Endocrine regulation of reproductive development and function in the male.

Sexual development is an ordered process that begins at the moment of fertilization and terminates with the production and transfer of viable gametes. The formation of the male gonad depends upon genes located on both sex chromosomes and autosomes. Differentiation and growth of the male reproductive system is directed by the fetal testis through the production of a putative peptide which causes the regression of the Mullerian ducts and the secretion of testosterone which virilizes the Wolffian duct and thereby directs the differentiation of the internal accessory structures of reproduction. A third hormone, dihydrotestosterone, is synthesized intracellularly from testosterone within the urogenital sinus and tubercle. The action of this hormone controls the formation of the prostate and the external genitalia characteristic of the male phenotype. The postnatal growth of the testis and accessory sex tissues follows a characteristic curvilinear pattern with the most prominent increments coincident with the onset in testosterone production. Spermatogonial differentiation may proceed in the absence of hypophyseal or gonadal hormones but the respective maturation divisions of primary and secondary spermatocytes and the completion of spermiogenesis are clearly dependent upon testicular steroids produced under the influence of LH. Germ cells differentiate in a unique environment created, in part, by the blood testis barrier which arises as a result of tight-junctional complexes formed between adjacent Sertoli cells. Sertoli cells actively secrete fluids and export an androgen binding protein under the influence of androgens and FSH. Maintenance of spermatogenesis depends on high intratubular concentrations of testosterone, provided in part by the steroidogenic actions of LH on the Leydig cell and, in part, by the production of androgen binding protein by the Sertoli cell. Thus, both gonadotropins act in concert to maintain germ cell production. Selective removal of either LH or FSH curtails sperm production but testosterone supplementation, in adequate amounts, allows spermatogenesis to proceed in the absence of the pituitary gland.