GSK-3? at the Crossroads in Regulating Protein Synthesis and Lipid Deposition in Zebrafish.

ABSTRACT: In this study, the mechanism by which GSK-3? regulates protein synthesis and lipid deposition was investigated in zebrafish (Danio rerio). The vector of pEGFP-N1-GSK-3? was constructed and injected into the muscle of zebrafish. It was found that the mRNA and protein expression of tuberous sclerosis complex 2 (TSC2) was significantly increased. However, the mRNA and protein expression of mammalian target of rapamycin (mTOR), p70 ribosomal S6 kinase 1 (S6K1), and 4E-binding protein 1 (4EBP1) was significantly decreased by the pEGFP-N1-GSK-3? vector in the muscle of zebrafish. In addition, the mRNA and protein expression of ?-catenin, CCAAT/enhancer binding protein ? (C/EBP?), and peroxisome proliferators-activated receptor ? (PPAR?) was significantly decreased, but the mRNA expression of fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), ATP-citrate lyase (ACL), and HMG-CoA reductase (HMGCR) was significantly increased by the pEGFP-N1-GSK-3? vector. The activity of FAS, ACC, ACL, and HMGCR as well as the content of triglyceride (TG), total cholesterol (TC), and nonesterified fatty acids (NEFA) were significantly increased by the pEGFP-N1-GSK-3? vector in the muscle of zebrafish. The content of free amino acids Arg, Lys, His, Phe, Leu, Ile, Val, and Thr was significantly decreased by the pEGFP-N1-GSK-3? vector. The results indicate that GSK-3? may participate in regulating protein synthesis via TSC2/mTOR signaling and regulating lipid deposition via ?-catenin in the muscle of zebrafish (Danio rerio).

SUBMITTER: Gu Y 

PROVIDER: S-EPMC6468354 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature