交感神经脂肪连接介导素驱动的脂解
Wenwen Zeng1, Roksana M Pirzgalska2, Mafalda M A Pereira2
1Laboratory of Molecular Genetics, The Rockefeller University, New York, NY 10021, USA; Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10021, USA.
Cell
|September 26, 2015
概括
瘦素激素通过同情神经直接接触脂肪细胞来触发脂肪的分解. 激活这些神经可以减少白色脂肪组织,
科学领域:
- 神经内分泌学
- 脂肪组织生物学
- 代谢调节
背景情况:
- 据悉,脂肪组织中的一个激素 - - 素 - - 刺激白脂肪的分解.
- 勒普调解脂质的确切机制,特别是神经通路的作用,需要进一步阐明.
研究的目的:
- 研究交感神经纤维在调解瘦素诱导的脂解中的作用.
- 描述神经脂肪结及其在脂肪代谢中的功能.
主要方法:
- 通过内存双光子显微镜可可视化神经脂肪相互作用.
- 对脂肪组织的交感输入的光遗传刺激.
- 基因操纵包括对多巴胺β-基酶的淘汰和对同情输入的切除.
主要成果:
- 交感神经纤维形成直接的神经脂肪结,包裹脂肪细胞.
- 这些神经的光遗传激活诱导局部脂解和减少白色脂肪质量.
- 对交感输入的切除或阻断了叶黄素刺激的脂解.
结论:
- 神经脂肪连接对于调解瘦素对白色脂肪组织的作用至关重要.
- 这些结点作为素作用的直接作用者.
- 向对脂肪组织的同情输入是一种潜在的减肥策略,可以绕过中枢素抵抗.
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