Sucrose nonfermenting AMPK-related kinase (SNARK) mediates contraction-stimulated glucose transport in mouse skeletal muscle

Ho-Jin Koh; Taro Toyoda; Nobuharu Fujii; Michelle M. Jung; Amee Rathod; R. Jan-Willem Middelbeek; Sarah J. Lessard; Jonas Thue Treebak; Katsuya Tsuchihara; Hiroyasu Esumi; Erik Richter; Jørgen Wojtaszewski; Michael F. Hirshman; Laurie J. Goodyear

doi:10.1073/pnas.1008131107

Sucrose nonfermenting AMPK-related kinase (SNARK) mediates contraction-stimulated glucose transport in mouse skeletal muscle

Ho-Jin Koh, Taro Toyoda, Nobuharu Fujii, Michelle M. Jung, Amee Rathod, R. Jan-Willem Middelbeek, Sarah J. Lessard, Jonas Thue Treebak, Katsuya Tsuchihara, Hiroyasu Esumi, Erik Richter, Jørgen Wojtaszewski, Michael F. Hirshman, Laurie J. Goodyear

67 Citations (Scopus)

Abstract

The signaling mechanisms that mediate the important effects of contraction to increase glucose transport in skeletal muscle are not well understood, but are known to occur through an insulinin-dependent mechanism. Muscle-specific knockout of LKB1, an upstream kinase for AMPK and AMPK-related protein kinases, significantly inhibited contraction-stimulated glucose transport. This finding, in conjunction with previous studies of ablated AMPKα2 activity showing no effect on contraction-stimulated glucose transport, suggests that one or more AMPK-related protein kinases are important for this process. Muscle contraction increased sucrose nonfermenting AMPK-related kinase (SNARK) activity, an effect blunted in the muscle-specific LKB1 knockout mice. Expression of a mutant SNARK in mouse tibialis anterior muscle impaired contraction-stimulated, but not insulin-stimulated, glucose transport. Whole-body SNARK heterozygotic knockout mice also had impaired contraction-stimulated glucose transport in skeletal muscle, and knockdown of SNARK in C2C12 muscle cells impaired sorbitol-stimulated glucose transport. SNARK is activated by muscle contraction and is a unique mediator of contraction-stimulated glucose transport in skeletal muscle.

Original language	English
Journal	Proceedings of the National Academy of Science of the United States of America
Volume	107
Issue number	35
Pages (from-to)	15541-15546
Number of pages	6
ISSN	0027-8424
DOIs	https://doi.org/10.1073/pnas.1008131107
Publication status	Published - 31 Aug 2010

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Koh, H-J., Toyoda, T., Fujii, N., Jung, M. M., Rathod, A., Middelbeek, R. J-W., Lessard, S. J., Treebak, J. T., Tsuchihara, K., Esumi, H., Richter, E., Wojtaszewski, J., Hirshman, M. F., & Goodyear, L. J. (2010). Sucrose nonfermenting AMPK-related kinase (SNARK) mediates contraction-stimulated glucose transport in mouse skeletal muscle. Proceedings of the National Academy of Science of the United States of America, 107(35), 15541-15546. https://doi.org/10.1073/pnas.1008131107

Sucrose nonfermenting AMPK-related kinase (SNARK) mediates contraction-stimulated glucose transport in mouse skeletal muscle. / Koh, Ho-Jin; Toyoda, Taro; Fujii, Nobuharu et al.

In: Proceedings of the National Academy of Science of the United States of America, Vol. 107, No. 35, 31.08.2010, p. 15541-15546.

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

Koh, H-J, Toyoda, T, Fujii, N, Jung, MM, Rathod, A, Middelbeek, RJ-W, Lessard, SJ, Treebak, JT, Tsuchihara, K, Esumi, H, Richter, E , Wojtaszewski, J, Hirshman, MF & Goodyear, LJ 2010, 'Sucrose nonfermenting AMPK-related kinase (SNARK) mediates contraction-stimulated glucose transport in mouse skeletal muscle', Proceedings of the National Academy of Science of the United States of America, vol. 107, no. 35, pp. 15541-15546. https://doi.org/10.1073/pnas.1008131107

