A longitudinal assessment of hormonal and physical alterations during normal puberty in boys. V. Rising leptin levels may signal the onset of puberty.
A longitudinal assessment of hormonal and physical alterations during normal puberty in boys. V. Rising leptin levels may signal the onset of puberty.
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DOI：
10.1210/jcem.82.4.3878
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发表时间：
1997-04
期刊：
影响因子：
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通讯作者：
C. Mantzoros;J. Flier;A. Rogol
中科院分区：
文献类型：
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作者：
C. Mantzoros;J. Flier;A. Rogol
瘦素是ob基因的产物，是一种脂肪细胞来源的激素，其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要影响。瘦素最近已被证明影响生殖功能的瘦素缺乏和正常的啮齿动物。由于青春期，性成熟和获得生殖能力的过程，已被提出由达到临界量和/或脂肪分布触发，我们研究了循环瘦素水平的变化是否可以代表负责触发人类青春期开始的激素信号。根据生殖器发育达到坦纳5期的时间，对8名青春期前男孩（研究开始时为坦纳生殖器1期或早期2期）进行了2.5-5.1年的纵向评价。在研究期间，每4个月获得用于测定瘦素、睾酮和硫酸脱氢表雄酮的血清。与青春期前的基线水平（青春期开始前8个月，定义为睾酮最初升高超过测定的检测限）相比，青春期开始前瘦素水平升高约50%，青春期开始后瘦素水平下降至约基线值（P < 0.01，通过ANOVA），保持稳定超过2年。尽管体重指数不断增加，但这些变化仍发生（P < 0.05，通过ANOVA）。瘦素和硫酸脱氢表雄酮浓度之间没有显着关联。总之，循环中的瘦素水平与这一假设是一致的，即这种分子是一个重要的信号，负责触发青春期的开始。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. Compared 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.