ArticleFish physiology and biochemistry2019
GSK3β inhibition suppresses the hepatic lipid accumulation in Schizothorax prenanti.
Article in Fish physiology and biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Cold acclimation promotes the fatty acid desaturation and glycerophospholipid metabolism of the visceral adipose tissue in the Schizothorax prenanti.Fish physiology and biochemistry · 2026Article
- 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
- Oxidative damages and antioxidant defences after feeding a single meal in rainbow trout.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
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Abstract
Glycogen synthase kinase-3β (GSK3β) is a serine/threonine kinase involved in the regulation of embryonic development, glycogen metabolism, protein synthesis, mitosis, and apoptosis. To understand the role of GSK3β in hepatic lipid accumulation of Schizothorax prenanti, we used lithium chloride (LiCl), a GSK3β inhibitor, to inhibit the expression and activity of GSK3β. LiCl increased levels of phosphorylation of GSK3β (Ser9) and decreased the protein level of GSK3β. Plasma TG, TC, and LDL-C levels were greatly decreased after LiCl treatment. Additionally, GSK3β inhibition significantly reduced the levels of hepatic triglyceride (TG) and decreased the expression of lipogenesis-related genes in liver. Interestingly, LiCl decreased levels of phosphorylation of STAT3 (Tyr705), and then inhibited the activity of STAT3. These results indicate that in vivo LiCl treatment, which inhibited GSK3β activity, effectively decreased hepatic lipid accumulation through STAT3 in Schizothorax prenanti.
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