调节脂肪组织的交感内置的丁-BDNF通路
Putianqi Wang1, Ken H Loh2, Michelle Wu1
1Laboratory of Molecular Genetics, Howard Hughes Medical Institute, The Rockefeller University, New York, NY, USA.
Nature
|July 24, 2020
概括
瘦素调节脂肪组织
科学领域:
- 代谢性疾病
- 神经内分泌学
- 脂肪组织生物学
背景情况:
- 瘦素基因突变导致肥胖和脂肪组织功能受损.
- 交感神经系统调节脂肪组织功能,如热生成和脂解.
- 莱普对交感功能的作用背后的机制是未知的.
研究的目的:
- 研究素在调节脂肪组织的交感内置中的作用.
- 阐明素对脂肪组织交感功能的神经通路.
- 确定参与瘦素调节能量平衡的下丘脑核.
主要方法:
- 研究肥胖小鼠和饮食诱导的肥胖小鼠.
- 使用慢性瘦素治疗.
- 在特定的神经元群体中利用了瘦素受体和BDNF基因的基因操纵.
- 评估了白色和棕色脂肪组织的同情内化.
主要成果:
- 瘦素缺乏会降低脂肪组织中的同情性内化.
- 莱普治疗恢复了交感内置,纠正了功能缺陷.
- 莱普的作用由下丘脑弧状核神经元 (AgRP和POMC) 和副腹核 (BDNF) 进行介导.
- 瘦素受体或BDNF的遗传删除会损害瘦素对内置的作用.
结论:
- 瘦素信号控制脂肪组织的交感内置可塑性.
- 一个涉及下垂体的神经通路对于莱普的作用至关重要.
- 这一途径对于维持能量平衡至关重要.
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