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由POMC神经元产生的IL-17A调节了饮食引起的肥胖症

Rosa Gallo¹, Ana Teijeiro¹, Mariana Angulo-Aguado¹

¹Growth Factors, Nutrients and Cancer Group, Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas, CNIO, 28029 Madrid, Spain.

|July 19, 2024

概括

干白素-17A (IL-17A) 通过亲opiomelanocortin (POMC) 神经元不会直接导致肥胖. 相反,POMC神经元产生IL-17A,这表明这些细胞与肥胖中的内分泌调节之间存在新的联系.

科学领域:

神经内分泌学神经内分泌学
免疫学免疫学免疫学
代谢性疾病研究研究

背景情况:

肥胖与低级炎症和IL-17A (IL-17A) 相关.
亲opiomelanocortin (POMC) 神经元调节养行为.
肥胖症中IL-17A和POMC神经元之间的相互作用尚未得到充分理解.

研究的目的:

在肥胖的背景下,研究IL-17A信号在POMC神经元中的作用.
为了确定IL-17A是否通过POMC神经元直接影响体重和脂肪.

主要方法:

在POMC神经元中产生IL-17A受体缺失的小鼠 (Il17ra-flox和Pomc-Cre).
评估体重,脂肪和基因表达,以应对高脂肪饮食.
分析了POMC神经元内的IL-17A表达.

主要成果:

在POMC神经元中删除IL-17A受体并没有改变体重或脂肪.
有Pomc-Cre转基因的小鼠显示体重增加和脂肪减少,独立于IL-17A信号传递.
发现POMC神经元表达IL-17A,而减少的POMC神经元数量与减少的IL-17A表达相关.

结论:

通过直接通过POMC神经元发出信号,IL-17A似乎不会诱导肥胖.
转基因Pomc-Cre本身可能会影响体重调节.
在产生IL-17A的POMC神经元和控制肥胖的内分泌系统之间存在一种新的交叉声.

关键词:

遗传学是一个遗传学.免疫学免疫学免疫学分子生物学分子生物学神经科学是一个神经科学.

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