Snhg3 improves glucose metabolism by promoting Sestrin2 expression in mice
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...
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| Main Author: | |
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| Format: | Article |
| Language: | zho |
| Published: |
Institute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College.
2025-06-01
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| Series: | Jichu yixue yu linchuang |
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| Online Access: | https://journal11.magtechjournal.com/Jwk_jcyxylc/fileup/1001-6325/PDF/1001-6325-2025-45-6-714.pdf |
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| Summary: | 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. |
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| ISSN: | 1001-6325 |