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选择性ERα减轻低垂体ER压力并调节高脂肪饮食的卵巢切除小鼠的能量平衡

Amr Ali Mohamed Abdelgawwad El-Sehrawy¹, Amirhosseinjaberi², Ehsan Zandi³

¹Internal medicine, Diabetes, Endocrinology and Metabolism, Mansoura University, Mansoura, Egypt.

Journal of biochemical and molecular toxicology

|August 21, 2025

概括

在肥胖小鼠中向激活雌激素受体α (ERα) 通过降低下丘脑内皮质网膜 (ER) 应激和增强素信号来降低体重和食物摄入量.

科学领域:

神经内分泌学
代谢调节
肥胖研究

背景情况:

肥胖源于能量失衡, 下丘脑对能量稳定至关重要.
雌激素受体α (ERα) 影响人体体重和能量摄入,但其精确的厌食机制尚不清楚.
下丘脑内质网膜 (ER) 的压力与肥胖的发病有关.

研究的目的:

在饮食引起的肥胖症中研究ERα激活对下丘脑ER压力的作用.
阐明ERα通过下丘脑路径调节能量摄入和体重的作用.

主要方法:

高脂肪饮食 (HFD) 诱导了卵巢切除 (OVX) 和卵巢完整的小鼠的肥胖.
在OVX-HFD小鼠中使用ERα激动剂 (PPT) 的治疗.
评估体重,能量摄入量,下丘脑神经Y (NPY),α-黑色素刺激激素 (α-MSH),瘦素信号传递 (JAK2/STAT3) 和ER压力标志物 (GRP78,ATF6).

主要成果:

卵巢切除加剧了HFD诱导的体重增加,增加了NPY,ER压力,并减少了α-MSH和瘦素信号.
在OVX-HFD小鼠中,PPT治疗显著降低了体重和能量摄入量.
PPT降低了下丘脑NPY,增加了α-MSH,降低了ER压力标志物,并增强了瘦素信号.

结论:

在高脂肪饮食的小鼠中,ERα激活可缓解肥胖.
激活ERα可以降低下丘脑的ER压力,并改善瘦素的敏感性.
有针对性的ERα调节是肥胖管理的潜在治疗策略.

关键词:

其他细胞内膜网应激大脑下垂体素的肥胖问题

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