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.

Highlights

  • Thyroid hormones play a crucial role in regulating development, differentiation, and metabolism in multiple mammalian tissues

  • Studies have demonstrated that thyroid hormones most notably T3 (3,5,3 -tri-iodothyronine) regulates Sertoli cell proliferation and differentiation during testis development including the assembly of the blood–testis barrier (BTB) [3,4,5]

  • Several idothyronine deiodinases and thyroid hormone transporters have been identified in the testis [7,8,9,10], illustrating that these enzymes and transporters necessary to maintain the homeostasis of thyroid hormone are present in the testis

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Summary

Thyroid hormone function in the rat testis

Edited by: Fátima Regina Mena Barreto Silva, Universidade Federal de Santa Catarina, Brazil. 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 express deiodinases, which are capable of converting the pro-hormoneT4 to the active thyroid hormone T3, or inactivating T3 or T4 to a non-biologically active form. 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

INTRODUCTION
Thyroid gland
Delays BTB assembly
Sertoli cell Leydig cell

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