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title = "Sucrose nonfermenting AMPK-related kinase (SNARK) mediates contraction-stimulated glucose transport in mouse skeletal muscle",

abstract = "The signaling mechanisms that mediate the important effects of contraction to increase glucose transport in skeletal muscle are not well understood, but are known to occur through an insulinin-dependent mechanism. Muscle-specific knockout of LKB1, an upstream kinase for AMPK and AMPK-related protein kinases, significantly inhibited contraction-stimulated glucose transport. This finding, in conjunction with previous studies of ablated AMPKα2 activity showing no effect on contraction-stimulated glucose transport, suggests that one or more AMPK-related protein kinases are important for this process. Muscle contraction increased sucrose nonfermenting AMPK-related kinase (SNARK) activity, an effect blunted in the muscle-specific LKB1 knockout mice. Expression of a mutant SNARK in mouse tibialis anterior muscle impaired contraction-stimulated, but not insulin-stimulated, glucose transport. Whole-body SNARK heterozygotic knockout mice also had impaired contraction-stimulated glucose transport in skeletal muscle, and knockdown of SNARK in C2C12 muscle cells impaired sorbitol-stimulated glucose transport. SNARK is activated by muscle contraction and is a unique mediator of contraction-stimulated glucose transport in skeletal muscle.",

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AU - Koh, Ho-Jin

AU - Toyoda, Taro

AU - Fujii, Nobuharu

AU - Jung, Michelle M.

AU - Rathod, Amee

AU - Middelbeek, R. Jan-Willem

AU - Lessard, Sarah J.

AU - Treebak, Jonas Thue

AU - Tsuchihara, Katsuya

AU - Esumi, Hiroyasu

AU - Richter, Erik

AU - Wojtaszewski, Jørgen

AU - Hirshman, Michael F.

AU - Goodyear, Laurie J.

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N2 - The signaling mechanisms that mediate the important effects of contraction to increase glucose transport in skeletal muscle are not well understood, but are known to occur through an insulinin-dependent mechanism. Muscle-specific knockout of LKB1, an upstream kinase for AMPK and AMPK-related protein kinases, significantly inhibited contraction-stimulated glucose transport. This finding, in conjunction with previous studies of ablated AMPKα2 activity showing no effect on contraction-stimulated glucose transport, suggests that one or more AMPK-related protein kinases are important for this process. Muscle contraction increased sucrose nonfermenting AMPK-related kinase (SNARK) activity, an effect blunted in the muscle-specific LKB1 knockout mice. Expression of a mutant SNARK in mouse tibialis anterior muscle impaired contraction-stimulated, but not insulin-stimulated, glucose transport. Whole-body SNARK heterozygotic knockout mice also had impaired contraction-stimulated glucose transport in skeletal muscle, and knockdown of SNARK in C2C12 muscle cells impaired sorbitol-stimulated glucose transport. SNARK is activated by muscle contraction and is a unique mediator of contraction-stimulated glucose transport in skeletal muscle.

AB - The signaling mechanisms that mediate the important effects of contraction to increase glucose transport in skeletal muscle are not well understood, but are known to occur through an insulinin-dependent mechanism. Muscle-specific knockout of LKB1, an upstream kinase for AMPK and AMPK-related protein kinases, significantly inhibited contraction-stimulated glucose transport. This finding, in conjunction with previous studies of ablated AMPKα2 activity showing no effect on contraction-stimulated glucose transport, suggests that one or more AMPK-related protein kinases are important for this process. Muscle contraction increased sucrose nonfermenting AMPK-related kinase (SNARK) activity, an effect blunted in the muscle-specific LKB1 knockout mice. Expression of a mutant SNARK in mouse tibialis anterior muscle impaired contraction-stimulated, but not insulin-stimulated, glucose transport. Whole-body SNARK heterozygotic knockout mice also had impaired contraction-stimulated glucose transport in skeletal muscle, and knockdown of SNARK in C2C12 muscle cells impaired sorbitol-stimulated glucose transport. SNARK is activated by muscle contraction and is a unique mediator of contraction-stimulated glucose transport in skeletal muscle.

U2 - 10.1073/pnas.1008131107

DO - 10.1073/pnas.1008131107

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JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

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ER -

Sucrose nonfermenting AMPK-related kinase (SNARK) mediates contraction-stimulated glucose transport in mouse skeletal muscle

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