Regulation of skeletal muscle oxidative capacity and insulin signaling by the Mitochondrial Rhomboid Protease PARL Civitarese, Anthony E., MacLean, Paul S., Carling, Stacy, Kerr-Bayles, Lyndal, McMillan, Ryan P., Pierce, Anson, Becker, Thomas C., Moro, Cedric, Finlayson, Jean, Lefort, Natalie, Newgard, Christopher B., Mandarino, Lawrence, Cefalu, William, Walder, Ken, Collier, Greg R., Hulver, Matthew W., Smith, Steven R. and Ravussin, Eric 2010, Regulation of skeletal muscle oxidative capacity and insulin signaling by the Mitochondrial Rhomboid Protease PARL, Cell metabolism, vol. 11, no. 5, pp. 412-426, doi: 10.1016/j.cmet.2010.04.004. Attached Files Name Description MIMEType Size Downloads walder-regulationof-2010.pdf Published version application/pdf 1.74MB 333 Title Regulation of skeletal muscle oxidative capacity and insulin signaling by the Mitochondrial Rhomboid Protease PARL Author(s) Civitarese, Anthony E. MacLean, Paul S. Carling, Stacy Kerr-Bayles, Lyndal McMillan, Ryan P. Pierce, Anson Becker, Thomas C. Moro, Cedric Finlayson, Jean Lefort, Natalie Newgard, Christopher B. Mandarino, Lawrence Cefalu, William Walder, Ken orcid.org/0000-0002-6758-4763 Collier, Greg R. Hulver, Matthew W. Smith, Steven R. Ravussin, Eric Journal name Cell metabolism Volume number 11 Issue number 5 Start page 412 End page 426 Total pages 15 Publisher Cell Press Place of publication Cambridge, Mass. Publication date 2010-05-05 ISSN 1550-4131 1932-7420 Keyword(s) humdisease Summary Type 2 diabetes mellitus (T2DM) and aging are characterized by insulin resistance and impaired mitochondrial energetics. In lower organisms, remodeling by the protease pcp1 (PARL ortholog) maintains the function and lifecycle of mitochondria. We examined whether variation in PARL protein content is associated with mitochondrial abnormalities and insulin resistance. PARL mRNA and mitochondrial mass were both reduced in elderly subjects and in subjects with T2DM. Muscle knockdown of PARL in mice resulted in malformed mitochondrial cristae, lower mitochondrial content, decreased PGC1α protein levels, and impaired insulin signaling. Suppression of PARL protein in healthy myotubes lowered mitochondrial mass and insulin-stimulated glycogen synthesis and increased reactive oxygen species production. We propose that lower PARL expression may contribute to the mitochondrial abnormalities seen in aging and T2DM. Language eng DOI 10.1016/j.cmet.2010.04.004 Field of Research 110306 Endocrinology Socio Economic Objective 920104 Diabetes HERDC Research category C1 Refereed article in a scholarly journal ERA Research output type C Journal article HERDC collection year 2010 Copyright notice ©2010, Elsevier Free to Read? Yes Persistent URL http://hdl.handle.net/10536/DRO/DU:30031578 Document type: Journal Article Collections: Faculty of Health School of Medicine Open Access Collection Related Links Link Description Connect to published version (restricted access) Go to link with your DU access privileges     Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved. Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au. Versions Version Filter Type Fri, 10 Dec 2010, 13:50:07 EST Mon, 13 Dec 2010, 08:27:42 EST Mon, 13 Dec 2010, 14:59:52 EST Tue, 14 Dec 2010, 08:52:36 EST Tue, 14 Dec 2010, 08:53:21 EST Tue, 14 Dec 2010, 08:54:40 EST Thu, 16 Jun 2011, 14:02:57 EST Mon, 15 Apr 2013, 13:48:45 EST Mon, 15 Apr 2013, 13:54:53 EST Mon, 19 Jan 2015, 11:15:07 EST Mon, 29 Jun 2015, 14:37:34 EST Tue, 05 Dec 2017, 10:45:12 EST Fri, 07 Sep 2018, 15:11:42 EST Filtered Full Citation counts:   Cited 61 times in TR Web of Science Cited 61 times in Scopus Search Google Scholar Access Statistics: 903 Abstract Views, 333 File Downloads  -  Detailed Statistics Created: Fri, 10 Dec 2010, 13:50:03 EST by Penny Andrews