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Is contraction-stimulated glucose transport feed forward-regulated by Ca2+?
AuthorsJensen TE, et al. Show all Journal
Exp Physiol. 2014 Aug 28. [Epub ahead of print]
Affiliation
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 sarcoplasmatic reticulum (SR) to initiate contraction. SR Ca(2+) release is widely believed to be a direct feed-forward regulator of the translocation of glucose transporter 4 (GLUT4) to the cell surface to facilitate transmembrane glucose transport. This review summarizes the evidence supporting the Ca(2+) feed-forward paradigm and its proposed signaling links to glucose transport regulation 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 muscle glucose transport. 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. This article is protected by copyright. All rights reserved.
AuthorsJensen TE, et al. Show all Journal
Exp Physiol. 2014 Aug 28. [Epub ahead of print]
Affiliation
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 sarcoplasmatic reticulum (SR) to initiate contraction. SR Ca(2+) release is widely believed to be a direct feed-forward regulator of the translocation of glucose transporter 4 (GLUT4) to the cell surface to facilitate transmembrane glucose transport. This review summarizes the evidence supporting the Ca(2+) feed-forward paradigm and its proposed signaling links to glucose transport regulation 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 muscle glucose transport. 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. This article is protected by copyright. All rights reserved.
