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Up-Regulation of Uncoupling Protein 3 Gene Expression by Fatty Acids and Agonists for PPARs in L6 Myotubes

Department of Medicine and Clinical Science (C.S., K.H., J.M., J.F., S.Y., H.I., H.M., Y.O., T.H., H.I., H.N., G.I., Y.Yo., K.N.), Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan; and Department of Life Science (K.H., Y.Ya.), Kyoto University Graduate School of Human and Environmental Studies, Kyoto 606-8507, Japan

Address all correspondence and requests for reprints to: Dr. Kiminori Hosoda, Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan. E-mail: kh{at}kuhp.kyoto-u.ac.jp

Uncoupling protein 3 (UCP3), which uncouples electron transport from ATP synthesis, is expressed at high levels in the skeletal muscle, an important organ in glucose and lipid metabolism. Because several reports proposed that fatty acids induced UCP3 gene expression in skeletal muscle in vivo, in the present study we examined the regulation of UCP3 gene expression by various fatty acids using L6 myotubes. UCP3 gene expression was increased in L6 myotubes by various fatty acids or by -bromopalmitate, a nonmetabolized derivative of palmitic acid. Because fatty acids are also known as agonists for PPARs, we examined the involvement of PPARs in the regulation of the UCP3 gene expression. L-165041, a PPAR agonist, increased UCP3 gene expression in L6 myotubes, whereas neither Wy 14,643, a PPAR agonist, nor Pioglitazone, a PPAR agonist, increased it. Therefore, we conclude that UCP3 gene expression is increased by the activation of PPAR in L6 myotubes and postulate that PPAR mediates at least some part of the increased UCP3 gene expression by fatty acids in skeletal muscle in vivo.

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