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根据能量平衡,表达神经Y神经元的弧形丁受体的功能发生变化

Nicola J Lee¹, Jennifer Oraha², Yue Qi³

¹Charles Perkins Centre, School of Medical Sciences, Faculty of Medicine and Health, University of Sydney, NSW, Australia; Garvan Institute of Medical Research, NSW, Australia; St Vincent's Clinical School, UNSW Sydney, NSW, Australia.

Molecular metabolism

|August 10, 2023

概括

通过NPY+神经元传递勒素信号可以促进脂肪燃烧和骨质. 然而,在高脂肪饮食下抗素可能会导致NPY负的神经元增加食物摄入量和体重.

科学领域:

神经科学是一个神经科学.
代谢过程中的代谢.
内分泌学在内分泌学.

背景情况:

素是能量恒温的关键调节剂,主要作用于下丘脑神经Y (NPY) 神经元.
在Npy神经元中选择性删除瘦素受体 (Lepr) 显著改变了脂肪和骨质之间的能量分区.
在能量平衡中,Npy-阳性Lepr (Npy+/Lepr+) 与Npy-负性Lepr (Npy-/Lepr+) 神经元的不同作用仍然不清楚.

研究的目的:

研究Npy+/Lepr+和Npy-/Lepr+神经元在调节养行为,能量恒温和身体组成方面的特定功能.
阐明了通过不同的下丘脑神经元群体传递勒丁信号的差异效应.

主要方法:

在男性Lepr^Cre/+和Lepr^Cre/+;Npy^Flp/+小鼠中利用了与腺相关的病毒载体的DREADD和INTRSECT技术.
评估了选择性激活Npy+/Lepr+或Npy-/Lepr+神经元对生理参数的影响.

主要成果:

激活Npy+/Lepr+神经元降低了呼吸系数,增加了食物摄入量 (在食小鼠中),并增强了棕色脂肪组织热生成和葡萄糖耐受性.
在高脂肪饮食 (HFD) 条件下,Npy-/Lepr+神经元的刺激增加了食物摄入量,体力活动和能量消耗.
慢性Npy+/Lepr+神经元刺激会增加骨质,而不影响体重,而Npy-/Lepr+刺激会增加体重和脂肪量.

结论:

通过Npy+/Lepr+神经元传递勒素信号,通过促进热生成,能量消耗和脂肪利用来调节能量分区.
长期HFD期间的勒素耐药性可能会将影响转移到Npy-/Lepr+神经元,可能会加剧过度进食和体重增加.

关键词:

骨头骨头骨头骨头这是一个可怕的恐惧.食物摄入量食物摄入量勒普丁是一种激素.没有任何的 Npy.热生成是一种热生成.

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