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新生大鼠睾丸中成年型莱迪希细胞的分化会因甲状腺功能减退而停滞。

Differentiation of adult Leydig cells in the neonatal rat testis is arrested by hypothyroidism.

作者信息

Mendis-Handagama S M, Ariyaratne H B, Teunissen van Manen K R, Haupt R L

机构信息

Department of Animal Science, College of Veterinary Medicine, The University of Tennessee, Knoxville, Tennessee 37996, USA.

出版信息

Biol Reprod. 1998 Aug;59(2):351-7. doi: 10.1095/biolreprod59.2.351.

Abstract

The effects of propyl thiouracil (PTU)-induced hypothyroidism on testicular interstitial cells and androgen secretion in vitro in the neonatal rat were investigated using Sprague Dawley rats of 1, 7, 14, and 21 days. The results revealed that the fetal Leydig cell (FLC) number per testis was unchanged between and within treatment groups at all ages tested. FLC size was 50% smaller in 21-day controls than in all other groups. Adult Leydig cells (ALCs) were present at Days 14 and 21 in controls but were absent in PTU rats. ALCs approximated FLCs of 21-day controls in size. ALC number per testis showed a sharp increase at Day 21. 11ss-HSD1-positive cells were absent in 21-day PTU testes, but a few were present in 21-day control testes. Testosterone secretion per testis was unchanged in 1- to 21-day controls and 7- to 21-day PTU rats. However, at Day 21, a significantly lower value was seen in controls compared to PTU rats. Testicular androstenedione secretion was not significantly different between control and PTU rats up to 14 days, but a sharp rise was observed in controls at Day 21. At this age, androstenedione levels in PTU rats were similar to those at younger ages. In summary, histological studies showed that hypothyroidism prevented the hypotrophy of FLC and the emergence of ALC in the neonatal rat testis, and agreed favorably with results concerning testicular androgen secretion in vitro. These findings suggest that thyroid hormones have a regulatory role in precursor cell differentiation into Leydig cells in the neonatal rat testis to establish the ALC population.

摘要

利用1日龄、7日龄、14日龄和21日龄的斯普拉格-道利大鼠,研究丙硫氧嘧啶(PTU)诱导的甲状腺功能减退对新生大鼠睾丸间质细胞和体外雄激素分泌的影响。结果显示,在所有测试年龄的治疗组之间及组内,每个睾丸的胎儿型睾丸间质细胞(FLC)数量均未改变。21日龄对照组的FLC大小比所有其他组小50%。对照组在14日龄和21日龄时存在成年型睾丸间质细胞(ALC),但PTU处理的大鼠中不存在。ALC大小与21日龄对照组的FLC相近。每个睾丸的ALC数量在21日龄时急剧增加。21日龄PTU处理的睾丸中不存在11β-羟基类固醇脱氢酶1(11β-HSD1)阳性细胞,但21日龄对照组睾丸中有少量存在。1至21日龄对照组和7至21日龄PTU处理的大鼠中,每个睾丸的睾酮分泌未改变。然而,在21日龄时,对照组的睾酮分泌值显著低于PTU处理的大鼠。在14天之前,对照组和PTU处理的大鼠睾丸雄烯二酮分泌无显著差异,但在21日龄时对照组雄烯二酮分泌急剧增加。在这个年龄,PTU处理的大鼠中雄烯二酮水平与较年轻年龄时相似。总之,组织学研究表明,甲状腺功能减退可防止新生大鼠睾丸中FLC的肥大和ALC的出现,这与体外睾丸雄激素分泌的结果一致。这些发现表明,甲状腺激素在新生大鼠睾丸中前体细胞分化为睾丸间质细胞以建立ALC群体方面具有调节作用。

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