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Institute of Agriculture and Forestry (M.H., D.I., A.T., Yu.K.), University of Tsukuba, Tsukuba-shi, Ibaraki 305-8572, Japan; and Precursory Research for Embryonic Science and Technology (Ya.K.), Japan Science and Technology Agency, Kawaguchi, Saitama 332-0012, Japan
Address all correspondence and requests for reprints to: M. Hirabayashi, Institute of Agriculture and Forestry, University of Tsukuba, Tsukuba-shi, Ibaraki 305-8572, Japan. E-mail: mhira{at}sakura.cc.tsukuba.ac.jp.
Although birds lack brown adipose tissue, a thermogenic organ found in mammals, they possess other thermogenic mechanisms. In the current studies, we examined the molecular mechanisms of avian thermogenesis by studying how chicks acquire cold tolerance. We found that the acquisition of cold tolerance corresponded with an increase in the redness of the skeletal muscle, suggesting an increase in slow-twitch muscle fiber. This was confirmed by histological analysis. In addition, in chicks acquiring cold tolerance, there was an enhanced expression of the chicken homologue of peroxisome proliferator-activated receptor-
coactivator-1
, a protein involved in adaptive thermogenesis in mammalian brown adipose tissue and in slow-twitch fiber formation in mammalian skeletal muscle. Subtraction and differential display techniques further showed that, when chicks acquired cold tolerance, the expression of genes associated with slow-twitch fibers increased, whereas those associated with fast-twitch fibers decreased. There was also an enhanced expression of mitochondrial oxidative genes. Together, these results suggest that transformation of skeletal muscle fiber from fast-twitch to slow-twitch is involved in the acquisition of thermogenesis in chicks.
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