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脑下垂体FTO上调调节BDNF,通过PI3K/Akt通路促进GnRH的表达,从而导致早期的青春期

Shaolian Zang¹, Yang Ouyang¹, Pin Li¹

¹Department of Endocrinology, Shanghai Children's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.

Frontiers in endocrinology

|November 17, 2025

概括

脂肪质量和与肥胖相关的 (FTO) 蛋白质通过m6A脱甲基化调节来自大脑的神经营养因子 (BDNF),影响淋巴激素释放激素 (GnRH) 表达和青春期时间. 这一途径对于理解和治疗早期青春期至关重要.

科学领域:

神经内分泌学神经内分泌学
分子生物学分子生物学
发展生物学发展生物学

背景情况:

青春期的开始是由下丘脑内释放性腺激素 (GnRH) 的神经元调节的.
脂肪质量和与肥胖相关的 (FTO) 蛋白质在下丘脑m6A甲基化中的作用及其对青春期发育期间GnRH表达的影响正在调查中.
了解FTO对神经营养素的调节是澄清早期青春期分子通路的关键.

研究的目的:

调查FTO如何调节在下丘脑中的神经质蛋白功能.
阐明FTO影响GnRH表达的分子途径.
为了澄清早期青春期背后的机制.

主要方法:

在雌性大鼠中使用甲基化RNA免疫沉降测序 (MeRIP-seq) 评估下丘脑m6A甲基化.
在女孩中测量了血清脑衍生神经营养因子 (BDNF) 中央早期青春期 (CPP) 和对照.
使用动物模型进行FTO过度表达/敲击和脑内内 (ICV) BDNF输送,分析BDNF/PI3K/Akt信号通路.

主要成果:

脑下垂体GnRH和FTO表达增加,而m6A甲基化在青春期下降.
在老鼠的早期青春期,在弧形核 (ARC) 中观察到BDNF mRNA的减少m6A甲基化.
通过m6A脱甲基化,FTO通过积极调节BDNF表达,激活BDNF/PI3K/Akt通路并影响青春期的开始.

结论:

通过调节BDNF m6A脱甲基化和激活BDNF/PI3K/Akt通路,FTO促进了GnRH的表达.
在青春期开始时,BDNF起着至关重要的作用.
这些发现为开发早期青春期治疗策略提供了洞察力.

关键词:

大脑衍生神经营养因子 (BDNF)与脂肪质量和肥胖相关的 (FTO)发生性腺激素释放激素 (GnRH)m6A甲基化的情况.青春期开始青春期开始

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