You Xiaoqing, Yang Wei, Li Xiuyun, Li Xiaoli, Huang Ying, Huang Congfu
Department of Pediatrics, Fuzhou First General Hospital Affiliated With Fujian Medical University, Fuzhou, Fujian, China.
Department of Pediatrics, Shenzhen Baoan Clinical Medical College of Guangdong Medical University (The People's Hospital of Baoan Shenzhen), Shenzhen, China.
J Endocrinol Invest. 2025 Jun 17. doi: 10.1007/s40618-025-02615-3.
The global rise in early pubertal activation is closely linked to dietary patterns and gut microbiota (GM) dysbiosis. This review synthesizes evidence on how GM-derived metabolites modulate hypothalamic maturation and pubertal timing through the gut-brain axis.
Following PRISMA guidelines, we conducted a systematic review of human and animal studies (PubMed, Medline, CNKI, Wanfang) up to October 2024, focusing on dietary impacts (high-fat/high-sugar) on GM composition and puberty onset. Inclusion criteria prioritized studies linking GM metabolites to HPGA activation.
High-fat/high-sugar diets reduce GM diversity and short-chain fatty acid (SCFA) production (e.g., butyrate, acetate), impair gut barrier integrity, and promote systemic inflammation. Dysbiosis in SCFA-producing taxa (Roseburia, Faecalibacterium) and neurotransmitter-modulating genera (Bifidobacterium, Lactobacillus) disrupts leptin/insulin signaling and kisspeptin-GnRH interactions, accelerating HPGA activation. Animal studies demonstrate SCFA supplementation delays puberty by reducing hypothalamic inflammation, while human data reveal ethnic and dietary variability in GM profiles. Western diets heighten altered pubertal timing risk via GM-mediated HPGA dysregulation, whereas fiber-rich Mediterranean diets exhibit protective effects.
GM dysbiosis and SCFA depletion are pivotal in diet-driven alterations of pubertal timing. Culturally adapted interventions targeting microbiota-metabolite interactions may mitigate risks of early puberty onset.
青春期过早启动的全球趋势与饮食模式和肠道微生物群（GM）失调密切相关。本综述综合了关于GM衍生代谢物如何通过肠-脑轴调节下丘脑成熟和青春期时间的证据。
遵循PRISMA指南，我们对截至2024年10月的人类和动物研究（PubMed、Medline、CNKI、万方）进行了系统综述，重点关注饮食（高脂肪/高糖）对GM组成和青春期开始的影响。纳入标准优先考虑将GM代谢物与下丘脑-垂体-性腺轴（HPGA）激活联系起来的研究。
高脂肪/高糖饮食会降低GM多样性和短链脂肪酸（SCFA）的产生（如丁酸、乙酸），损害肠道屏障完整性，并促进全身炎症。产生SCFA的类群（罗斯氏菌属、粪杆菌属）和调节神经递质的属（双歧杆菌属、乳酸杆菌属）的失调会破坏瘦素/胰岛素信号传导和促性腺激素释放激素（Kisspeptin-GnRH）相互作用，加速HPGA激活。动物研究表明，补充SCFA可通过减轻下丘脑炎症来延迟青春期，而人类数据显示GM谱存在种族和饮食差异。西方饮食通过GM介导的HPGA失调增加青春期时间改变的风险，而富含纤维的地中海饮食则具有保护作用。
GM失调和SCFA消耗在饮食驱动的青春期时间改变中起关键作用。针对微生物群-代谢物相互作用的文化适应性干预措施可能会降低青春期过早开始的风险。
