Kinetics of GLUT4 trafficking in rat and human skeletal muscle

H K R Karlsson, A V Chibalin, H A Koistinen, J Yang, Francoise Koumanov, H Wallberg-Henriksson, J R Zierath, Geoffrey D Holman

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Abstract

OBJECTIVE-In skeletal muscle, insulin stimulates glucose transport activity three- to fourfold, and a large part of this stimulation is associated with a net translocation of GLUT4 from an intracellular compartment to the cell surface. We examined the extent to which insulin or the AMP-activated protein kinase activator AICAR can lead to a stimulation of the exocytosis limb of the GLUT4 translocation pathway and thereby account for the net increase in glucose transport activity.
RESEARCH DESIGN AND METHODS-Using a biotinylated photoaffinity label, we tagged endogenous GLUT4 and studied the kinetics of exocytosis of the tagged protein in rat and human skeletal muscle in response to insulin or AICAR. Isolated epitrochlearis muscles were obtained from male Wistar rats. Vastus lateralis skeletal muscle strips were prepared from open muscle biopsies obtained from six healthy men (age 39 +/- 11 years and BMI 25.8 +/- 0.8 kg/m(2)).
RESULTS-In rat epitrochlearis muscle, insulin exposure leads to a sixfold stimulation of the GLUT4 exocytosis rate (with basal and insulin-stimulated rate constants of 0.010 and 0.067 min(-1), respectively). In human vastus lateralis muscle, insulin stimulates GLUT4 translocation by a similar sixfold increase in the exocytosis rate constant (with basal and insulin-stimulated rate constants of 0.011 and 0.075 min(-1), respectively). In contrast, AICAR treatment does not markedly increase exocytosis in either rat or human muscle.
CONCLUSIONS-Insulin stimulation of the GLUT4 exocytosis rate constant is sufficient to account for most of the observed increase in glucose transport activity in rat and human muscle.
Original languageEnglish
Pages (from-to)847-854
Number of pages8
JournalDiabetes
Volume58
Issue number4
Early online date2 Feb 2009
DOIs
Publication statusPublished - Apr 2009

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Exocytosis
Skeletal Muscle
Insulin
Muscles
Quadriceps Muscle
Glucose
Photoaffinity Labels
AMP-Activated Protein Kinases
Wistar Rats
Research Design
Extremities
Biopsy
AICA ribonucleotide
Proteins

Cite this

Karlsson, H. K. R., Chibalin, A. V., Koistinen, H. A., Yang, J., Koumanov, F., Wallberg-Henriksson, H., ... Holman, G. D. (2009). Kinetics of GLUT4 trafficking in rat and human skeletal muscle. Diabetes, 58(4), 847-854. https://doi.org/10.2337/db08-1539

Kinetics of GLUT4 trafficking in rat and human skeletal muscle. / Karlsson, H K R; Chibalin, A V; Koistinen, H A; Yang, J; Koumanov, Francoise; Wallberg-Henriksson, H; Zierath, J R; Holman, Geoffrey D.

In: Diabetes, Vol. 58, No. 4, 04.2009, p. 847-854.

Research output: Contribution to journalArticle

Karlsson, HKR, Chibalin, AV, Koistinen, HA, Yang, J, Koumanov, F, Wallberg-Henriksson, H, Zierath, JR & Holman, GD 2009, 'Kinetics of GLUT4 trafficking in rat and human skeletal muscle', Diabetes, vol. 58, no. 4, pp. 847-854. https://doi.org/10.2337/db08-1539
Karlsson HKR, Chibalin AV, Koistinen HA, Yang J, Koumanov F, Wallberg-Henriksson H et al. Kinetics of GLUT4 trafficking in rat and human skeletal muscle. Diabetes. 2009 Apr;58(4):847-854. https://doi.org/10.2337/db08-1539
Karlsson, H K R ; Chibalin, A V ; Koistinen, H A ; Yang, J ; Koumanov, Francoise ; Wallberg-Henriksson, H ; Zierath, J R ; Holman, Geoffrey D. / Kinetics of GLUT4 trafficking in rat and human skeletal muscle. In: Diabetes. 2009 ; Vol. 58, No. 4. pp. 847-854.
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abstract = "OBJECTIVE-In skeletal muscle, insulin stimulates glucose transport activity three- to fourfold, and a large part of this stimulation is associated with a net translocation of GLUT4 from an intracellular compartment to the cell surface. We examined the extent to which insulin or the AMP-activated protein kinase activator AICAR can lead to a stimulation of the exocytosis limb of the GLUT4 translocation pathway and thereby account for the net increase in glucose transport activity. RESEARCH DESIGN AND METHODS-Using a biotinylated photoaffinity label, we tagged endogenous GLUT4 and studied the kinetics of exocytosis of the tagged protein in rat and human skeletal muscle in response to insulin or AICAR. Isolated epitrochlearis muscles were obtained from male Wistar rats. Vastus lateralis skeletal muscle strips were prepared from open muscle biopsies obtained from six healthy men (age 39 +/- 11 years and BMI 25.8 +/- 0.8 kg/m(2)). RESULTS-In rat epitrochlearis muscle, insulin exposure leads to a sixfold stimulation of the GLUT4 exocytosis rate (with basal and insulin-stimulated rate constants of 0.010 and 0.067 min(-1), respectively). In human vastus lateralis muscle, insulin stimulates GLUT4 translocation by a similar sixfold increase in the exocytosis rate constant (with basal and insulin-stimulated rate constants of 0.011 and 0.075 min(-1), respectively). In contrast, AICAR treatment does not markedly increase exocytosis in either rat or human muscle. CONCLUSIONS-Insulin stimulation of the GLUT4 exocytosis rate constant is sufficient to account for most of the observed increase in glucose transport activity in rat and human muscle.",
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AU - Karlsson, H K R

