在高脂肪饮食养的小鼠中,SIRT1控制了肠内分泌原始细胞的增殖
Masaomi Miura1, Masaki Igarashi2, Ryosuke Isotani1
1Department of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Cellular and molecular gastroenterology and hepatology
|August 20, 2023
概括
肠道中的Sirtuin 1 (SIRT1) 通过通过Wnt/β-catenin信号传递控制原生细胞的增殖来调节肠内分泌细胞数量. 这一发现为代谢疾病治疗提供了新的见解.
科学领域:
- 代谢研究的研究.
- 细胞生物学 细胞生物学
- 胃肠病学 胃肠病学
背景情况:
- 肠内分泌细胞 (EECs) 在调节新陈代谢方面发挥着至关重要的作用.
- 增加EEC可能为2型糖尿病和肥胖症提供治疗潜力.
- 赛尔图因1 (SIRT1) 是一种关键的蛋白脱乙酶,参与细胞调节.
研究的目的:
- 研究SIRT1在调节肠道EECs数量的作用.
- 了解SIRT1如何影响EEC及其对代谢健康的贡献.
- 探索SIRT1调节对代谢障碍的治疗影响.
主要方法:
- 使用了具有特定Sirt1破坏 (VilKO,NgnKO) 或过度表达 (Sir2d) 的转基因小鼠.
- 进行高脂肪饮食 (HFD) 和评估代谢参数,如GLP-1和葡萄糖水平.
- 使用分子和组织学技术分析了肠道组织,EEC和有机体.
主要成果:
- 在肠表皮或原生细胞中SIRT1的干扰增加了HFD养小鼠的EEC和GLP-1产量.
- 相反,SIRT1过度表达或禁食会降低EEC和祖细胞增殖.
- 这些变化与Wnt/β-catenin信号的改变有关,抑制抑制了EEC的增加.
结论:
- 肠道SIRT1通过Wnt/β-catenin信号调节肠内分泌前体细胞 (EEPC) 增殖.
- 在饮食诱导的代谢条件下,SIRT1在控制EEC数量方面发挥了以前未知的作用.
- 向肠道SIRT1可能是针对肥胖和2型糖尿病的新疗法策略.
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