HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 295/3/E545    most recent 90259.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Long, Y. C. Articles by Zierath, J. R. Search for Related Content PubMed PubMed Citation Articles by Long, Y. C. Articles by Zierath, J. R.

REVIEWS

Influence of AMP-activated protein kinase and calcineurin on metabolic networks in skeletal muscle

¹Department of Molecular Medicine and Surgery, Karolinska Institutet, Section of Integrative Physiology, Stockholm, Sweden; and ²Howard Hughes Medical Institute, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts

Submitted 28 February 2008 ; accepted in final form 4 June 2008

ABSTRACT

Skeletal muscle fibers differ considerably in their metabolic and physiological properties. Skeletal muscle displays a high degree of metabolic flexibility, which allows the myofibers to adapt to various physiological demands by shifting energy substrate utilization. Transcriptional events play a pivotal role in the metabolic adaptations of skeletal muscle. The expression of genes essential for skeletal muscle glucose and lipid metabolism is tightly coordinated in support of a shift in substrate utilization. AMP-activated protein kinase (AMPK) and calcineurin (a calcium-regulated serine/threonine protein phosphatase) regulate skeletal muscle metabolic gene expression programs in response to changes in the energy status and levels of neuronal input, respectively. AMPK and calcineurin activate transcriptional regulators such as peroxisome proliferator-activated receptor- coactivator-1 and myocyte enhancer factor as well as increase skeletal muscle oxidative capacity and mitochondrial gene expression. Activation of either the AMPK or calcineurin pathway can also enhance the glycogen storage capacity and insulin sensitivity in skeletal muscle. Characterization of pathways governing skeletal muscle metabolism offers insight into physiological and pharmacological strategies to prevent or ameliorate peripheral insulin resistance associated with metabolic disorders such as type 2 diabetes.

adenosine 5'-monophosphate-activated protein kinase

This article has been cited by other articles:

				B. K. Pedersen Edward F. Adolph Distinguished Lecture: Muscle as an endocrine organ: IL-6 and other myokines J Appl Physiol, October 1, 2009; 107(4): 1006 - 1014. [Abstract] [Full Text] [PDF]

				M. Murgia, T. E. Jensen, M. Cusinato, M. Garcia, E. A. Richter, and S. Schiaffino Multiple signalling pathways redundantly control glucose transporter GLUT4 gene transcription in skeletal muscle J. Physiol., September 1, 2009; 587(17): 4319 - 4327. [Abstract] [Full Text] [PDF]