Adult testicular enlargement induced by neonatal hypothyroidism is accompanied by increased Sertoli and germ cell numbers.

Abstract

Our previous studies have shown that transient neonatal hypothyroidism, induced by treatment with the reversible goitrogen 6-propyl-2-thiouracil (PTU), increases testicular size and daily sperm production in the adult rat by up to 82% and 136%, respectively. The objective of the present study was to examine morphological and functional changes in adult seminiferous tubules associated with PTU-induced increases in testicular size and sperm production. Sprague-Dawley rats were treated with PTU from birth to day 25 or left untreated; for morphometry, all testes were fixed by vascular perfusion at 90 days of age. Although testicular weight was increased 62% in treated rats, gross pathological changes were not evident in these organs, and spermatogenesis appeared morphologically normal. The percent area of testis occupied by seminiferous tubules was equal in control and treated testes, but mean seminiferous tubule diameter and length were increased in the PTU-treated testis. The adult number of Sertoli cells in treated testes was increased by 157%, and the numbers of leptotene spermatocytes and round spermatids were increased 84% and 93%, respectively. These results demonstrate that increases in Sertoli cell numbers result in increased sperm production and support the idea that Sertoli cells are the major regulators of the magnitude of sperm production. Although the round spermatid to Sertoli cell ratio was reduced by nearly 30%, the number of round spermatids per g testis was increased by 14%. This increased efficiency of sperm production was accomplished by an increased density of Sertoli cells along the basement membrane and an increased height of the seminiferous epithelium. Despite the large increase in Sertoli cell numbers in treated rats, Northern blot analysis using Sertoli cell-specific cDNA probes for transferrin and androgen-binding protein indicated that relative steady state levels of mRNAs per Sertoli cell for these two secretory proteins were similar in control and treated rats at 90 days of age.

Consequences of a low litter birth weight phenotype for postnatal lean growth performance and neonatal testicular morphology in the pig

“…It has been demonstrated that Sertoli cells provide the environment that protects and nourishes germ cells and supports their development to viable sperm (França and Chiarini-Garcia, 2005) and Sertoli cell proliferation in pigs begins during the prenatal period (McCoard et al, 2002) and continues after birth (Swanlund et al, 1995;França et al, 2000). A critical period of Sertoli cell proliferation occurs during the first 3 weeks after birth (McCoard et al, 2003) and the total number of Sertoli cells achieved will determine testicle size in adulthood, as well as the sperm production capacity (Cooke et al, 1992;Hess et al, 1993). More recently, Flowers (2008) has reported beneficial effects on sperm production for prospective artificial insemination (AI) boars with improved pre-weaning growth, which was achieved by rearing these boars in smaller litters during lactation.…”

Van Wyk and Grumbach Syndrome (A Syndrome of Incomplete Isosexual Precocity and Juvenile Hypothyroidism)

“…Hence, such precocity is now thought to be incomplete sexual precocity. A similar precocity is known to occur in males also [7,8]. In most boys with juvenile hypothyroidism and precocity, the testes are enlarged because of increase in size of the seminiferous tubules.…”

Spermatogenic Defects in a New Inbred Strain SD/gShi Male Rat with Small Testes.

“…These quantitative and qualitative histopathological findings indicate suppression of the number of spermatocytes and spermatids supported by one Sertoli cell, due to reduced proliferation of preleptotene spermatocytes, resulting in suppression of total sperm production. On the other hand, it is well documented that the number of Sertoli cells per testis determines the theoretical maximum of sperm production [10][11][12][13] and that Sertoli cell replication in the rat occurs during fetal and neonatal life [14][15][16][17]. The total number of Sertoli cells in the testis and the proliferation of Sertoli cells in the fetal and neonatal phase of SD/gShi male rats are yet to be investigated.…”

“…SD/gShi males (7-12 animals/age) and SD males (5-10 animals/age) were weighed and necropsied at 3,4,5,6,8,10,12,15,17,20,25 and 35 weeks of age. Rats were anesthetized using ether, and blood samples were collected.…”