 kinetics', Communicative & Integrative Biology, vol. 3, no. 3, pp. 260-262. https://doi.org/10.4161/cib.3.3.11457
Stöckli, Jacqueline ; Fazakerley, Daniel J ; Coster, Adelle C F ; Holman, Geoffrey D ; James, David E. / Muscling in on GLUT4 kinetics. In: Communicative & Integrative Biology. 2010 ; Vol. 3, No. 3. pp. 260-262.
@article{9293513ea769457fac56a08d7b6ced53,
title = "Muscling in on GLUT4 kinetics",
abstract = "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.",
author = "Jacqueline St{\"o}ckli and Fazakerley, {Daniel J} and Coster, {Adelle C F} and Holman, {Geoffrey D} and James, {David E}",
note = "Addendum to: Fazakerley DJ, Holman GD, Marley A, James DE, St{\"o}ckli 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.",
year = "2010",
doi = "10.4161/cib.3.3.11457",
language = "English",
volume = "3",
pages = "260--262",
journal = "Communicative & Integrative Biology",
issn = "1942-0889",
publisher = "Landes Bioscience",
number = "3",

}

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

VL - 3

SP - 260

EP - 262

JO - Communicative & Integrative Biology

JF - Communicative & Integrative Biology

SN - 1942-0889

IS - 3

ER -