| Literature DB >> 31782040 |
Dongwu Liu1,2, Yaqi Gu3, Qiuxiang Pang3, Qiang Han4, Ao Li3, Weiwei Wu3, Xiuzhen Zhang3, Qilong Shi5, Lanlan Zhu5, Hairui Yu6, Qin Zhang7.
Abstract
In this study, the mechanism that VC inhibits lipid deposition through GSK-3β/mTOR signaling was investigated in the liver of Danio rerio. The results indicated that 0.5- and 1.0-g/kg VC treatments activated mTOR signaling by inhibiting GSK-3β expression. The mRNA expression of FAS, ACC, and ACL, as well as the content of TG, TC, and NEFA, was decreased by 0.5- and 1.0-g/kg VC treatments. Moreover, to confirm GSK-3β playing a key role in regulating TSC2 and mTOR, GSK-3β RNA was interfered and the activity of GSK-3β was inhibited by 25- and 50-mg/L LiCl treatments, respectively. The results indicated that GSK-3β inactivation played a significant role in inducing mTOR signaling and inhibiting lipid deposition. VC treatments could induce mTOR signaling by inhibiting GSK-3β, and mTOR further participated in regulating lipid deposition by controlling lipid profile in the liver of zebrafish.Entities:
Keywords: Danio rerio; GSK-3β; Lipid deposition; Liver; Vitamin C; mTOR
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Year: 2019 PMID： 31782040 DOI： 10.1007/s10695-019-00727-1
Source DB: PubMed Journal: Fish Physiol Biochem ISSN： 0920-1742 Impact factor: 2.794