ArticleFish physiology and biochemistry2016
GSK-3b participates in the regulation of hepatic lipid deposition in large yellow croaker (Larmichthys crocea).
Article in Fish physiology and biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- Dual phosphorylation of glycogen synthase kinase 3β differentially integrates metabolic programs to determine T cell immunity across vertebrates.Cellular and molecular life sciences : CMLS · 2025Article
- Vitamin C inhibits lipid deposition through GSK-3β/mTOR signaling in the liver of zebrafish.Fish physiology and biochemistry · 2020Article
- GSK3β inhibition suppresses the hepatic lipid accumulation in Schizothorax prenanti.Fish physiology and biochemistry · 2019Article
- Duplication and gene expression patterns of β-catenin in Nile tilapia.Fish physiology and biochemistry · 2018Article
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5 authors at 1 institution in 1 country.
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Abstract
In this study, the participation of glycogen synthase kinase-3β (GSK-3β) in the lipid deposition was investigated in the liver of large yellow croaker (Larmichthys crocea) by LiCl treatment. It was found that the expression of GSK-3β and peroxisome proliferator-activated receptor-γ (PPARγ) was inhibited, but the expression of β-catenin was induced by LiCl treatment. Furthermore, the gene expression and activity of fatty acid synthetase (FAS) and lipoprotein lipase (LPL) in the liver was inhibited by LiCl treatment. The content of total cholesterol (TC), triglyceride (TG), and non-estesterified fatty acid in the liver, as well as TC, TG, and low-density lipoprotein cholesterol in plasma, was decreased by LiCl treatment. However, high-density lipoprotein cholesterol in plasma was increased, and the number of lipid droplets in the liver was decreased by LiCl treatment. The results indicate that GSK-3β/β-catenin may participate in regulating LPL and FAS through PPARγ in the liver of large yellow croaker, which will lead to the inhibition of hepatic lipid deposition.
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