A longitudinal assessment of hormonal and physical alterations during normal puberty in boys .5. Rising leptin levels may signal the onset of puberty
A longitudinal assessment of hormonal and physical alterations during normal puberty in boys .5. Rising leptin levels may signal the onset of puberty
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DOI：
10.1210/jc.82.4.1066
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发表时间：
1997-04-01
影响因子：
5.8
通讯作者：
Rogol, AD
中科院分区：
文献类型：
--
作者：
Mantzoros, CS;Flier, JS;Rogol, AD
瘦素是ob基因的产物，是一种脂肪细胞衍生的激素，它向大脑发出脂肪组织能量储存量的信号，并对能量稳态和神经内分泌功能产生重大影响。瘦素最近被证明会影响瘦素缺乏和正常啮齿类动物的生殖功能。由于青春期（性成熟和生殖能力的获得过程）被认为是由达到临界数量和/或脂肪分布触发的，我们研究了循环瘦素水平的变化是否可以代表触发人类青春期开始的激素信号。8名青春期前男孩（Tanner生殖器发育阶段1或研究开始时的Tanner生殖器发育阶段2早期）根据Tanner生殖器发育阶段5的时间进行了2.5-5.1年的纵向评估。在研究期间，每4个月采集一次血清，用于测定瘦素、睾酮和硫酸脱氢表雄酮。与青春期前基线水平（青春期开始前8个月，由睾酮初始升高高于检测限定义）相比，瘦素水平在青春期开始前上升了约50%，在青春期开始后下降到接近基线值（P < 0.01，方差分析），保持稳定超过2年。这些变化发生在体重指数不断增加的情况下（P < 0.05，方差分析）。瘦素与硫酸脱氢表雄酮浓度之间无显著关联。总之，循环瘦素的水平与这种分子是触发青春期开始的重要信号的假设是一致的。在青春期开始前瘦素水平激增的刺激因素目前尚不清楚。
Leptin, the product of the ob gene, is an adipocyte-derived hormone that signals the amount of adipose tissue energy stores to the brain and exerts major effects on energy homeostasis and neuroendocrine function. Leptin has recently been shown to affect reproductive function in leptin-deficient and normal rodents. As puberty, the process of sexual maturation and acquisition of reproductive competence, has been proposed to be triggered by the attainment of a critical amount and/or distribution of fat, we examined whether changes in circulating leptin levels could represent the hormonal signal responsible for triggering the onset of puberty in humans. Eight prepubertal boys (Tanner genital stage 1 or early stage 2 at the initiation of the study) were evaluated longitudinally for 2.5-5.1 yr depending on when Tanner stage 5 of genital development was achieved. Sera for the determination of leptin, testosterone, and dehydroepiandrosterone sulfate were obtained every 4 months during the period of the study. Com pared to baseline prepubertal levels (8 months before the onset of puberty, as defined by the initial rise in testosterone above the detection limit of the assay), leptin levels rose by approximately 50% just before the onset of puberty and decreased to approximately baseline values after the initiation of puberty (P < 0.01, by ANOVA), remaining stable for more than 2 yr. These changes occurred despite constantly increasing body mass index (P < 0.05, by ANOVA). No significant association between leptin and dehydroepiandrosterone sulfate concentrations was detected. in conclusion, the levels of circulating leptin are consistent with the hypothesis that this molecule is an important signal responsible for triggering the onset of puberty. The stimulus for a surge in leptin levels just before the onset of puberty is currently unknown.