An acetylation rheostat for the control of muscle energy homeostasis

    1. Johan Auwerx
    1. Laboratory of Integrative and Systems Physiology (LISP/NCEM), Life Science Faculty, Institute of Bioengineering, École Polytechnique Fédérale de Lausanne (EPFL), Station 15, CH-1015 Lausanne, Switzerland
    1. Correspondence should be addressed to J Auwerx; Email: admin.auwerx{at}


    In recent years, the role of acetylation has gained ground as an essential modulator of intermediary metabolism in skeletal muscle. Imbalance in energy homeostasis or chronic cellular stress, due to diet, aging, or disease, translate into alterations in the acetylation levels of key proteins which govern bioenergetics, cellular substrate use, and/or changes in mitochondrial content and function. For example, cellular stress induced by exercise or caloric restriction can alter the coordinated activity of acetyltransferases and deacetylases to increase mitochondrial biogenesis and function in order to adapt to low energetic levels. The natural duality of these enzymes, as metabolic sensors and effector proteins, has helped biologists to understand how the body can integrate seemingly distinct signaling pathways to control mitochondrial biogenesis, insulin sensitivity, glucose transport, reactive oxygen species handling, angiogenesis, and muscle satellite cell proliferation/differentiation. Our review will summarize the recent developments related to acetylation-dependent responses following metabolic stress in skeletal muscle.

    • Received 8 July 2013
    • Revision received 28 August 2013
    • Accepted 30 August 2013
    • Made available online as an Accepted Preprint 2 September 2013
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