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母体甲状腺功能减退对雌性大鼠后代青春期发育的影响。

Effects of Maternal Hypothyroidism on the Pubertal Development in Female Rat Offspring.

作者信息

Park Jin-Soo, Lee Sung-Ho

机构信息

Department of Biotechnology, Sangmyung University, Seoul 03016, Korea.

出版信息

Dev Reprod. 2021 Jun;25(2):83-91. doi: 10.12717/DR.2021.25.2.83. Epub 2021 Jun 30.

DOI:10.12717/DR.2021.25.2.83
PMID:34386643
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8328481/
Abstract

The present study was performed to investigate the effect of maternal hypothyroidism and puberty onset in female rat pups. To do this, we employed propylthiouracil (PTU) to prepare a hypothyroid rat model. Pregnant rats were treated with PTU (0.025%) in drinking water from gestational day 14 to postnatal day 21 of offspring. Comparison of general indices such as body and tissue weights and puberty indices such as vaginal opening (VO) and tissue histology between control and PTU-treated rats were conducted. There was no significant difference in the date of VO between control and PTU group. The body weights of the PTU group were significantly lower, only 36.8% of the control group (<0.001). Although the absolute thyroid weight was not changed by PTU treatment, the relative weight increased significantly about 2.8 times (<0.001), indicating that hypothyroidism was successfully induced. On the other hand, the absolute weights of the ovary and uterus were markedly decreased by PTU administration (<0.001), and the relative weight was not significantly changed. The ovarian histology of PTU group revealed the advanced state of differentiation (i.e., presence of corpora lutea). Inversely, the uterine histology of PTU group showed underdeveloped structures compared those in control group. Taken together, the present study demonstrates that our maternal hypothyroidism model resulted in minimal effect on pubertal development symbolized by VO despite of huge retardation in somatic growth. More sophisticatedly designed hypothyroidism model will be helpful to achieve a better understanding of pubertal development and related disorders.

摘要

本研究旨在探讨母体甲状腺功能减退与雌性幼鼠青春期启动之间的关系。为此,我们使用丙硫氧嘧啶(PTU)制备甲状腺功能减退大鼠模型。从妊娠第14天至子代出生后第21天,给怀孕大鼠饮用含0.025% PTU的水。对对照组和PTU处理组大鼠的一般指标(如体重和组织重量)以及青春期指标(如阴道开口(VO)和组织组织学)进行比较。对照组和PTU组之间VO日期无显著差异。PTU组的体重显著降低,仅为对照组的36.8%(<0.001)。虽然PTU处理未改变甲状腺的绝对重量,但相对重量显著增加约2.8倍(<0.001),表明成功诱导了甲状腺功能减退。另一方面,PTU给药显著降低了卵巢和子宫的绝对重量(<0.001),相对重量无显著变化。PTU组的卵巢组织学显示分化程度较高(即存在黄体)。相反,PTU组的子宫组织学显示与对照组相比结构发育不全。综上所述,本研究表明,尽管我们的母体甲状腺功能减退模型导致躯体生长严重迟缓,但对以VO为标志的青春期发育影响最小。设计更精密的甲状腺功能减退模型将有助于更好地理解青春期发育及相关疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f16f/8328481/5f61fb3bf451/dr-25-2-83-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f16f/8328481/bfdcf7440f4f/dr-25-2-83-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f16f/8328481/0e22a344a3e3/dr-25-2-83-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f16f/8328481/16c6b47d4cc0/dr-25-2-83-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f16f/8328481/5f61fb3bf451/dr-25-2-83-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f16f/8328481/bfdcf7440f4f/dr-25-2-83-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f16f/8328481/0e22a344a3e3/dr-25-2-83-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f16f/8328481/16c6b47d4cc0/dr-25-2-83-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f16f/8328481/5f61fb3bf451/dr-25-2-83-g4.jpg

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Ameliorating effect of postweaning exposure to antioxidant on disruption of hippocampal neurogenesis induced by developmental hypothyroidism in rats.
断奶后暴露于抗氧化剂对发育性甲状腺功能减退诱导的大鼠海马神经发生破坏的改善作用。
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Global epidemiology of hyperthyroidism and hypothyroidism.全球甲状腺功能亢进症和甲状腺功能减退症的流行病学。
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Discovery of GnIH and Its Role in Hypothyroidism-Induced Delayed Puberty.促性腺激素抑制激素(GnIH)的发现及其在甲状腺功能减退症所致青春期延迟中的作用。
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