Irisin ameliorates hepatic glucose/lipid metabolism and enhances cell survival in insulin-resistant human HepG2 cells through adenosine monophosphate-activated protein kinase signaling
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- 作者：Wing Yan So ; zoe_sweet1012@hotmail.com" class="auth_mail" title="E-mail the corresponding author ; Po Sing Leung ; psleung@cuhk.edu.hk" class="auth_mail" title="E-mail the corresponding author
- 关键词：ACC ; acetyl-CoA-carboxylase ; AMPK ; adenosine monophosphate-activated protein kinase ; BrdU ; bromodeoxyuridine ; CaMKKβ ; Ca2+/calmodulin-dependent protein kinase kinase β ; ERK ; extracellular signal-regulated kinase ; FAS ; fatty acid synthase ; FNDC5 ; fibronectin type III domain containing 5 ; FoxO1 ; forkhead box protein O1 ; GSK3 ; glycogen synthase kinase 3 ; HGHI ; high glucose-high insulin ; LKB1 ; liver kinase B1 ; MEK ; mitogen-activated protein kinase ; NGNI ; normal glucose-normal insulin ; PEPCK ; phospho
- 刊名：International Journal of Biochemistry and Cell Biology
- 出版年：2016
- 出版时间：September 2016
- 年：2016
- 卷：78
- 期：Complete
- 页码：237-247
- 全文大小：2812 K
文摘
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Irisin activates LKB1/AMPK signaling pathway in HepG2 cells.
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Irisin ameliorates derangement of lipid and glucose metabolism via AMPK activation.
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Irisin alleviates hepatic insulin resistance via AMPK activation.
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Irisin enhances HepG2 cell survival through AMPK/ERK pathway.