Contraction-stimulated glucose transport in muscle is controlled by AMPK and mechanical stress but not sarcoplasmatic reticulum Ca2+ release

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Standard

Contraction-stimulated glucose transport in muscle is controlled by AMPK and mechanical stress but not sarcoplasmatic reticulum Ca2+ release. / Jensen, Thomas Elbenhardt; Sylow, Lykke; Rose, Adam John; Madsen, Agnete Louise Bjerregaard; Angin, Yeliz; Maarbjerg, Stine J; Richter, Erik A.

I: Molecular Metabolism, Bind 3, Nr. 7, 2014, s. 742-753.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Jensen, TE, Sylow, L, Rose, AJ, Madsen, ALB, Angin, Y, Maarbjerg, SJ & Richter, EA 2014, 'Contraction-stimulated glucose transport in muscle is controlled by AMPK and mechanical stress but not sarcoplasmatic reticulum Ca2+ release', Molecular Metabolism, bind 3, nr. 7, s. 742-753. https://doi.org/10.1016/j.molmet.2014.07.005

APA

Jensen, T. E., Sylow, L., Rose, A. J., Madsen, A. L. B., Angin, Y., Maarbjerg, S. J., & Richter, E. A. (2014). Contraction-stimulated glucose transport in muscle is controlled by AMPK and mechanical stress but not sarcoplasmatic reticulum Ca2+ release. Molecular Metabolism, 3(7), 742-753. https://doi.org/10.1016/j.molmet.2014.07.005

Vancouver

Jensen TE, Sylow L, Rose AJ, Madsen ALB, Angin Y, Maarbjerg SJ o.a. Contraction-stimulated glucose transport in muscle is controlled by AMPK and mechanical stress but not sarcoplasmatic reticulum Ca2+ release. Molecular Metabolism. 2014;3(7):742-753. https://doi.org/10.1016/j.molmet.2014.07.005

Author

Jensen, Thomas Elbenhardt ; Sylow, Lykke ; Rose, Adam John ; Madsen, Agnete Louise Bjerregaard ; Angin, Yeliz ; Maarbjerg, Stine J ; Richter, Erik A. / Contraction-stimulated glucose transport in muscle is controlled by AMPK and mechanical stress but not sarcoplasmatic reticulum Ca2+ release. I: Molecular Metabolism. 2014 ; Bind 3, Nr. 7. s. 742-753.

Bibtex

@article{8614d1ce7088414586e29d63345a1348,
title = "Contraction-stimulated glucose transport in muscle is controlled by AMPK and mechanical stress but not sarcoplasmatic reticulum Ca2+ release",
abstract = "Understanding how muscle contraction orchestrates insulin-independent muscle glucose transport may enable development of hyperglycemia-treating drugs. The prevailing concept implicates Ca(2+) as a key feed forward regulator of glucose transport with secondary fine-tuning by metabolic feedback signals through proteins such as AMPK. Here, we demonstrate in incubated mouse muscle that Ca(2+) release is neither sufficient nor strictly necessary to increase glucose transport. Rather, the glucose transport response is associated with metabolic feedback signals through AMPK, and mechanical stress-activated signals. Furthermore, artificial stimulation of AMPK combined with passive stretch of muscle is additive and sufficient to elicit the full contraction glucose transport response. These results suggest that ATP-turnover and mechanical stress feedback are sufficient to fully increase glucose transport during muscle contraction, and call for a major reconsideration of the established Ca(2+) centric paradigm.",
author = "Jensen, {Thomas Elbenhardt} and Lykke Sylow and Rose, {Adam John} and Madsen, {Agnete Louise Bjerregaard} and Yeliz Angin and Maarbjerg, {Stine J} and Richter, {Erik A.}",
note = "CURIS 2014 NEXS 324",
year = "2014",
doi = "10.1016/j.molmet.2014.07.005",
language = "English",
volume = "3",
pages = "742--753",
journal = "Molecular Metabolism",
issn = "2212-8778",
publisher = "Elsevier",
number = "7",

}

RIS

TY - JOUR

T1 - Contraction-stimulated glucose transport in muscle is controlled by AMPK and mechanical stress but not sarcoplasmatic reticulum Ca2+ release

AU - Jensen, Thomas Elbenhardt

AU - Sylow, Lykke

AU - Rose, Adam John

AU - Madsen, Agnete Louise Bjerregaard

AU - Angin, Yeliz

AU - Maarbjerg, Stine J

AU - Richter, Erik A.

N1 - CURIS 2014 NEXS 324

PY - 2014

Y1 - 2014

N2 - Understanding how muscle contraction orchestrates insulin-independent muscle glucose transport may enable development of hyperglycemia-treating drugs. The prevailing concept implicates Ca(2+) as a key feed forward regulator of glucose transport with secondary fine-tuning by metabolic feedback signals through proteins such as AMPK. Here, we demonstrate in incubated mouse muscle that Ca(2+) release is neither sufficient nor strictly necessary to increase glucose transport. Rather, the glucose transport response is associated with metabolic feedback signals through AMPK, and mechanical stress-activated signals. Furthermore, artificial stimulation of AMPK combined with passive stretch of muscle is additive and sufficient to elicit the full contraction glucose transport response. These results suggest that ATP-turnover and mechanical stress feedback are sufficient to fully increase glucose transport during muscle contraction, and call for a major reconsideration of the established Ca(2+) centric paradigm.

AB - Understanding how muscle contraction orchestrates insulin-independent muscle glucose transport may enable development of hyperglycemia-treating drugs. The prevailing concept implicates Ca(2+) as a key feed forward regulator of glucose transport with secondary fine-tuning by metabolic feedback signals through proteins such as AMPK. Here, we demonstrate in incubated mouse muscle that Ca(2+) release is neither sufficient nor strictly necessary to increase glucose transport. Rather, the glucose transport response is associated with metabolic feedback signals through AMPK, and mechanical stress-activated signals. Furthermore, artificial stimulation of AMPK combined with passive stretch of muscle is additive and sufficient to elicit the full contraction glucose transport response. These results suggest that ATP-turnover and mechanical stress feedback are sufficient to fully increase glucose transport during muscle contraction, and call for a major reconsideration of the established Ca(2+) centric paradigm.

U2 - 10.1016/j.molmet.2014.07.005

DO - 10.1016/j.molmet.2014.07.005

M3 - Journal article

C2 - 25353002

VL - 3

SP - 742

EP - 753

JO - Molecular Metabolism

JF - Molecular Metabolism

SN - 2212-8778

IS - 7

ER -

ID: 126384314