类酸通过TGR5/cAMP信号通路抑制食欲
Shuang Liu1, Xiaoling Chen1, Daiwen Chen1
1Key Laboratory for Animal Disease-Resistance Nutrition of China Ministry of Education, Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu, Sichuan, PR China.
The Journal of nutritional biochemistry
|January 22, 2025
概括
氨酸 (OA) 通过激活高田G蛋白结合受体5 (TGR5) 和下丘脑中的循环腺单酸 (cAMP) 途径来抑制食欲,这为抗肥胖提供了潜在的策略.
科学领域:
- 内分泌学 在内分泌学.
- 神经科学是一个神经科学.
- 药理学 药理学是指药理学的学科.
背景情况:
- 肥胖是一个日益严重的健康问题,抑制食欲是管理的关键策略.
- 已知胆酸通过Takeda G蛋白结合受体5 (TGR5) 抑制食欲,但其下游信号分子循环腺单酸 (cAMP) 的作用尚未完全理解.
- 类酸 (OA) 是一种植物衍生的化合物,模仿胆酸,并呈现出潜在的治疗途径.
研究的目的:
- 为了研究食补充醇酸 (OA) 对食欲调节的影响.
- 阐明TGR5/cAMP信号通路在OA介导的食欲抑制中的作用.
- 探索OA对下丘脑食欲调节因子的影响.
主要方法:
- 在基本饮食的同时,小鼠被食补充了OA (50mg/kg,100mg/kg) 或tauroursodeoxycholic acid (TUDCA,30mg/kg) 的饮食.
- 分析了胃口刺激和抑制因素的下丘脑基因表达.
- 在用OA治疗的N38细胞中评估了TGR5激活和cAMP信号.
- 在OA治疗和TGR5/cAMP抑制后,测量了阿古蒂相关 (AgRP) 表达和分泌.
主要成果:
- 在小鼠中,OA和TUDCA补充剂都显著抑制了食欲.
- 甲醇和TUDCA改变了下丘脑基因表达,降低了食欲刺激剂的调节,并提高了食欲抑制剂的调节.
- 甲激活了下丘脑中的TGR5信号传递.
- 甲醇降低了阿古蒂相关 (AgRP) 的表达和分泌,这种效应因TGR5和cAMP抑制而减弱.
结论:
- 饮食中的醇酸 (OA) 有效地抑制食欲.
- 氨酸通过在下丘脑中激活TGR5/cAMP信号通路来发挥其抑制食欲的作用.
- 氧化可能通过调节下丘脑胃口控制机制来代表一种新的治疗肥胖症的药物.
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