雌激素通过NAMPT控制的ER应激路径防止年龄相关的色脂肪生成失败
bioRxiv : the preprint server for biology
|September 11, 2023
概括
雌激素 (E2) 治疗可以抵消与年龄相关的小鼠色脂肪细胞形成的下降. 这一过程涉及尼古丁胺酸基转移酶 (NAMPT) 信号,减轻ER压力和改善代谢健康.
科学领域:
- 代谢性疾病研究研究.
- 内分泌学 在内分泌学.
- 细胞生物学 细胞生物学
背景情况:
- 热生色脂肪细胞对代谢健康至关重要,但随着年龄的增长而下降.
- 与年龄相关的衰退会影响能量消耗和葡萄糖平衡.
- 雌激素 (E2) 水平随着年龄的增长而下降,可能有助于这种下降.
研究的目的:
- 研究雌激素 (E2) 在抵消与年龄相关的色脂肪细胞衰减中的作用.
- 阐明分子机制,包括NAMPT信号和ER压力,是E2对色脂肪细胞影响的基础.
主要方法:
- 用雌激素治疗老年小鼠 (E2).
- 评估色脂肪细胞的形成,能量消耗和耐葡萄糖的评价.
- 对NAMPT信号和ER压力标志物的调查.
- 对NAMPT信号的遗传和药理向.
主要成果:
- 在老年小鼠中,雌激素 (E2) 治疗恢复了寒冷诱导的色脂肪细胞形成.
- E2治疗增加了能量消耗和改善了葡萄糖耐受性.
- 尼古丁胺酸基转移酶 (NAMPT) 被确定为E2诱导的色脂肪生成的关键媒介.
- 向NAMPT信号恢复了色脂肪细胞的形成,通过增加周周血管脂肪细胞的前代细胞和抑制ER压力.
结论:
- 雌激素 (E2) 和NAMPT信号抗击与年龄相关的色脂肪细胞功能障碍.
- 准NAMPT信号可以通过增加原生细胞来恢复色脂肪细胞的形成.
- E2-NAMPT控制的ER压力是依赖年龄的色脂肪细胞损伤的关键调节者.
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