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First published online April 18, 2008
Journal of Experimental Biology 211, 1448-1455 (2008)
Published by The Company of Biologists 2008
doi: 10.1242/jeb.014951
Role of the PGC-1 family in the metabolic adaptation of goldfish to diet and temperature
Department of Biology, Queen's University, Kingston, ON K7L 3N6, Canada
* Author for correspondence (e-mail: chris.moyes{at}queensu.ca)
Accepted 4 March 2008
In mammals, the peroxisome proliferator-activated receptor (PPAR) 
coactivator-1 (PGC-1) family members and their binding partners orchestrate
remodelling in response to diverse challenges such as diet, temperature and
exercise. In this study, we exposed goldfish to three temperatures (4, 20 and
35°C) and to three dietary regimes (food deprivation, low fat and high
fat) and examined the changes in mitochondrial enzyme activities and
transcript levels for metabolic enzymes and their genetic regulators in red
muscle, white muscle, heart and liver. When all tissues and conditions were
pooled, there were significant correlations between the mRNA for the PGC-1
coactivators (both 
and β) and mitochondrial transcripts (citrate
synthase), metabolic gene regulators including PPAR, PPARβ and
nuclear respiratory factor-1 (NRF-1). PGC-1β was the better predictor of
the NRF-1 axis, whereas PGC-1 was the better predictor of the PPAR axis
(PPAR, PPARβ, medium chain acyl CoA dehydrogenase). In contrast to
these intertissue/developmental patterns, the response of individual tissues
to physiological stressors displayed no correlations between mRNA for PGC-1
family members and either the NRF-1 or PPAR axes. For example, in skeletal
muscles, low temperature decreased PGC-1 transcript levels but
increased mitochondrial enzyme activities (citrate synthase and cytochrome
oxidase) and transcripts for COX IV and NRF-1. These results suggest that in
goldfish, as in mammals, there is a regulatory relationship between (i) NRF-1
and mitochondrial gene expression and (ii) PPARs and fatty acid oxidation gene
expression. In contrast to mammals, there is a divergence in the roles of the
coactivators, with PGC-1 linked to fatty acid oxidation through
PPAR, and PGC-1β with a more prominent role in mediating
NRF-1-dependent control of mitochondrial gene expression, as well as
distinctions between their respective roles in development and physiological
responsiveness.
Key words: PPAR, NRF-1, mitochondria, transcriptional regulation
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