Volume 28, Issue S1 820.1
Nutrition
Free Access

PGC-1α-mediated branched-chain amino acid metabolism in the skeletal muscle (820.1)

Yukino Hatazawa

Yukino Hatazawa

Tokyo Medical and Dental University, Tokyo, Japan

Kyoto Prefectural University, Kyoto, Japan

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Miki Tadaishi

Miki Tadaishi

National Institute of Health and Nutrition, Tokyo, Japan

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Yuta Nagaike

Yuta Nagaike

University of Shizuoka, Shizuoka, Japan

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Akihito Morita

Akihito Morita

University of Shizuoka, Shizuoka, Japan

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Yoshihiro Ogawa

Yoshihiro Ogawa

Tokyo Medical and Dental University, Tokyo, Japan

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Osamu Ezaki

Osamu Ezaki

Showa Women’s University, Tokyo, Japan

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Yasuyuki Kitaura

Yasuyuki Kitaura

Nagoya University, Nagoya, Japan

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Yoshiharu Shimomura

Yoshiharu Shimomura

Nagoya University, Nagoya, Japan

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Yasutomi Kamei

Yasutomi Kamei

Kyoto Prefectural University, Kyoto, Japan

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Shinji Miura

Shinji Miura

University of Shizuoka, Shizuoka, Japan

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Abstract

PGC-1α is a co-activator of various nuclear receptors and other transcription factors. In skeletal muscles, the role of PGC-1α in fibre type specificity, mitochondrial biogenesis, angiogenesis and improved exercise performance has been demonstrated. Branched-chain amino acid (BCAA) metabolism primarily occurs in the skeletal muscles. In this study, microarray analysis revealed that the BCAA catabolic pathway was co-ordinately activated in the skeletal muscles of transgenic mice overexpressing PGC-1α. Using murine skeletal muscle and cultured cells overexpressing PGC-1α, we investigated whether PGC-1α stimulates BCAA metabolism by increasing the expression of enzymes involved in BCAA metabolism. Transgenic mice specifically overexpressing PGC-1α in the skeletal muscles increased the expression of branched-chain aminotransferase (BCAT) 2 and branched-chain α-keto acid dehydrogenase (BCKDH), which catabolize BCAA. The amount of BCAA in the skeletal muscles was significantly decreased in the transgenic mice compared with that in the wild-type mice, suggesting the activation of muscle BCAA metabolism by PGC-1α. In C2C12 myoblast cells, the overexpression of PGC-1α significantly increased the expression of BCAT2 and BCKDH. In conclusion, PGC-1α in the skeletal muscles is likely to contribute significantly to BCAA metabolism.