Potential role of TBC1D4 in enhanced post-exercise insulin action in human skeletal muscle

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Potential role of TBC1D4 in enhanced post-exercise insulin action in human skeletal muscle. / Treebak, Jonas Thue; Frøsig, Christian; Pehmøller, Christian; Chen, Shuai; Maarbjerg, Stine Just; Brandt, Nina; Mackintosh, C.; Zierath, J. R.; Hardie, D. G.; Kiens, Bente; Richter, Erik A.; Pilegaard, Henriette; Wojtaszewski, Jørgen.

In: Diabetologia, Vol. 52, No. 5, 2009, p. 891-900.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Treebak, JT, Frøsig, C, Pehmøller, C, Chen, S, Maarbjerg, SJ, Brandt, N, Mackintosh, C, Zierath, JR, Hardie, DG, Kiens, B, Richter, EA, Pilegaard, H & Wojtaszewski, J 2009, 'Potential role of TBC1D4 in enhanced post-exercise insulin action in human skeletal muscle', Diabetologia, vol. 52, no. 5, pp. 891-900. https://doi.org/10.1007/s00125-009-1294-y

APA

Treebak, J. T., Frøsig, C., Pehmøller, C., Chen, S., Maarbjerg, S. J., Brandt, N., Mackintosh, C., Zierath, J. R., Hardie, D. G., Kiens, B., Richter, E. A., Pilegaard, H., & Wojtaszewski, J. (2009). Potential role of TBC1D4 in enhanced post-exercise insulin action in human skeletal muscle. Diabetologia, 52(5), 891-900. https://doi.org/10.1007/s00125-009-1294-y

Vancouver

Treebak JT, Frøsig C, Pehmøller C, Chen S, Maarbjerg SJ, Brandt N et al. Potential role of TBC1D4 in enhanced post-exercise insulin action in human skeletal muscle. Diabetologia. 2009;52(5):891-900. https://doi.org/10.1007/s00125-009-1294-y

Author

Treebak, Jonas Thue ; Frøsig, Christian ; Pehmøller, Christian ; Chen, Shuai ; Maarbjerg, Stine Just ; Brandt, Nina ; Mackintosh, C. ; Zierath, J. R. ; Hardie, D. G. ; Kiens, Bente ; Richter, Erik A. ; Pilegaard, Henriette ; Wojtaszewski, Jørgen. / Potential role of TBC1D4 in enhanced post-exercise insulin action in human skeletal muscle. In: Diabetologia. 2009 ; Vol. 52, No. 5. pp. 891-900.

Bibtex

@article{fc3ee5500e4b11de8478000ea68e967b,
title = "Potential role of TBC1D4 in enhanced post-exercise insulin action in human skeletal muscle",
abstract = "Aims/Hypothesis: TBC1 domain family, member 4 (TBC1D4; also known as AS160) is a cellular signalling intermediate to glucose transport regulated by insulin-dependent and -independent mechanisms. Skeletal muscle insulin sensitivity is increased after acute exercise by an unknown mechanism that does not involve modulation at proximal insulin signalling intermediates. We hypothesised that signalling through TBC1D4 is involved in this effect of exercise as it is a common signalling element for insulin and exercise. Methods: Insulin-regulated glucose metabolism was evaluated in 12 healthy moderately trained young men 4 h after one-legged exercise at basal and during a euglycaemic-hyperinsulinaemic clamp. Vastus lateralis biopsies were taken before and immediately after the clamp. Results: Insulin stimulation increased glucose uptake in both legs, with greater effects (~80%, p < 0.01) in the previously exercised leg. TBC1D4 phosphorylation, assessed using the phospho-AKT (protein kinase B)substrate antibody and phospho- and site-specific antibodies targeting six phosphorylation sites on TBC1D4, increased at similar degrees to insulin stimulation in the previously exercised and rested legs (p < 0.01). However, TBC1D4 phosphorylation on Ser-318, Ser-341, Ser-588 and Ser-751 was higher in the previously exercised leg, both in the absence and in the presence of insulin (p < 0.01; Ser-588, p = 0.09; observed power = 0.39). 14-3-3 binding capacity for TBC1D4 increased equally (p < 0.01) in both legs during insulin stimulation. Conclusion/Interpretation: We provide evidence for site-specific phosphorylation of TBC1D4 in human skeletal muscle in response to physiological hyperinsulinaemia. The data support the idea that TBC1D4 is a nexus for insulin- and exercise-responsive signals that may mediate increased insulin action after exercise.",
author = "Treebak, {Jonas Thue} and Christian Fr{\o}sig and Christian Pehm{\o}ller and Shuai Chen and Maarbjerg, {Stine Just} and Nina Brandt and C. Mackintosh and Zierath, {J. R.} and Hardie, {D. G.} and Bente Kiens and Richter, {Erik A.} and Henriette Pilegaard and J{\o}rgen Wojtaszewski",
note = "CURIS 2009 5200 011",
year = "2009",
doi = "10.1007/s00125-009-1294-y",
language = "English",
volume = "52",
pages = "891--900",
journal = "Diabetologia",
issn = "0012-186X",
publisher = "Springer",
number = "5",

}

RIS

TY - JOUR

T1 - Potential role of TBC1D4 in enhanced post-exercise insulin action in human skeletal muscle

AU - Treebak, Jonas Thue

AU - Frøsig, Christian

AU - Pehmøller, Christian

AU - Chen, Shuai

AU - Maarbjerg, Stine Just

AU - Brandt, Nina

AU - Mackintosh, C.

