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在巨细胞中,乙氨基基和2型细胞因子信号调节功能色脂肪的发展

Yifu Qiu¹, Khoa D Nguyen¹, Justin I Odegaard¹

¹Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA 94158-9001, USA.

|June 7, 2014

概括

研究人员发现了一条新途径,涉及乙氨基酸和IL-4/13,激活色脂肪,以防御感冒和肥胖. 这一发现为治疗肥胖症提供了潜在的目标.

科学领域:

细胞生物学细胞生物学
免疫学免疫学免疫学
代谢过程中的代谢.

背景情况:

色脂肪,表达UCP1,可以抵御感冒和肥胖.
寒冷诱导的色脂肪的发育途径尚不清楚.

研究的目的:

为了识别控制色脂肪热生成的高效电路.
探索肥胖治疗的治疗潜力.

主要方法:

在小鼠中研究了冷诱导的色脂肪生物发生.
利用了对乙氨基细胞和IL-4/13信号传递的遗传损失.
给热中性小鼠使用IL-4.

主要成果:

鉴定出埃奥西诺菲尔,IL-4/13,以及替代性激活的巨细胞作为白色脂肪发热电路.
遗传或信号损失导致受寒感应的色脂肪形成受损.
在scWAT中的巨细胞激活诱导了用于色的catecholamine生产.
服用IL-4增加了色脂肪,改善了肥胖症.

结论:

发现了控制色脂肪生物生成的气流电路.
在冷诱导的色脂肪中证明了乙氨基和IL-4/13的作用.
提供了针对这种电路治疗肥胖症的证据.

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