Meisami E, Sendera T J, Clay L B
Department of Physiology and Biophysics, University of Illinois, Urbana 61801.
J Endocrinol. 1992 Dec;135(3):495-505. doi: 10.1677/joe.0.1350495.
The effects of various durations of postnatal hypothyroidism followed by recovery were studied on testicular growth in Long-Evans and Sprague-Dawley rats from birth to 7 months. Hypothyroidism was induced by adding propylthiouracil (PTU) in drinking water (0.1%, w/v). Recovery was induced by withdrawal of PTU. Testicular growth was reduced in rat pups by 20, 65 and 90% at days 10, 25 and 50. Upon withdrawal of PTU at weaning (25 days), testicular growth resumed and became compensatory; catch-up growth occurred by day 65. Paradoxically, testicular growth progressively increased, surpassing the control weights by 40, 50 and 100% at days 75, 90 and 210. Maximal testicular growth rate in the recovery group was 35% higher, occurred 2 weeks later and lasted 2 weeks longer than controls. Testes of rats subjected to prolonged postnatal hypothyroidism (60 or 120 days) also showed recovery and hypertrophy, amounting to nearly twice the normal maximal growth levels, after at least 6 months of recovery. Body weights of recovering rats remained always significantly below those of controls. When the suckling pups were exposed to short, week-long regimes of PTU treatment, only rats treated during the early postnatal weeks (days 1-8 or 9-16) had enlarged testes; PTU treatment during the late suckling period (days 17-24) or later had no effects. Total duration of hypothyroidism in the suckling period was positively correlated with testicular enlargement. The results indicate that hypothyroidism early in life is stimulatory to testicular growth, resulting in a paradoxical twofold increase in final testicular size which occurs even if hypothyroidism is prolonged. These effects occur similarly in different strains of rat with differing sized testes. It is suggested that there is a sensitive period for this effect, i.e. during the first 2 weeks after birth. The marked plasticity of testicular growth as shown by its recovery and hypertrophy, even after long periods of hypothyroid retardation, is unique in the body and may be a useful model for studying hormonal factors regulating testicular growth and for animal breeding and research into infertility.
研究了出生后不同时长的甲状腺功能减退随后恢复对Long-Evans和Sprague-Dawley大鼠从出生到7个月睾丸生长的影响。通过在饮用水中添加丙硫氧嘧啶（PTU，0.1%，w/v）诱导甲状腺功能减退。通过停用PTU诱导恢复。在出生后第10、25和50天，幼鼠的睾丸生长分别减少了20%、65%和90%。在断奶时（25天）停用PTU后，睾丸生长恢复并出现代偿性生长；到第65天出现追赶生长。矛盾的是，睾丸生长逐渐增加，在第75、90和210天时超过对照体重的40%、50%和100%。恢复组的最大睾丸生长速率比对照组高35%，发生时间晚2周，持续时间长2周。经历出生后长期甲状腺功能减退（60或120天）的大鼠睾丸在至少6个月的恢复后也显示出恢复和肥大，达到正常最大生长水平的近两倍。恢复中的大鼠体重始终显著低于对照组。当哺乳幼鼠接受为期一周的短期PTU治疗时，只有在出生后早期（第1 - 8天或第9 - 16天）接受治疗的大鼠睾丸增大；哺乳后期（第17 - 24天）或更晚接受PTU治疗则没有影响。哺乳期甲状腺功能减退的总时长与睾丸增大呈正相关。结果表明，生命早期的甲状腺功能减退对睾丸生长有刺激作用，导致最终睾丸大小出现矛盾的两倍增长，即使甲状腺功能减退持续时间延长也会如此。这些效应在不同睾丸大小的大鼠品系中表现相似。提示存在该效应的敏感期，即出生后的前2周。睾丸生长即使在长期甲状腺功能减退延迟后仍能恢复和肥大，显示出显著的可塑性，这在身体中是独特的，可能是研究调节睾丸生长的激素因素以及动物育种和不育研究的有用模型。
