Thyroid Hormone Effects on Male Reproductive Physiology

Summary

Thyroid hormones, chiefly triiodothyronine (T3) and thyroxine (T4), exert profound influence on male reproductive function by modulating testicular development, steroidogenesis and spermatogenesis. Within the testis, T3 and T4 act via thyroid hormone receptors in Sertoli, Leydig and germ cells to regulate cell proliferation, differentiation and intercellular communication. Deiodinase enzymes present in testicular tissue finely tune local conversion of T4 to active T3 or to inactive metabolites, ensuring stage-specific hormone action during the epithelial cycle of sperm production. Adequate thyroid status supports Leydig cell production of testosterone through stimulation of steroidogenic enzymes, while Sertoli cell maturation and the assembly of the blood–testis barrier are highly sensitive to thyroidal signals. Both hypo- and hyperthyroid states perturb gonadotropin release from the pituitary, disrupt the hypothalamic-pituitary-gonadal axis and lead to altered sperm quality, semen parameters and testicular histology. Developmental hypothyroidism may cause transient testicular underdevelopment followed by compensatory Sertoli cell proliferation and macroorchidism, whereas adult thyroid dysfunction often manifests as subfertility, reduced libido and changes in erectile function. Globally, recognition of thyroid–reproductive crosstalk has widened opportunities for diagnostic assessment and therapeutic intervention in endocrine-related male infertility, emphasising the need for integrated management of thyroid disorders in reproductive health care.

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Thyroid Hormone Effects on Male Reproductive Physiology publication trend

The graph below shows the total number of articles in thyroid hormone effects on male reproductive physiology across all publications each year (not limited to Nature Index journals).

Technical terms

Thyroid hormones (THs): Endocrine hormones (T3 and T4) produced by the thyroid gland that regulate metabolism, growth and development.

Deiodinases: Enzymes that activate or inactivate thyroid hormones by removing iodine atoms, modulating local hormone action.

Sertoli cells: Somatic cells in the seminiferous epithelium that support germ cell development and form the blood–testis barrier.

Leydig cells: Interstitial cells responsible for testosterone synthesis in response to luteinising hormone.

Spermatogenesis: The multistage process of sperm production, involving mitotic, meiotic and differentiation phases within the testis.

Hypothyroidism: A state of insufficient thyroid hormone production resulting in metabolic and developmental disturbances.

References

  1. Perinatal exposure to environmental chemicals that disrupt thyroid function can perturb testis development. Environmental Pollution (2024).
  2. Kisspeptin-10 Improves Testicular Redox Status but Does Not Alter the Unfolded Protein Response (UPR) That Is Downregulated by Hypothyroidism in a Rat Model. International Journal of Molecular Sciences (2024).
  3. Methimazole-induced congenital hypothyroidism affects gonocytes differentiation and arrests meiosis: role of Sertoli cells. Frontiers in Cell and Developmental Biology (2024).
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