van Weissenbruch M M, Delemarre-van de Waal H A
Department of Paediatrics, Research Institute for Clinical and Experimental Neurosciences, VU University Medical Centre, Amsterdam, The Netherlands.
Horm Res. 2006;65 Suppl 3:105-11. doi: 10.1159/000091514. Epub 2006 Apr 10.
Fetal growth retardation appears to be associated with an increased risk of premature adrenarche, early puberty, polycystic ovary syndrome and associated fertility problems. In a rat model of intrauterine growth retardation, based on ligation of the uterine arteries, the onset of puberty was delayed in female pups, with anovulation during the first cycle. The ovaries showed a lower number of follicles. The onset of puberty was also delayed in male pups. Testosterone production was lower in these growth-retarded rats compared with controls. The relationship between birth weight and the onset of puberty and pubertal progression in different cohorts of healthy children has been examined. In girls, no differences were observed in timing and progression of puberty, including age of menarche, between groups of different birth weights. In boys, a relatively delayed onset of puberty was observed in those with low birth weight, with a normally timed progression. In children with low birth weight, particularly boys, higher dehydroepiandrosterone levels were found compared with children with a normal birth weight, indicating an overactive adrenal gland in children with low birth weight. These data indicate that impaired fetal growth may have long-lasting effects on pubertal development. The fact that results of human studies on the relationship between fetal growth and the onset of puberty are often controversial may be explained by the heterogeneity of children born small for gestational age with respect to the intrauterine insult that they experience. From rat studies, it is clear that a serious intrauterine insult associated with growth failure can lead to dysregulation of puberty and gonadal function.
胎儿生长受限似乎与肾上腺初现提前、性早熟、多囊卵巢综合征及相关生育问题的风险增加有关。在基于子宫动脉结扎的宫内生长受限大鼠模型中，雌性幼崽的青春期开始延迟，且第一个周期无排卵。卵巢中的卵泡数量较少。雄性幼崽的青春期开始也延迟。与对照组相比，这些生长受限大鼠的睾酮生成较低。已对不同队列健康儿童的出生体重与青春期开始及青春期发育进程之间的关系进行了研究。在女孩中，不同出生体重组之间在青春期的时间和进程方面，包括月经初潮年龄，未观察到差异。在男孩中，出生体重低的个体青春期开始相对延迟，但发育进程时间正常。与出生体重正常的儿童相比，出生体重低的儿童，尤其是男孩，脱氢表雄酮水平较高，这表明出生体重低的儿童肾上腺功能亢进。这些数据表明，胎儿生长受损可能对青春期发育产生长期影响。关于胎儿生长与青春期开始之间关系的人体研究结果往往存在争议，这一事实可能是由于小于胎龄儿在宫内所经历的损伤存在异质性所致。从大鼠研究中可以清楚地看出，与生长失败相关的严重宫内损伤可导致青春期和性腺功能失调。
