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PGC-1α and exercise: important partners in combating insulin resistance Russell, Aaron 2005, PGC-1α and exercise: important partners in combating insulin resistance, Current diabetes reviews, vol. 1, no. 2, pp. 175-181. Attached Files Name Description MIMEType Size Downloads Title PGC-1α and exercise: important partners in combating insulin resistance Author(s) Russell, Aaron Journal name Current diabetes reviews Volume number 1 Issue number 2 Start page 175 End page 181 Publisher Bentham Science Publishers Ltd Place of publication Bussum, Netherlands Publication date 2005 ISSN 1573-3998 Keyword(s) diabetes skeletal muscle PPAR mitochondria obesity Summary Diabetes and obesity are characterised by an impairment in mitochondrial function resulting in a decrease in glucose and fatty acid oxidation, respiration and an increase in intramuscular triglycerides (IMTG's) and insulin resistance. Peroxisome proliferator-activated receptor (PPAR)-ggr coactivator 1agr (PGC-1agr) is a nuclear transcriptional coactivator which regulates several important metabolic processes including, mitochondrial biogenesis, adaptive thermogenesis, respiration, insulin secretion and gluconeogenesis. In addition, PGC-1agr has been shown to increase the percentage of oxidative type I muscle fibres, with the latter responsible for the majority of insulin stimulated glucose uptake. PGC-1agr also co-activates PPAR's agr, bgr/dgr and ggr which are important transcription factors of genes regulating lipid and glucose metabolism. Exercise causes mitochondrial biogenesis, improves skeletal muscle fatty acid oxidation capacity and insulin sensitivity, therefore making it an important intervention for the treatment of insulin resistance. The expression of PGC-1agr mRNA is reduced in diabetic subjects, however, it is rapidly induced in response to interventions which signal alterations in metabolic requirements, such as exercise. Because of the important role of PGC-1agr in the control of energy metabolism and insulin sensitivity, it is seen as a candidate factor in the etiology of type 2 diabetes and a drug target for its therapeutic treatment. Language eng Field of Research 060199 Biochemistry and Cell Biology not elsewhere classified Socio Economic Objective 970106 Expanding Knowledge in the Biological Sciences HERDC Research category C1.1 Refereed article in a scholarly journal Copyright notice ©2005, Bentham Science Publishers Ltd Persistent URL http://hdl.handle.net/10536/DRO/DU:30004083 Document type: Journal Article Collections: School of Exercise and Nutrition Sciences Centre for Physical Activity and Nutrition Research 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. Versions Version Filter Type Wed, 14 Jan 2009, 10:43:18 EST Fri, 09 Apr 2010, 13:02:38 EST Tue, 10 Dec 2013, 14:44:53 EST Filtered Full Citation counts: Cited 13 times in Scopus Search Google Scholar Access Statistics: 438 Abstract Views, 0 File Downloads  -  Detailed Statistics Created: Mon, 07 Jul 2008, 09:11:35 EST

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