AU - Zierath, J. R.

AU - Hardie, D. G.

AU - Kiens, Bente

AU - Richter, Erik A.

AU - Pilegaard, Henriette

AU - Wojtaszewski, Jørgen

N1 - CURIS 2009 5200 011

PY - 2009

Y1 - 2009

N2 - Aims/Hypothesis: TBC1 domain family, member 4 (TBC1D4; also known as AS160) is a cellular signalling intermediate to glucose transport regulated by insulin-dependent and -independent mechanisms. Skeletal muscle insulin sensitivity is increased after acute exercise by an unknown mechanism that does not involve modulation at proximal insulin signalling intermediates. We hypothesised that signalling through TBC1D4 is involved in this effect of exercise as it is a common signalling element for insulin and exercise. Methods: Insulin-regulated glucose metabolism was evaluated in 12 healthy moderately trained young men 4 h after one-legged exercise at basal and during a euglycaemic-hyperinsulinaemic clamp. Vastus lateralis biopsies were taken before and immediately after the clamp. Results: Insulin stimulation increased glucose uptake in both legs, with greater effects (~80%, p < 0.01) in the previously exercised leg. TBC1D4 phosphorylation, assessed using the phospho-AKT (protein kinase B)substrate antibody and phospho- and site-specific antibodies targeting six phosphorylation sites on TBC1D4, increased at similar degrees to insulin stimulation in the previously exercised and rested legs (p < 0.01). However, TBC1D4 phosphorylation on Ser-318, Ser-341, Ser-588 and Ser-751 was higher in the previously exercised leg, both in the absence and in the presence of insulin (p < 0.01; Ser-588, p = 0.09; observed power = 0.39). 14-3-3 binding capacity for TBC1D4 increased equally (p < 0.01) in both legs during insulin stimulation. Conclusion/Interpretation: We provide evidence for site-specific phosphorylation of TBC1D4 in human skeletal muscle in response to physiological hyperinsulinaemia. The data support the idea that TBC1D4 is a nexus for insulin- and exercise-responsive signals that may mediate increased insulin action after exercise.

AB - Aims/Hypothesis: TBC1 domain family, member 4 (TBC1D4; also known as AS160) is a cellular signalling intermediate to glucose transport regulated by insulin-dependent and -independent mechanisms. Skeletal muscle insulin sensitivity is increased after acute exercise by an unknown mechanism that does not involve modulation at proximal insulin signalling intermediates. We hypothesised that signalling through TBC1D4 is involved in this effect of exercise as it is a common signalling element for insulin and exercise. Methods: Insulin-regulated glucose metabolism was evaluated in 12 healthy moderately trained young men 4 h after one-legged exercise at basal and during a euglycaemic-hyperinsulinaemic clamp. Vastus lateralis biopsies were taken before and immediately after the clamp. Results: Insulin stimulation increased glucose uptake in both legs, with greater effects (~80%, p < 0.01) in the previously exercised leg. TBC1D4 phosphorylation, assessed using the phospho-AKT (protein kinase B)substrate antibody and phospho- and site-specific antibodies targeting six phosphorylation sites on TBC1D4, increased at similar degrees to insulin stimulation in the previously exercised and rested legs (p < 0.01). However, TBC1D4 phosphorylation on Ser-318, Ser-341, Ser-588 and Ser-751 was higher in the previously exercised leg, both in the absence and in the presence of insulin (p < 0.01; Ser-588, p = 0.09; observed power = 0.39). 14-3-3 binding capacity for TBC1D4 increased equally (p < 0.01) in both legs during insulin stimulation. Conclusion/Interpretation: We provide evidence for site-specific phosphorylation of TBC1D4 in human skeletal muscle in response to physiological hyperinsulinaemia. The data support the idea that TBC1D4 is a nexus for insulin- and exercise-responsive signals that may mediate increased insulin action after exercise.

U2 - 10.1007/s00125-009-1294-y

DO - 10.1007/s00125-009-1294-y

M3 - Journal article

C2 - 19252894

VL - 52

SP - 891

EP - 900

JO - Diabetologia

JF - Diabetologia

SN - 0012-186X

IS - 5

ER -

ID: 11207093