肥胖的青春期前儿童具有高的自由IGF-1水平,尽管降低了帕帕利辛水平,但增长加速
Álvaro Martín-Rivada1,2,3, Gabriel Á Martos-Moreno1,2,3,4, Santiago Guerra-Cantera1,2,3,4
1Department of Endocrinology, Hospital Infantil Universitario Niño Jesús, Madrid E-28009, Spain.
The Journal of clinical endocrinology and metabolism
|April 25, 2024
概括
儿童肥胖与更高的胰岛素样生长因子 (IGF-I) 和IGF-II水平有关,可能导致增长加速. 肥胖儿童的体重减轻使一些生长因子正常化,并改变了巴巴素 (PAPP-A,PAPP-A2) 和斯坦尼素 (STC1,STC2) 的水平.
科学领域:
- 儿科内分泌学 儿科内分泌学
- 增长激素研究轴研究
- 儿童代谢障碍 儿童代谢障碍
背景情况:
- 儿童肥胖与增长的增强和增长激素-胰岛素类生长因子 (GH-IGF) 轴的改变有关.
- 帕帕利辛 (PAPP-A,PAPP-A2) 和斯坦尼奥卡尔辛 (STC1,STC2) 在儿科肥胖症中的IGF生物可用性中的作用仍未得到研究.
研究的目的:
- 研究儿童肥胖和随后减肥对PAPP-A,PAPP-A2,STC1和STC2血清水平的影响.
- 检查这些因素与IGF生物可用性,生长参数和其他GH-IGF系统组件之间的关系.
主要方法:
- 在诊断时和减肥后研究了患有严重肥胖的青春期前儿童 (n=150).
- 将肥胖儿童与206名年龄和性别匹配的健康对照进行了比较.
- 测量了PAPP-A,PAPP-A2,STC1,STC2,IGF-I,IGF-II,IGF结合蛋白和胰岛素的血清度.
主要成果:
- 肥胖儿童呈现较低的PAPP-A,PAPP-A2和STC2,但较高的总/自由IGF-I,完整的IGFBP-3,酸可变子单元 (ALS),IGF-II和胰岛素.
- 没有发现BMI或身高z-score与测量的生物化学参数之间的相关性.
- 减肥导致IGF-II,胰岛素和ALS降低,IGFBP-2,IGFBP-5,STC2和PAPP-A的增加.
结论:
- 在肥胖儿童中循环IGF-I,IGF-II和胰岛素的升高可能导致加速生长和骨成熟.
- 在青春期前肥胖症中观察到的生长变化中,STC2可能起作用.
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