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Am J Physiol Regul Integr Comp Physiol (January 23, 2003). doi:10.1152/ajpregu.00579.2002
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Submitted on September 17, 2002
Accepted on January 18, 2003

Tissue-specific depression of mitochondrial proton leak and substrate oxidation in hibernating arctic ground squirrels

Jamie L Barger1*, Martin D Brand2, Brian M Barnes3, and Bert B Boyer3

1 Institute of Arctic Biology, University of Alaska Fairbanks, Fairbanks, AK, USA; Wisconsin Primate Research Center, University of Wisconsin Madison, Madison, WI, USA
2 Medical Research Council, Dunn Human Nutrition Unit, Cambridge, United Kingdom
3 Institute of Arctic Biology, University of Alaska Fairbanks, Fairbanks, AK, USA

* To whom correspondence should be addressed. E-mail: jbarger{at}primate.wisc.edu.

A significant proportion of standard metabolic rate is devoted to driving mitochondrial proton leak, and this futile cycle may be a site of metabolic control during hibernation. To determine if the proton leak pathway is decreased during metabolic depression related to hibernation, mitochondria were isolated from liver and skeletal muscle of non-hibernating (active) and hibernating arctic ground squirrels (Spermophilus parryii). At an assay temperature of 37°C, state 3 and state 4 respiration rates and state 4 membrane potential were significantly depressed in liver mitochondria isolated from hibernators. In contrast, state 3 and state 4 respiration rates and membrane potentials were unchanged during hibernation in skeletal muscle mitochondria. The decrease in oxygen consumption of liver mitochondria was achieved by reduced activity of the set of reactions generating the proton gradient but not by a lowered proton permeability. These results suggest that mitochondrial proton conductance is unchanged during hibernation and that the reduced metabolism in hibernators is a partial consequence of tissue-specific depression of substrate oxidation.




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