de Ridder C M, Thijssen J H, Bruning P F, Van den Brande J L, Zonderland M L, Erich W B
Janus Jongbloed Research Centre, Department of Physiology and Sports Medicine, University of Utrecht, The Netherlands.
J Clin Endocrinol Metab. 1992 Aug;75(2):442-6. doi: 10.1210/jcem.75.2.1639945.
The rate at which girls progress through the stages of puberty in relation to body fat mass and body fat distribution and its relation to their hormonal profiles was studied. Sixty-eight schoolgirls participated in a longitudinal study during 3 yr. The girls were divided into subgroups with increasing skinfold thicknesses and waist-hip ratio. They were also grouped depending on Tanner's breast development classification (M2 and M3). The age at M2 was only marginally correlated with the menarcheal age, but the age at M2 and the time interval from that age to menarche was negatively correlated. Age at the onset of puberty was not related to body fat mass or distribution. The rate of pubertal development after pubertal stage M3 was negatively related to the body fat mass. Age at M2 was only correlated with estrone (E1), while the rate of pubertal development was associated with higher FSH, E1, estradiol (E2), the fraction of E2 that was not bound to sex-hormone-binding globulin (non-sex-hormone-binding globulin bound E2) and androstenedione plasma levels at the onset of puberty. Body fat distribution, rather than body fat mass was related to the total and the non-sex-hormone-binding globulin bound plasma levels of E2 and testosterone at the onset of puberty. Changes in body fat distribution in early female puberty were chiefly related to the waist circumferences. We found no evidence that body fat mass or body fat distribution triggers the onset of puberty. Body fat distribution was related to early pubertal endocrine activity. Body fat mass was negatively related to the rate of pubertal development toward menarche, but no clear indications for an endocrine-related process is found. We conclude that onset of puberty and menarche are not parallel pubertal events, and that early pubertal plasma E1, E2 and androstenedione levels are predictors for the rate of pubertal development toward menarche. We propose that the control of the onset of puberty and maturation of the hypothalamic-pituitary gonadal axis, with regard to negative feedback control, are at least partially independent. This induces on the average a "catch up" pubertal maturation in girls with a late onset of puberty.
研究了女孩青春期各阶段进展速度与体脂量、体脂分布的关系及其与激素水平的关系。68名女学生参与了一项为期3年的纵向研究。根据皮褶厚度和腰臀比增加将女孩分为亚组。还根据坦纳乳房发育分级（M2和M3）进行分组。M2时的年龄与初潮年龄仅呈微弱相关，但M2时的年龄以及从该年龄到初潮的时间间隔呈负相关。青春期开始的年龄与体脂量或分布无关。青春期M3阶段后的发育速度与体脂量呈负相关。M2时的年龄仅与雌酮（E1）相关，而青春期发育速度与青春期开始时较高的促卵泡生成素（FSH）、E1、雌二醇（E2）、未与性激素结合球蛋白结合的E2部分（非性激素结合球蛋白结合E2）和雄烯二酮血浆水平相关。青春期开始时，体脂分布而非体脂量与E2和睾酮的总血浆水平及非性激素结合球蛋白结合血浆水平相关。女性青春期早期体脂分布的变化主要与腰围有关。我们没有发现证据表明体脂量或体脂分布会触发青春期开始。体脂分布与青春期早期内分泌活动有关。体脂量与初潮前青春期发育速度呈负相关，但未发现与内分泌相关过程的明确迹象。我们得出结论，青春期开始和初潮不是平行的青春期事件，青春期早期血浆E1、E2和雄烯二酮水平是初潮前青春期发育速度的预测指标。我们提出，就负反馈控制而言，青春期开始和下丘脑 - 垂体 - 性腺轴成熟的控制至少部分是独立的。这平均会导致青春期开始较晚的女孩出现“追赶性”青春期成熟。
