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SUN-594 Pubertal Timing and Hormonal Correlates in Male Obesity

机译:Sun-594青春期时机和荷尔蒙在雄性肥胖症中相关

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摘要

An early, normal or delayed pubertal onset have been described in overweight/ obese males(1). A greater prepubertal adiposity has been associated with a greater risk for delayed puberty in males, but an underlying mechanism was not explored(2). We investigated whether an increased testosterone aromatization or an higher degree of low-grade inflammation might be more prevalent in obese males with a delay in genital development. Pubertal status assessment by Tanner staging and measurement of morning serum testosterone, estradiol, leptin, and hSCRP by standard laboratory methods were performed in 191 male adolescents, aged between 10 and 18.6 yr (median 12.8 yr) with overweight (BMI z-score > 1.3), starting an ambulatory (n = 138) or a residential weight loss program (n = 55). Their median (range) BMI z-score was 2.32 (1.34 – 3.38). Delayed / slow and early / rapid genital development was defined by a Tanner genital stage respectively above the 90th or below 10th percentile age distribution (national Flemish standards of 2004). In 3 males pubertal development was advanced, while in 34 it was delayed. In the remaining 154 adolescents genital stage was normally timed. Males with a delayed timing or progression of genital development were older (median(range) age:14.8 (11.6-18.6) yr vs 12.3 (10-18.6) yr; p< 0.005) and shorter (height sds: -0.55 (-1.90- 1.48) vs 0.49 (-3 – 3.19); p < 0.005), and had a higher birthweight (birthweight z-score: 0.15(-3.51-2.75) vs -0.34(-4.7-3.30); p = 0.058), but a similar BMI and waist z-score in comparison with males with a normally timed puberty. Median serum estradiol, leptin, and hSCRP concentrations did not differ significantly between those with a normal or a delayed pubertal onset or progression. In conclusion, pubertal delay is more frequently observed than early puberty in males referred to obesity clinics. Neither low grade inflammation nor increased estradiol production appear to be associated with a later onset of slower progression of genital development in male obesity. References (1) Li W et al. Int J Environ Res Public Health. 2017 Oct 24;14(10) (2) Lee JM et al. Arch Pediatr Adolesc Med. 2010 Feb;164(2):139-44.
机译:超重/肥胖男性(1)描述了早期,正常或延迟的青春期发作。更高的预接种肥胖与男性延迟青春期的风险有更大的风险,但没有探索潜在的机制(2)。我们研究了睾酮芳香化或更高程度的低级炎症是否可能在肥胖的雄性中具有更普遍的毒性发育。由标准实验室方法的Tanner睾酮,雌二醇,瘦素和HSCRP的Tanner分期和测量的普及塔尔现状评估在191个雄性青少年中进行,年龄在10至18.6毫升(中位数12.8 yr)之间,超重(BMI Z分数> 1.3 ),启动动态(n = 138)或住宅减肥计划(n = 55)。他们的中位数(范围)BMI Z分数为2.32(1.34 - 3.38)。延迟/缓慢和早期/快速发展是由分别高于第90次或低于第10百分点的年龄分布(2004年国家佛罗里野标准)的Tanner生殖器阶段。在3个男性普国普国开发先进,而在34岁时被推迟。在剩下的154个青少年中,生殖器阶段通常是定时的。具有延迟时间或生殖器发育的延迟的雄性(中位数(范围)年龄:14.8(11.6-18.6)YR与12.3(10-18.6)Yr; P <0.005)和更短(高度SDS:-0.55(-1.90 - 1.48)与0.49(-3 - 3.19); p <0.005),出生重量较高(出生重量Z分数:0.15(-3.51-2.75)vs -0.34(-4.7-3.30); p = 0.058),但与具有通常定时青春期的男性相比,类似的BMI和腰部Z分数。中间血清雌二醇,瘦素和HSCRP浓度在正常或延迟的青春期发作或进展之间没有显着差异。总之,青春期延迟比肥胖诊所的男性早期青春期更常见。既不是低级炎症也不增加雌二醇产量似乎与雄性肥胖症生殖器发育较慢进展的后期发作相关。参考文献(1)Li W等人。 int j Environ Res公共健康。 2017年10月24日; 14(10)(2)Lee JM等人。 Arch Pedias Adolesc Med。 2010年2月; 164(2):139-44。

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