Basic & Clinical Medicine ›› 2025, Vol. 45 ›› Issue (6): 714-719.doi: 10.16352/j.issn.1001-6325.2025.06.0714

• Original Articles • Previous Articles     Next Articles

Snhg3 improves glucose metabolism by promoting Sestrin2 expression in mice

ZHANG Minglong1, 2, GAO Mingyue2, XIE Xianghong2, GUO Zeyu2, LIU Xiaojun2, YAN Li1*   

  1. 1. Department of Pathophysiology; 2. Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences CAMS, School of Basic Medicine PUMC, Beijing 100005, China
  • Received:2025-02-27 Revised:2025-03-21 Online:2025-06-05 Published:2025-05-26

Abstract: Objective To investigate the role of long non-coding RNA-small nucleolar RNA host gene 3(lncRNA-Snhg3) and its regulatory mechanism in the hepatic glucose metabolism of mice. Methods Adenovirus Snhg3 was over-expressed by the tail vein injection in db/db mice, and then glucose tolerance and pyruvate tolerance were measured. The mRNA expression of mouse liver gluconeogenesis-related genes phosphoenolpyruvate carboxylase(Pepck) and glucose-6-phosphatase(G6pc) and stress-inducing protein 2(Sestrin2,Sesn2,a gene adjacent to Snhg3) were detected by RT-qPCR. The dual luciferase reporter assay was used to detect the effect of Snhg3 on the Sesn2 promoter activity in 293T cells. Results Snhg3 over-expression improved glucose tolerance and pyruvate tolerance in db/db mice. Snhg3 over-expression inhibited the mRNA of gluconeogenesis genes of Pepck(P<0.05) and G6pc(P<0.05), while promoted the mRNA of Sesn2(P<0.01). Meanwhile,Snhg3 over-expression promoted Sesn2 promoter activity in 293T cells(P<0.05). Conclusions Snhg3 improves glucose metabolism in mice by promoting Sestrin2 expression.

Key words: small nucleolar RNA host gene 3(Snhg3), hepatic gluconeogenesis, stress-inducing protein 2(Sestrin 2)

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