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.
In: Experimental Physiology, Vol. 99, No. 12, 2014, p. 1562-1568.Research output: Contribution to journal › Journal article › Research › peer-review
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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