Thyroid Hormone Function in the Rat Testis

Abstract

Thyroid hormones are emerging regulators of testicular function since Sertoli, germ, and Leydig cells are found to express thyroid hormone receptors (TRs). These testicular cells also express deiodinases, which are capable of converting the pro-hormone T4 to the active thyroid hormone T3, or inactivating T3 or T4 to a non-biologically active form. Furthermore, thyroid hormone transporters are also found in the testis. Thus, the testis is equipped with the transporters and the enzymes necessary to maintain the optimal level of thyroid hormone in the seminiferous epithelium, as well as the specific TRs to execute thyroid hormone action in response to different stages of the epithelial cycle of spermatogenesis. Studies using genetic models and/or goitrogens (e.g., propylthiouracil) have illustrated a tight physiological relationship between thyroid hormone and testicular function, in particular, Sertoli cell differentiation status, mitotic activity, gap junction function, and blood–testis barrier assembly. These findings are briefly summarized and discussed herein.

Retinoid signaling controls spermatogonial differentiation by regulating expression of replication-dependent core histone genes

“…However, we feel this result is unlikely because the knockout of the Vdr or Ppar still results in the completion of spermatogenesis although with a reduced sperm count (Blomberg Jensen et al, 2013;Yao et al, 2015). In addition, male mice lacking individual thyroid receptor genes or both TRalpha1 and TRbeta1 (also known as Thra and Thrb, respectively) are still fertile, and inactivation of TRalpha1 actually results in a larger testis with enhanced Sertoli and germ cell numbers (Cooke, 1991;Gao et al, 2014;Gothe et al, 1999;Holsberger et al, 2005). Therefore, the observations from Gely-Pernot et al and our findings that germ-cell mutants exhibit complete defects in spermatogonial differentiation identical to VAD mice reveal that RARs could act both with and without an RXR, or that RXRs could act both with and without an RAR, in germ cells.…”

Maternal Nutrition during Pregnancy Affects Testicular and Bone Development, Glucose Metabolism and Response to Overnutrition in Weaned Horses Up to Two Years

“…Another hypothesis would have been an effect of hormones: T3, leptin, insulin and IGF-1 plasma concentrations are known to increase with improved nutritional status in the fetus and neonate [31,79]. These hormones are directly active on testes [80,81]. Insulin and IGF-1 regulate Sertoli cell proliferation and FSH action in mice [80] and T3 affects Sertoli cell differentiation and blood-testis barrier assembly [81].…”

“…These hormones are directly active on testes [80,81]. Insulin and IGF-1 regulate Sertoli cell proliferation and FSH action in mice [80] and T3 affects Sertoli cell differentiation and blood-testis barrier assembly [81]. At 6 months of age, however, no differences were found in insulin levels and glucose metabolism, T3, and IGF-1 levels in both groups of foals [31], but there is no information available on earlier stages.…”

Sertoli cells are the target of environmental toxicants in the testis – a mechanistic and therapeutic insight

“…BPA is an EDC that exerts its effect by binding to estrogen receptors, ARs and/or thyroid hormone receptors [34]. Because these steroid receptors are found in Sertoli cells [35,36], BPA can exert its effects via these receptors to impair Sertoli cell function. Emerging epidemiological and experimental evidence indicates that BPA has adverse effects on male reproductive function following in utero and fetal/neonatal exposure because adults are more tolerant to BPA [37-39], perhaps due to its short half-life, < 2 h [39].…”