| Literature DB >> 24726723 |
Taro Usui1, Kazuo Kajita1, Toshiko Kajita1, Ichiro Mori1, Takayuki Hanamoto1, Takahide Ikeda1, Hideyuki Okada1, Koichiro Taguchi1, Yoshihiko Kitada1, Hiroyuki Morita1, Tsutomu Sasaki2, Tadahiro Kitamura2, Takashi Sato3, Itaru Kojima4, Tatsuo Ishizuka5.
Abstract
Androgen reduces fat mass, although the underlying mechanisms are unknown. Here, we examined the effect of testosterone on heat production and mitochondrial biogenesis. Testosterone-treated mice exhibited elevated heat production. Treatment with testosterone increased the expression level of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α), ATP5B and Cox4 in skeletal muscle, but not that in brown adipose tissue and liver. mRNA levels of genes involved in mitochondrial biogenesis were elevated in skeletal muscle isolated from testosterone-treated male mice, but were down-regulated in androgen receptor deficient mice. These results demonstrated that the testosterone-induced increase in energy expenditure is derived from elevated mitochondrial biogenesis in skeletal muscle.Entities:
Keywords: Androgen receptor deficient mice; Mitochondrial biogenesis; Skeletal muscle; Testosterone
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Year: 2014 PMID: 24726723 DOI: 10.1016/j.febslet.2014.03.051
Source DB: PubMed Journal: FEBS Lett ISSN: 0014-5793 Impact factor: 4.124