Lycopene promotes a fast-to-slow fiber type transformation through Akt/FoxO1 signaling pathway and miR-22-3p
Autor: | Hui Yan, Bing Yu, Ping Zheng, Yuheng Luo, Wanxue Wen, Xiaoling Chen, Jun He, Daiwen Chen, Zhiqing Huang, Jie Yu |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
Medicine (miscellaneous) FOXO1 Muscle fiber type transformation Akt/FoxO1 signaling Wortmannin 03 medical and health sciences chemistry.chemical_compound Mice 0404 agricultural biotechnology Lycopene Downregulation and upregulation Lactate dehydrogenase miR-22-3p TX341-641 Protein kinase B 030109 nutrition & dietetics Nutrition and Dietetics Myogenesis Nutrition. Foods and food supply 04 agricultural and veterinary sciences musculoskeletal system 040401 food science Cell biology chemistry C2C12 myotubes Signal transduction Food Science |
Zdroj: | Journal of Functional Foods, Vol 80, Iss, Pp 104430-(2021) |
ISSN: | 1756-4646 |
Popis: | This study investigated molecular mechanisms of lycopene regulating muscle fiber type transformation in vitro and in vivo. Remarkably, TNNI1 protein level was increased, while TNNI2 protein level was decreased in C2C12 myotubes and in mice after lycopene treatment. Lycopene also enhanced enzyme activities of succinic dehydrogenase and malate dehydrogenase and reduced lactate dehydrogenase activity. Meanwhile, lycopene markedly upregulated the protein expressions of P-Akt and P-FoxO1 and decreased FoxO1 protein level. However, specific blocking Akt/FoxO1 signaling by wortmannin effectively eliminated lycopene-induced upregulation of slow MyHC and downregulation of fast MyHC in C2C12 myotubes. In addition, lycopene effectively inhibited miR-22-3p expression in C2C12 myotubes and in mice, whereas miR-22-3p mimics attenuated transformation from fast glycolytic fiber to slow oxidative fiber caused by lycopene. Our findings provided the first evidence that lycopene promoted muscle fiber type transformation from fast-twitch to slow-twitch through Akt/FoxO1 pathway and miR-22-3p. |
Databáze: | OpenAIRE |
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