Arctigenin efficiently enhanced sedentary mice treadmill endurance.

Physical inactivity is considered as one of the potential risk factors for the development of type 2 diabetes and other metabolic diseases, while endurance exercise training could enhance fat oxidation that is associated with insulin sensitivity improvement in obesity. AMP-activated protein kinase (...

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Autores principales:	Xuan Tang, Jingjing Zhuang, Jing Chen, Liang Yu, Lihong Hu, Hualiang Jiang, Xu Shen
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/832be60fa0b840bc86627fea13390162
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spelling	oai:doaj.org-article:832be60fa0b840bc86627fea133901622021-11-18T06:47:09ZArctigenin efficiently enhanced sedentary mice treadmill endurance.1932-620310.1371/journal.pone.0024224https://doaj.org/article/832be60fa0b840bc86627fea133901622011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21887385/?tool=EBIhttps://doaj.org/toc/1932-6203Physical inactivity is considered as one of the potential risk factors for the development of type 2 diabetes and other metabolic diseases, while endurance exercise training could enhance fat oxidation that is associated with insulin sensitivity improvement in obesity. AMP-activated protein kinase (AMPK) as an energy sensor plays pivotal roles in the regulation of energy homeostasis, and its activation could improve glucose uptake, promote mitochondrial biogenesis and increase glycolysis. Recent research has even suggested that AMPK activation contributed to endurance enhancement without exercise. Here we report that the natural product arctigenin from the traditional herb Arctium lappa L. (Compositae) strongly increased AMPK phosphorylation and subsequently up-regulated its downstream pathway in both H9C2 and C2C12 cells. It was discovered that arctigenin phosphorylated AMPK via calmodulin-dependent protein kinase kinase (CaMKK) and serine/threonine kinase 11(LKB1)-dependent pathways. Mice treadmill based in vivo assay further indicated that administration of arctigenin improved efficiently mice endurance as reflected by the increased fatigue time and distance, and potently enhanced mitochondrial biogenesis and fatty acid oxidation (FAO) related genes expression in muscle tissues. Our results thus suggested that arctigenin might be used as a potential lead compound for the discovery of the agents with mimic exercise training effects to treat metabolic diseases.Xuan TangJingjing ZhuangJing ChenLiang YuLihong HuHualiang JiangXu ShenPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 8, p e24224 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Xuan Tang Jingjing Zhuang Jing Chen Liang Yu Lihong Hu Hualiang Jiang Xu Shen Arctigenin efficiently enhanced sedentary mice treadmill endurance.
description	Physical inactivity is considered as one of the potential risk factors for the development of type 2 diabetes and other metabolic diseases, while endurance exercise training could enhance fat oxidation that is associated with insulin sensitivity improvement in obesity. AMP-activated protein kinase (AMPK) as an energy sensor plays pivotal roles in the regulation of energy homeostasis, and its activation could improve glucose uptake, promote mitochondrial biogenesis and increase glycolysis. Recent research has even suggested that AMPK activation contributed to endurance enhancement without exercise. Here we report that the natural product arctigenin from the traditional herb Arctium lappa L. (Compositae) strongly increased AMPK phosphorylation and subsequently up-regulated its downstream pathway in both H9C2 and C2C12 cells. It was discovered that arctigenin phosphorylated AMPK via calmodulin-dependent protein kinase kinase (CaMKK) and serine/threonine kinase 11(LKB1)-dependent pathways. Mice treadmill based in vivo assay further indicated that administration of arctigenin improved efficiently mice endurance as reflected by the increased fatigue time and distance, and potently enhanced mitochondrial biogenesis and fatty acid oxidation (FAO) related genes expression in muscle tissues. Our results thus suggested that arctigenin might be used as a potential lead compound for the discovery of the agents with mimic exercise training effects to treat metabolic diseases.
format	article
author	Xuan Tang Jingjing Zhuang Jing Chen Liang Yu Lihong Hu Hualiang Jiang Xu Shen
author_facet	Xuan Tang Jingjing Zhuang Jing Chen Liang Yu Lihong Hu Hualiang Jiang Xu Shen
author_sort	Xuan Tang
title	Arctigenin efficiently enhanced sedentary mice treadmill endurance.
title_short	Arctigenin efficiently enhanced sedentary mice treadmill endurance.
title_full	Arctigenin efficiently enhanced sedentary mice treadmill endurance.
title_fullStr	Arctigenin efficiently enhanced sedentary mice treadmill endurance.
title_full_unstemmed	Arctigenin efficiently enhanced sedentary mice treadmill endurance.
title_sort	arctigenin efficiently enhanced sedentary mice treadmill endurance.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/832be60fa0b840bc86627fea13390162
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Arctigenin efficiently enhanced sedentary mice treadmill endurance.

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