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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.

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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
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
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
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
Persistent URL http://hdl.handle.net/10536/DRO/DU:30031578

Document type: Journal Article
Collections: School of Medicine
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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.