期刊
MOLECULAR METABOLISM
卷 3, 期 7, 页码 742-753出版社
ELSEVIER
DOI: 10.1016/j.molmet.2014.07.005
关键词
Exercise; Skeletal muscle; Ca2+; AMPK; Stretch
资金
- Novo Nordisk Fonden [NNF14OC0010641, NNF12OC1016400, NNF14OC0012319] Funding Source: researchfish
Understanding how muscle contraction orchestrates insulin-independent muscle glucose transport may enable development of hyperglycemia treating drugs. The prevailing concept implicates Ca2+ 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 Ca2+ 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 Ca2+ centric paradigm. (C) 2014 The Authors. Published by Elsevier GmbH. This is an open access article under the CC BY-NC-ND license (http.creativecommons.org/licenses/by-nc-nd/3.0/).
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