Key Laboratory for Animal Disease-Resistance Nutrition of China Ministry of Education, Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu, Sichuan, People's Republic of China.
Key Laboratory of Animal Disease-Resistant Nutrition of Sichuan Province, Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu, Sichuan, People's Republic of China.
Anim Biotechnol. 2022 Apr;33(2):330-338. doi: 10.1080/10495398.2021.1892709. Epub 2021 Mar 11.
Leucine can promote slow-twitch muscle fibers formation, and this effect may be mediated by AMPK signaling pathway. In addition, adiponectin (AdipoQ) plays an important role in regulation of muscle fiber type transformation. AdipoQ is located in the upstream of AMPK and its secretion can be regulated by leucine. Therefore, the aim of this study was to explore whether leucine affects muscle fiber type transformation through AdipoQ signaling pathway. Our data showed that 4 mM leucine significantly increased protein expression levels of slow MyHC, Myoglobin, Troponin I-SS, AdipoQ, AdipoR1, phospho-AMPK (p-AMPK) and PGC-1α and mRNA expression levels of AMPKα2, PGC-1α, AdipoQ and AdipoR1, and significantly decreased fast MyHC protein expression. In addition, 4 mM leucine significantly increased the SDH activity while significantly decreased the LDH activity. However, knockdown of AdipoR1 expression by AdipoR1-siRNA abolished leucine-induced upregulation of protein expressions of slow MyHC, AdipoR1, p-AMPK, PGC-1α and NRF1, mRNA expressions of MyHC I, MyHC IIa, AdipoR1, AMPKα2 and PGC-1α, ATP5G, TFAM and NRF1, and mtDNA level, as well as downregulation of protein expression of fast MyHC and mRNA expression of MyHC IIb. Together, our data revealed that leucine promotes muscle fiber type transformation from fast-twitch to slow-twitch through AdipoQ signaling pathway.
亮氨酸可以促进慢肌纤维的形成，这种作用可能是通过 AMPK 信号通路介导的。此外，脂联素（AdipoQ）在调节肌纤维类型转换中起着重要作用。AdipoQ 位于 AMPK 的上游，其分泌可以被亮氨酸调节。因此，本研究旨在探讨亮氨酸是否通过 AdipoQ 信号通路影响肌纤维类型转换。我们的数据表明，4mmol/L 的亮氨酸显著增加了慢肌肌球蛋白重链、肌红蛋白、肌钙蛋白 I-SS、AdipoQ、AdipoR1、磷酸化 AMPK（p-AMPK）和 PGC-1α 的蛋白表达水平，以及 AMPKα2、PGC-1α、AdipoQ 和 AdipoR1 的 mRNA 表达水平，同时显著降低了快肌肌球蛋白重链的蛋白表达。此外，4mmol/L 的亮氨酸显著增加了琥珀酸脱氢酶（SDH）的活性，同时显著降低了乳酸脱氢酶（LDH）的活性。然而，AdipoR1-siRNA 敲低 AdipoR1 表达后，亮氨酸诱导的慢肌肌球蛋白重链、AdipoR1、p-AMPK、PGC-1α 和 NRF1 的蛋白表达上调，MyHC I、MyHC IIa、AdipoR1、AMPKα2 和 PGC-1α、ATP5G、TFAM 和 NRF1 的 mRNA 表达，以及线粒体 DNA 水平的上调，以及快肌肌球蛋白重链蛋白表达的下调和 MyHC IIb 的 mRNA 表达的下调均被消除。综上所述，我们的数据表明，亮氨酸通过 AdipoQ 信号通路促进肌纤维类型从快肌向慢肌转化。
