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Am J Physiol Endocrinol Metab (September 9, 2008). doi:10.1152/ajpendo.90408.2008
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Submitted on April 30, 2008
Revised on August 19, 2008
Accepted on August 31, 2008

The Time Course of High Fat Diet Induced Reductions in Adipose Tissue Mitochondrial Proteins: Potential Mechanisms and the Relationship to Glucose Intolerance

Lindsey Sutherland1, Lauren Capozzi1, Joan Turchinsky1, Rhonda C. Bell1, and David C Wright1*

1 University of Alberta

* To whom correspondence should be addressed. E-mail: David.Wright{at}afhe.ualberta.ca.

Increasing evidence suggests that reduced adipose tissue mitochondrial content is associated with the pathogenesis of type 2 diabetes. These investigations have utilized severely insulin resistant rodent models. Thus, it is difficult to ascertain the potential mechanisms which initiate these changes and if reductions in adipose mitochondria are an initiating event in the development of impaired glucose homeostasis. Thus, we sought to determine the time course of high fat diet induced reductions of mitochondrial content in epididymal adipose tissue in relation to changes in purported mediators of mitochondrial biogenesis, and the development of impaired glucose homeostasis. Male Wistar rats were fed a high fat diet (~59% of Kcals from fat) for 2, 4 or 6 weeks. Six weeks of high fat feeding resulted in reductions in CORE1, COXIV, cytochrome C, HSP60, relative mtDNA copy number and PGC-1 expression. These changes were not associated with decreases in eNOS and AMPK or increases in markers of oxidative stress. Interestingly, ex vivo treatment of adipose tissue cultures with palmitate led to decreases in PGC-1 expression and COXIV and CORE1 protein content as observed in vivo. Thus, the high fat diet induced reductions in adipose tissue mitochondrial proteins may be mediated by increases in plasma fatty acids. Importantly, reductions in adipose tissue mitochondrial content occurred after the development of impaired glucose homeostasis. Thus, reductions in adipose tissue mitochondrial proteins are most likely not a causal event in the development of impaired glucose homeostasis.




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