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GSK3β inhibition suppresses the hepatic lipid accumulation in Schizothorax prenanti

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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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Funding

This study was supported by the grants from the National Natural Science Foundation of China (31602148).

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Contributions

L.W. and Y.W. conceived and designed the experiments; X.Z. performed the experiments; L.W. wrote the paper; W. L., L.Z., and S.Y. analyzed the data; and Z.L. and D.C. contributed reagents/materials/analysis tools.

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Correspondence to Linjie Wang.

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All research involving animals was conducted according to the Regulations for the Administration of Affairs Concerning Experimental Animals (Ministry of Science and Technology, China, revised in June 2004) and approved by the Institutional Animal Care and Use Committee at the College of Animal Science and Technology, Sichuan Agricultural University, Sichuan, China, under permit No. DKYB20110807.

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The authors declare that they have no competing interests.

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Wang, Y., Zhan, X., Luo, W. et al. GSK3β inhibition suppresses the hepatic lipid accumulation in Schizothorax prenanti. Fish Physiol Biochem 45, 1953–1961 (2019). https://doi.org/10.1007/s10695-019-00691-w

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  • DOI: https://doi.org/10.1007/s10695-019-00691-w

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