AU - Chibalin, A V

AU - Koistinen, H A

AU - Yang, J

AU - Koumanov, Francoise

AU - Wallberg-Henriksson, H

AU - Zierath, J R

AU - Holman, Geoffrey D

N1 - ADA will submit the final print versions of articles to PubMed Central. Articles will be accessible on PubMed Central 12 months after the date of final publication in Diabetes.

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Y1 - 2009/4

N2 - OBJECTIVE-In skeletal muscle, insulin stimulates glucose transport activity three- to fourfold, and a large part of this stimulation is associated with a net translocation of GLUT4 from an intracellular compartment to the cell surface. We examined the extent to which insulin or the AMP-activated protein kinase activator AICAR can lead to a stimulation of the exocytosis limb of the GLUT4 translocation pathway and thereby account for the net increase in glucose transport activity. RESEARCH DESIGN AND METHODS-Using a biotinylated photoaffinity label, we tagged endogenous GLUT4 and studied the kinetics of exocytosis of the tagged protein in rat and human skeletal muscle in response to insulin or AICAR. Isolated epitrochlearis muscles were obtained from male Wistar rats. Vastus lateralis skeletal muscle strips were prepared from open muscle biopsies obtained from six healthy men (age 39 +/- 11 years and BMI 25.8 +/- 0.8 kg/m(2)). RESULTS-In rat epitrochlearis muscle, insulin exposure leads to a sixfold stimulation of the GLUT4 exocytosis rate (with basal and insulin-stimulated rate constants of 0.010 and 0.067 min(-1), respectively). In human vastus lateralis muscle, insulin stimulates GLUT4 translocation by a similar sixfold increase in the exocytosis rate constant (with basal and insulin-stimulated rate constants of 0.011 and 0.075 min(-1), respectively). In contrast, AICAR treatment does not markedly increase exocytosis in either rat or human muscle. CONCLUSIONS-Insulin stimulation of the GLUT4 exocytosis rate constant is sufficient to account for most of the observed increase in glucose transport activity in rat and human muscle.

AB - OBJECTIVE-In skeletal muscle, insulin stimulates glucose transport activity three- to fourfold, and a large part of this stimulation is associated with a net translocation of GLUT4 from an intracellular compartment to the cell surface. We examined the extent to which insulin or the AMP-activated protein kinase activator AICAR can lead to a stimulation of the exocytosis limb of the GLUT4 translocation pathway and thereby account for the net increase in glucose transport activity. RESEARCH DESIGN AND METHODS-Using a biotinylated photoaffinity label, we tagged endogenous GLUT4 and studied the kinetics of exocytosis of the tagged protein in rat and human skeletal muscle in response to insulin or AICAR. Isolated epitrochlearis muscles were obtained from male Wistar rats. Vastus lateralis skeletal muscle strips were prepared from open muscle biopsies obtained from six healthy men (age 39 +/- 11 years and BMI 25.8 +/- 0.8 kg/m(2)). RESULTS-In rat epitrochlearis muscle, insulin exposure leads to a sixfold stimulation of the GLUT4 exocytosis rate (with basal and insulin-stimulated rate constants of 0.010 and 0.067 min(-1), respectively). In human vastus lateralis muscle, insulin stimulates GLUT4 translocation by a similar sixfold increase in the exocytosis rate constant (with basal and insulin-stimulated rate constants of 0.011 and 0.075 min(-1), respectively). In contrast, AICAR treatment does not markedly increase exocytosis in either rat or human muscle. CONCLUSIONS-Insulin stimulation of the GLUT4 exocytosis rate constant is sufficient to account for most of the observed increase in glucose transport activity in rat and human muscle.

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