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Elevated mitochondrial biogenesis in skeletal muscle is associated with testosterone‐induced body weight loss in male mice
Author(s) -
Usui Taro,
Kajita Kazuo,
Kajita Toshiko,
Mori Ichiro,
Hanamoto Takayuki,
Ikeda Takahide,
Okada Hideyuki,
Taguchi Koichiro,
Kitada Yoshihiko,
Morita Hiroyuki,
Sasaki Tsutomu,
Kitamura Tadahiro,
Sato Takashi,
Kojima Itaru,
Ishizuka Tatsuo
Publication year - 2014
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2014.03.051
Subject(s) - mitochondrial biogenesis , endocrinology , medicine , skeletal muscle , testosterone (patch) , androgen receptor , coactivator , mitochondrion , adipose tissue , biology , brown adipose tissue , thermogenin , androgen , microbiology and biotechnology , transcription factor , prostate cancer , gene , hormone , biochemistry , cancer
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.