PUBLICATION

Vitamin C inhibits lipid deposition through GSK-3β/mTOR signaling in the liver of zebrafish

Authors
Liu, D., Gu, Y., Pang, Q., Han, Q., Li, A., Wu, W., Zhang, X., Shi, Q., Zhu, L., Yu, H., Zhang, Q.
ID
ZDB-PUB-191130-15
Date
2019
Source
Fish physiology and biochemistry   46(1): 383-394 (Journal)
Registered Authors
Keywords
Danio rerio, GSK-3β, Lipid deposition, Liver, Vitamin C, mTOR
MeSH Terms
  • Animals
  • Ascorbic Acid*
  • Glycogen Synthase Kinase 3 beta/metabolism*
  • Lipid Metabolism
  • Lipids
  • Liver
  • Signal Transduction
  • TOR Serine-Threonine Kinases/metabolism*
  • Zebrafish/physiology*
  • Zebrafish Proteins/metabolism*
  • beta Catenin
PubMed
31782040 Full text @ Fish Physiol. Biochem.
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.
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