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Am J Physiol Endocrinol Metab 297: E340-E348, 2009. First published May 19, 2009; doi:10.1152/ajpendo.90610.2008
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Knockout of the predominant conventional PKC isoform, PKC{alpha}, in mouse skeletal muscle does not affect contraction-stimulated glucose uptake

Thomas E. Jensen,1 Stine J. Maarbjerg,1 Adam J. Rose,1 Michael Leitges,2 and Erik A. Richter1

1Molecular Physiology Group, Copenhagen Muscle Research Centre, Department of Exercise and Sport Sciences, Section of Human Physiology, University of Copenhagen, Copenhagen, Denmark; and 2The Biotechnology Centre of Oslo, University of Oslo, Blindern, Oslo, Norway

Submitted 20 July 2008 ; accepted in final form 15 May 2009

Conventional (c) protein kinase C (PKC) activity has been shown to increase with skeletal muscle contraction, and numerous studies using primarily pharmacological inhibitors have implicated cPKCs in contraction-stimulated glucose uptake. Here, to confirm that cPKC activity is required for contraction-stimulated glucose uptake in mouse muscles, contraction-stimulated glucose uptake ex vivo was first evaluated in the presence of three commonly used cPKC inhibitors (calphostin C, Gö-6976, and Gö-6983) in incubated mouse soleus and extensor digitorum longus (EDL) muscles. All potently inhibited contraction-stimulated glucose uptake by 50–100%, whereas both Gö compounds, but not calphostin C, inhibited insulin-stimulated glucose uptake modestly. AMP-activated protein kinase (AMPK) and eukaryotic elongation factor 2 phosphorylation was unaffected by the blockers. PKC{alpha} was estimated to account for ~97% of total cPKC protein expression in skeletal muscle. However, in muscles from PKC{alpha} knockout (KO) mice, neither contraction- nor phorbol ester-stimulated glucose uptake ex vivo differed compared with the wild type. Furthermore, the effects of calphostin C and Gö-6983 on contraction-induced glucose uptake were similar in muscles lacking PKC{alpha} and in the wild type. It can be concluded that PKC{alpha}, representing ~97% of cPKC in skeletal muscle, is not required for contraction-stimulated glucose uptake. Thus the effect of the PKC blockers on glucose uptake is either nonspecific working on other parts of contraction-induced signaling or the remaining cPKC isoforms are sufficient for stimulating glucose uptake during contractions.

protein kinase C


Address for reprint requests and other correspondence: E. A. Richter, Molecular Physiology Group, Copenhagen Muscle Research Centre, Dept. of Exercise and Sport Sciences, Section of Human Physiology, Univ. of Copenhagen, Universitetsparken 13, DK-2100 Denmark (e-mail: ERichter{at}ifi.ku.dk)






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