Is contraction-stimulated glucose transport feedforward regulated by Ca2+?

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Is contraction-stimulated glucose transport feedforward regulated by Ca2+? / Jensen, Thomas Elbenhardt; Angin, Yeliz; Sylow, Lykke; Richter, Erik A.

I: Experimental Physiology, Bind 99, Nr. 12, 2014, s. 1562-1568.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

Jensen, TE, Angin, Y, Sylow, L & Richter, EA 2014, 'Is contraction-stimulated glucose transport feedforward regulated by Ca2+?', Experimental Physiology, bind 99, nr. 12, s. 1562-1568. https://doi.org/10.1113/expphysiol.2014.081679

APA

Jensen, T. E., Angin, Y., Sylow, L., & Richter, E. A. (2014). Is contraction-stimulated glucose transport feedforward regulated by Ca2+? Experimental Physiology, 99(12), 1562-1568. https://doi.org/10.1113/expphysiol.2014.081679

Vancouver

Jensen TE, Angin Y, Sylow L, Richter EA. Is contraction-stimulated glucose transport feedforward regulated by Ca2+? Experimental Physiology. 2014;99(12):1562-1568. https://doi.org/10.1113/expphysiol.2014.081679

Author

Jensen, Thomas Elbenhardt ; Angin, Yeliz ; Sylow, Lykke ; Richter, Erik A. / Is contraction-stimulated glucose transport feedforward regulated by Ca2+?. I: Experimental Physiology. 2014 ; Bind 99, Nr. 12. s. 1562-1568.

Bibtex

@article{c90df7ffb6c84873a6042b80d5bfcbdf,
title = "Is contraction-stimulated glucose transport feedforward regulated by Ca2+?",
abstract = "In many cell types, Ca(2+) signals to increase the movement and surface membrane insertion of vesicles. In skeletal muscle, Ca(2+) is predominantly released from the sarcoplasmic reticulum (SR) to initiate contraction. Sarcoplasmic reticulum Ca(2+) release is widely believed to be a direct feedforward regulator of the translocation of glucose transporter 4 to the cell surface to facilitate transmembrane glucose transport. This review summarizes the evidence supporting the Ca(2+) feedforward model and its proposed signalling links to regulation of glucose transport in skeletal muscle and other cell types. The literature is contrasted against our recent findings suggesting that SR Ca(2+) release is neither essential nor adequate to stimulate glucose transport in muscle. Instead, feedback signals through AMPK and mechanical stress are likely to account for most of contraction-stimulated glucose transport. A revised working model is proposed, in which muscle glucose transport during contraction is not directly regulated by SR Ca(2+) release but rather responds exclusively to feedback signals activated secondary to cross-bridge cycling and tension development.",
author = "Jensen, {Thomas Elbenhardt} and Yeliz Angin and Lykke Sylow and Richter, {Erik A.}",
note = "CURIS 2014 NEXS 297",
year = "2014",
doi = "10.1113/expphysiol.2014.081679",
language = "English",
volume = "99",
pages = "1562--1568",
journal = "Experimental Physiology",
issn = "0958-0670",
publisher = "Wiley-Blackwell",
number = "12",

}

RIS

TY - JOUR

T1 - Is contraction-stimulated glucose transport feedforward regulated by Ca2+?

AU - Jensen, Thomas Elbenhardt

AU - Angin, Yeliz

AU - Sylow, Lykke

AU - Richter, Erik A.

N1 - CURIS 2014 NEXS 297

PY - 2014

Y1 - 2014

N2 - In many cell types, Ca(2+) signals to increase the movement and surface membrane insertion of vesicles. In skeletal muscle, Ca(2+) is predominantly released from the sarcoplasmic reticulum (SR) to initiate contraction. Sarcoplasmic reticulum Ca(2+) release is widely believed to be a direct feedforward regulator of the translocation of glucose transporter 4 to the cell surface to facilitate transmembrane glucose transport. This review summarizes the evidence supporting the Ca(2+) feedforward model and its proposed signalling links to regulation of glucose transport in skeletal muscle and other cell types. The literature is contrasted against our recent findings suggesting that SR Ca(2+) release is neither essential nor adequate to stimulate glucose transport in muscle. Instead, feedback signals through AMPK and mechanical stress are likely to account for most of contraction-stimulated glucose transport. A revised working model is proposed, in which muscle glucose transport during contraction is not directly regulated by SR Ca(2+) release but rather responds exclusively to feedback signals activated secondary to cross-bridge cycling and tension development.

AB - In many cell types, Ca(2+) signals to increase the movement and surface membrane insertion of vesicles. In skeletal muscle, Ca(2+) is predominantly released from the sarcoplasmic reticulum (SR) to initiate contraction. Sarcoplasmic reticulum Ca(2+) release is widely believed to be a direct feedforward regulator of the translocation of glucose transporter 4 to the cell surface to facilitate transmembrane glucose transport. This review summarizes the evidence supporting the Ca(2+) feedforward model and its proposed signalling links to regulation of glucose transport in skeletal muscle and other cell types. The literature is contrasted against our recent findings suggesting that SR Ca(2+) release is neither essential nor adequate to stimulate glucose transport in muscle. Instead, feedback signals through AMPK and mechanical stress are likely to account for most of contraction-stimulated glucose transport. A revised working model is proposed, in which muscle glucose transport during contraction is not directly regulated by SR Ca(2+) release but rather responds exclusively to feedback signals activated secondary to cross-bridge cycling and tension development.

U2 - 10.1113/expphysiol.2014.081679

DO - 10.1113/expphysiol.2014.081679

M3 - Journal article

C2 - 25172886

VL - 99

SP - 1562

EP - 1568

JO - Experimental Physiology

JF - Experimental Physiology

SN - 0958-0670

IS - 12

ER -

ID: 125242599