在对PrRP的食反应中,Prlhr/GPR10和Npffr2/GPR74的作用
Yi Wang1, Weiwei Qiu2, Stace Kernodle3
1Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA; Department of Metabolism and Endocrinology, National Clinical Research Center for Metabolic Diseases, the Second Xiangya Hospital, Central South University, Changsha, 410000, China.
Molecular metabolism
|January 4, 2025
概括
该研究发现,阻断两种PrRP受体 (Prlhr和Npffr2) 是必要的,以消除NTSPrlh神经元激活的抑制食欲的影响. 然而,PrRP 模拟 p52 独立于这些受体减少了食.
科学领域:
- 神经科学是一个神经科学.
- 内分泌学 在内分泌学.
- 肥胖问题研究研究
背景情况:
- 在NTS (孤独通道核) 中的神经元调节食物摄入.
- 在NTS中,表达前素释放激素 (Prlh) 的神经元 (NTSPrlh) 抑制食和体重,特别是在高脂肪饮食 (HFD) 中.
- Prlh编码神经PrRP,其信号与食欲控制有关.
研究的目的:
- 研究PrRP受体GPR10 (Prlhr) 和GPR74 (Npffr2) 在调解NTS神经元信号传递对食物摄入量和体重的影响中的作用.
- 要确定PrRP模拟物p52的厌食作用是否依赖Prlhr和Npffr2.2.
主要方法:
- 使用了缺乏PrRP受体GPR10 (Prlhr) 和/或GPR74 (Npffr2) 的转基因小鼠.
- 研究了NTSPrlh神经元 (NTSPrlhOX小鼠) 中增强Prlh表达对这些受体缺乏小鼠的食物摄入量和体重的影响.
- 用PrRP模拟物p52来评估其对食的影响,独立于研究的受体.
主要成果:
- 在受HFD养的对照小鼠中,PRLHR对于限制食物摄入量和体重至关重要.
- 为了消除在NTSPrlhOX小鼠中观察到的食物摄入限制,需要Prlhr和Npffr2的联合缺席.
- PrRP 模拟 p52 抑制了 Prlhr 和 Npffr2.2 的独立养.
结论:
- 无论是Prlhr还是Npffr2,都能促进NTSPrlh介导的食物摄入量和体重抑制.
- PrRP 模拟 p52 通过与 Prlhr 和 Npffr2.2 不同的系统发挥其厌食作用.
- 虽然Prlhr对生理体重增加的抑制至关重要,但当NTSPrlh信号增强时,任何受体都可以帮助减轻肥胖.
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