Chronic AMPK activity dysregulation produces myocardial insulin resistance in the human Arg302Gln-PRKAG2 glycogen storage disease mouse model

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dc.contributor.authorThorn, Stephanie L
dc.contributor.authorGollob, Michael H
dc.contributor.authorHarper, Mary-Ellen
dc.contributor.authorBeanlands, Rob S
dc.contributor.authorDekemp, Robert A
dc.contributor.authorDaSilva, Jean N
dc.date.accessioned2014-10-01T02:16:07Z
dc.date.available2014-10-01T02:16:07Z
dc.date.created2013
dc.date.issued2013
dc.identifier.citationThorn et al. EJNMMI Research 2013, 3:48
dc.identifier.urihttp://hdl.handle.net/10393/31668
dc.identifier.urihttp://www.ejnmmires.com/content/3/1/48
dc.description.abstractThe cardiac PRKAG2 mutation in the γ2-subunit of adenosine monophosphate activated kinase (AMPK) is characterized by excessive glycogen deposition, hypertrophy, frequent arrhythmias, and progressive conduction system disease. We investigated whether myocardial glucose uptake (MGU) was augmented following insulin stimulation in a mouse model of the PRKAG2 cardiac syndrome.
dc.language.isoen
dc.titleChronic AMPK activity dysregulation produces myocardial insulin resistance in the human Arg302Gln-PRKAG2 glycogen storage disease mouse model
dc.typeArticle
dc.identifier.doi10.1186/2191-219X-3-48
CollectionPublications en libre accès financées par uOttawa // uOttawa financed open access publications

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