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Endocrine Research Unit, Mayo Clinic and Foundation, Rochester, Minnesota 55905
Uncoupling protein (UCP)-2 and -3 mediate mitochondrial (mt) proton leak in vitro and are potential
regulators of energy expenditure and ATP production. Aging is
associated with alteration of tissue functions, suggesting impaired
mtATP production. To determine whether age-related changes in UCP
expression occur, we measured the transcript levels of UCP-2 and -3 in
skeletal muscle, liver, and heart in 6- and 27-mo-old rats. UCP-2
transcripts were higher in old animals in the white (+100%) and red
(+70%, both P < 0.04) gastrocnemius muscle and in the
liver (+300%, P < 0.03), whereas they were comparable
in the heart in both age groups. UCP-2 transcript levels correlated
positively with mitochondrial-encoded cytochrome c oxidase
transcripts normalized for mtDNA (P < 0.01) and
negatively with mtDNA copy number (P < 0.001). UCP-3
transcripts were lower in the less oxidative white (
50%,
P < 0.04) and unchanged in the more oxidative red
(15%, P = 0.41) gastrocnemius muscle in old animals.
Similar changes at protein level were confirmed by UCP-2 protein in
aging liver (+300%, P < 0.01) and UCP-2 (+85%, P < 0.05) and UCP-3 (30%, P = 0.4)
protein in aging mixed gastrocnemius muscle. Aging is thus associated
with tissue-specific changes of UCP-2 and -3 gene expression. Increased
UCP-2 expression may limit ATP production and is related to
mitochondrial gene expression in aging muscles and liver. Different
age-related changes may reflect differential regulation of UCP-2 and -3 in skeletal muscle. The current data suggest a potential role of
uncoupling proteins to alter energy production in aging tissues.
energy metabolism; mitochondria; adenosine 5'-triphosphate; proton leak
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