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脂肪组织中尼古丁胺酸基转移酶的过度表达阻止了肥胖小鼠的代谢功能障碍

Daniel Ferguson, Elise I Gadson, Kathleen R Markan

bioRxiv : the preprint server for biology

|November 19, 2025

概括

在脂肪细胞中过度表达NAMPT可以通过改善NAD+水平和与肝脏的通信来保护雄性小鼠免受代谢功能障碍. 这突出了NAD+代谢通过细胞外囊泡影响肥胖的新方法.

科学领域:

代谢性疾病是一种代谢性疾病.
内分泌学在内分泌学.
分子生物学分子生物学

背景情况:

尼古丁胺胺氨基二核酸 (NAD+) 对于能量代谢至关重要.
尼古丁胺胺酸基转移酶 (NAMPT) 维持NAD+水平.
减少脂肪细胞NAMPT与衰老和肥胖中的代谢功能障碍有关.

研究的目的:

研究改变脂肪细胞NAMPT对小鼠代谢功能障碍和器官间通信的影响.
探索细胞外囊泡 (EVs) 在调解这些效应中的作用.

主要方法:

产生的脂肪细胞特异性NAMPT过度表达 (ANOV) 和淘汰赛 (ANKO) 鼠标模型.
评估了高脂肪饮食的代谢参数 (炎症,耐葡萄糖,胰岛素抵抗) 的反应.
分析了肝脏的胰岛素信号传递,NAD+含量和脂肪酸.
从小鼠模型中分离了EV,并测试了它们对HepG2细胞和WT肥胖小鼠的影响.

主要成果:

雄性ANOV小鼠被保护免受饮食诱导的代谢功能障碍.
雌性ANOV小鼠的保护性较低,可能是由于内源性NAMPT的高.
ANOV小鼠肝脏表现出改善的胰岛素信号传递,增加的NAD+含量和减少的脂肪酸.
来自ANOV小鼠的EV改善了HepG2胰岛素信号和肥胖小鼠的葡萄糖耐受性.
来自ANKO小鼠的EV抑制了HepG2胰岛素信号;抑制EV释放改善了ANKO雌性中的葡萄糖耐受性.

结论:

脂肪细胞NAMPT在调节全身代谢健康方面发挥着重要作用.
脂肪细胞中的NAD+代谢通过EVs影响器官间的通信,特别是与肝脏的通信.
向脂肪细胞的NAD+代谢和EV信号传递,为代谢功能障碍提供了一个潜在的治疗策略.

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