诺奇-PDGFRβ轴抑制棕色脂肪细胞前代的分化在早期产后小鼠
Zuoxiao Shi1, Shaolei Xiong2, Ruoci Hu1
1Department of Physiology and Biophysics, College of Medicine, University of Illinois Chicago, Chicago, IL 60612, USA; Department of Pharmaceutical Sciences, University of Illinois Chicago, Chicago, IL 60612, USA.
Developmental cell
|April 3, 2024
概括
研究人员确定了负责棕色脂肪发育的特定细胞. 抑制这些细胞中的Notch信号促进棕色脂肪生成,可能对抗肥胖和糖尿病.
科学领域:
- 细胞生物学 细胞生物学
- 代谢疾病研究研究
背景情况:
- 棕色脂肪生成对代谢健康至关重要,但原始细胞的身份和调节仍然不清楚.
- 了解棕色脂肪细胞原始细胞 (APC) 是开发肥胖和糖尿病治疗的关键.
研究的目的:
- 为了确定特定的原始细胞和调节机制驱动棕色脂肪生成.
- 研究Notch/PDGFRβ轴在调节棕色脂肪组织 (BAT) 扩张和代谢功能的作用.
主要方法:
- 在体内谱系追踪和小鼠模型被用来追踪祖细胞的贡献.
- 在特定的细胞群中对Notch信号进行了操纵.
- 在接受高脂肪,高糖饮食的小鼠中进行了代谢评估.
主要成果:
- 血小板衍生生长因子受体β (PDGFRβ) + 皮质细胞产生发育性棕色脂肪细胞,而T-box 18 (TBX18) + 皮质细胞在整个生命中以特定的存储方式贡献.
- 在PDGFRβ+细胞周围细胞中隙抑制通过降低PDGFRβ的调节促进棕色脂肪生成.
- 抑制PDGFRβ+细胞中的Notch信号改善了高脂肪,高糖饮食的小鼠的葡萄糖和代谢障碍.
结论:
- 诺奇/PDGFRβ轴负面调节发育性棕色脂肪生成.
- 这一轴的抑制促进棕色脂肪组织的扩张,增强新陈代谢健康,为肥胖和糖尿病提供治疗潜力.
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