Kythreotis Alexandros K, Nicolaou Marina, Mitsinga Eirini, Daher Habib, Skordis Nicos
Derby Hospital, Derby DE22 3NE, UK.
Addenbrookes Hospital, Cambridge CB2 0QQ, UK.
Children (Basel). 2025 May 25;12(6):679. doi: 10.3390/children12060679.
This overview explores the complex relationship between environmental factors, particularly obesity, and the timing of puberty, with a focus on how hormonal and genetic interactions are influenced by external conditions. Puberty (gonadarche) is characterised by the activation of the hypothalamic-pituitary-gonadal (HPG) axis. The onset and progression of puberty vary significantly among individuals, primarily due to genetic factors, with key genes like kisspeptin 1 () and makorin ring finger protein 3 () playing a crucial role. Cohesively, this paper emphasises that environmental factors, particularly obesity and exposure to endocrine-disrupting chemicals (EDCs), have become significant influences on the timing of puberty. Childhood obesity has risen significantly in recent decades and the age of pubertal onset has declined over the same period. Obesity greatly disrupts hormone regulation in pre-pubertal children. Leptin accelerates the onset of puberty in girls but not in boys. The underlying mechanism is proposed to be the increase in / signalling. On the contrary, excess leptin in boys suppresses testosterone production by increasing oestrogen conversion. Low adiponectin in obese girls may contribute to earlier puberty due to a reduced inhibition of / signalling. Low adiponectin in boys is linked to delayed puberty due to its role in maintaining insulin sensitivity and testosterone production. Hyperinsulinemia influences pubertal timing through central and peripheral mechanisms. Insulin acting synergistically with leptin promotes the earlier onset of puberty in girls but not in boys. The effects of exposure to certain EDCs-mostly obesogenic chemicals that mimic the action of natural hormones-on the timing of puberty remain unclear; hence, further research on this topic is needed. Addressing and preventing obesity in children could potentially mitigate these alterations in pubertal timing.
本综述探讨了环境因素，尤其是肥胖与青春期时间之间的复杂关系，重点关注外部条件如何影响激素和基因的相互作用。青春期（性腺发育）的特征是下丘脑 - 垂体 - 性腺（HPG）轴的激活。青春期的开始和进展在个体之间差异很大，主要是由于遗传因素，关键基因如亲吻素1（ ）和马克林环指蛋白3（ ）起着至关重要的作用。本文一致强调，环境因素，尤其是肥胖和接触内分泌干扰化学物质（EDCs），已成为青春期时间的重要影响因素。近几十年来，儿童肥胖率显著上升，同时青春期开始的年龄有所下降。肥胖极大地扰乱了青春期前儿童的激素调节。瘦素加速女孩青春期的开始，但对男孩没有影响。其潜在机制被认为是 / 信号的增加。相反，男孩体内过量的瘦素通过增加雌激素转化来抑制睾酮的产生。肥胖女孩中脂联素水平低可能由于对 / 信号的抑制减少而导致青春期提前。男孩中脂联素水平低与青春期延迟有关，因为它在维持胰岛素敏感性和睾酮产生方面发挥作用。高胰岛素血症通过中枢和外周机制影响青春期时间。胰岛素与瘦素协同作用促进女孩青春期提前开始，但对男孩没有影响。接触某些EDCs（大多是模拟天然激素作用的致肥胖化学物质）对青春期时间的影响仍不清楚；因此，需要对该主题进行进一步研究。解决和预防儿童肥胖可能会减轻青春期时间的这些变化。
