4.5 Article

Insulin acutely improves mitochondrial function of rat and human skeletal muscle by increasing coupling efficiency of oxidative phosphorylation

期刊

BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS
卷 1837, 期 2, 页码 270-276

出版社

ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbabio.2013.10.012

关键词

Skeletal muscle cells; Insulin sensitivity; Oxidative phosphorylation; Mitochondrial coupling efficiency; Cell respiratory control; Mitochondrial proton leak

资金

  1. Medical Research Council [G1100165]
  2. Plymouth University
  3. Medical Research Council [G1100165] Funding Source: researchfish
  4. MRC [G1100165] Funding Source: UKRI

向作者/读者索取更多资源

Insulin is essential for the regulation of fuel metabolism and triggers the uptake of glucose by skeletal muscle. The imported glucose is either stored or broken down, as insulin stimulates glycogenesis and ATP synthesis. The mechanism by which ATP production is increased is incompletely understood at present and, generally, relatively little functional information is available on the effect of insulin on mitochondrial function. In this paper we have exploited extracellular flux technology to investigate insulin effects on the bioenergetics of rat (L6) and human skeletal muscle myoblasts and myotubes. We demonstrate that a 20-min insulin exposure significantly increases (i) the cell respiratory control ratio, (ii) the coupling efficiency of oxidative phosphorylation, and (iii) the glucose sensitivity of anaerobic glycolysis. The improvement of mitochondrial function is explained by an insulin-induced immediate decrease of mitochondrial proton leak. Palmitate exposure annuls the beneficial mitochondrial effects of insulin. Our data improve the mechanistic understanding of insulin-stimulated ATP synthesis, and reveal a hitherto undisclosed insulin sensitivity of cellular bioenergetics that suggests a novel way of detecting insulin responsiveness of cells. (C) 2013 The Authors. Published by Elsevier B.V. All rights reserved.

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