In contrast to female eggs, sperm are continually produced throughout a man's lifetime. During spermatogenesis and transport through the male reproductive tract, the male spermatozoa are transformed into a highly specialized cell with its own motility and enzymatic capacity to penetrate the egg. Epididymal function must be normal and the accessory glands must be functional to produce normal seminal plasma. An intact nervous system is also required to permit penile erection and normal ejaculation.
UCSF is a leader in reproductive health, achieving consistently high pregnancy rates, and we offer a comprehensive array of evaluation and treatment options for men with fertility concerns. We recognize that the process of resolving infertility can be difficult, and we are committed to caring for each patient with knowledge, understanding and respect.
Abstract Normal testicular function is dependent upon hormones acting through endocrine and paracrine pathways both in vivo and in vitro. Publication types Review. Substances Hormones. The effect of a null mutation in the follicle-stimulating hormone receptor gene on mouse reproduction. Impairing follicle-stimulating hormone FSH signaling in vivo : targeted disruption of the FSH receptor leads to aberrant gametogenesis and hormonal imbalance.
Effects of testosterone on spermatogenic cell populations in the adult rat. Testosterone effects on spermatogenesis in the gonadotropin-releasing hormone-immunized rat.
FSH immunoneutralization acutely impairs spermatogonial development in normal adult rats. Mol Hum Reprod. Preferential beta-arrestin signalling at low receptor density revealed by functional characterization of the human FSH receptor A V mutation.
Analysis of protein-coding genetic variation in 60, humans. Nature — Male hypogonadism resulting from mutations in the genes for gonadotropin subunits and their receptors. In: Winters S, Huhtaniemi I, editors. Gonadotroph adenomas in men produce biologically active follicle-stimulating hormone.
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J Pediatr. Sexual precocity—genetic bases of central precocious puberty and autonomous gonadal activation. Endocr Dev. Female mice expressing constitutively active mutants of FSH receptor present with a phenotype of premature follicle depletion and estrogen excess. Research resource: the dynamic transcriptional profile of sertoli cells during the progression of spermatogenesis.
Oligonucleotide microarray analysis of gene expression in follicle-stimulating hormone-treated rat Sertoli cells. Follicle-stimulating hormone induced changes in gene expression of murine testis. Identification of Sertoli cell-specific transcripts in the mouse testis and the role of FSH and androgen in the control of Sertoli cell activity.
BMC Genomics Kruppel-like factor 4 is involved in functional differentiation of testicular Sertoli cells. Dev Biol. Reprogramming sertoli cells into pluripotent stem cells. Cell Reprogram — Atypical development of Sertoli cells and impairment of spermatogenesis in the hypogonadal hpg mouse. J Anat. Gene expression profiling of mouse Sertoli cell lines. Cell Tissue Res. FSH regulates the formation of adherens junctions and ectoplasmic specialisations between rat Sertoli cells in vitro and in vivo.
Stanton PG. Regulation of the blood-testis barrier. Defective Wnt3 expression by testicular Sertoli cells compromise male fertility. Retinoic acid induces Sertoli cell paracrine signals for spermatogonia differentiation but cell autonomously drives spermatocyte meiosis. Follicle-stimulating hormone and leukemia inhibitory factor regulate Sertoli cell retinol metabolism. Activity of retinoic acid receptor-alpha is directly regulated at its protein kinase A sites in response to follicle-stimulating hormone signaling.
Apoptosis in testis germ cells: developmental changes in gonadotropin dependence and localization to selective tubule stages. Developmentally distinct in vivo effects of FSH on proliferation and apoptosis during testis maturation. An early and massive wave of germinal cell apoptosis is required for the development of functional spermatogenesis. EMBO J. Gen Comp Endocrinol. Aquaporins in the human testis and spermatozoa - identification, involvement in sperm volume regulation and clinical relevance.
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Russell LD, Clermont Y. Degeneration of germ cells in normal, hypophysectomized and hormone treated hypophysectomized rats. Anat Rec. Normal prenatal but arrested postnatal sexual development of luteinizing hormone receptor knockout LuRKO mice. Infertility with defective spermatogenesis and hypotestosteronemia in male mice lacking the androgen receptor in Sertoli cells. A Sertoli cell-selective knockout of the androgen receptor causes spermatogenic arrest in meiosis.
Pituitary-testicular function of prostatic cancer patients during treatment with a gonadotropin-releasing hormone agonist analog. Circulating hormone levels. Assessment of the androgen environment within the human testis: minimally invasive method to obtain intratesticular fluid. Serum LH correlates highly with intratesticular steroid levels in normal men. Induction of spermatogenesis by androgens in gonadotropin-deficient hpg mice.
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Overlapping dose responses of spermatogenic and extragonadal testosterone actions jeopardize the principle of hormonal male contraception. Testosterone replacement therapy induces spermatogenesis and partially restores fertility in luteinizing hormone receptor knockout mice.
A new LH receptor splice mutation responsible for male hypogonadism with subnormal sperm production in the propositus, and infertility with regular cycles in an affected sister. Hum Reprod. Normal spermatogenesis in a man with mutant luteinizing hormone.
N Engl J Med. Eur J Endocrinol. Burgues S, Calderon MD. Subcutaneous self-administration of highly purified follicle stimulating hormone and human chorionic gonadotrophin for the treatment of male hypogonadotrophic hypogonadism. Spanish collaborative group on male hypogonadotropic hypogonadism. Repeated intramuscular injections of testosterone undecanoate for substitution therapy in hypogonadal men.
Clin Endocrinol. The functional significance of FSH in spermatogenesis and the control of its secretion in male primates. Hormones play an organizational role, priming the body to behave in a certain way once puberty begins, and an activational role, referring to changes in hormones during adolescence that trigger behavioral and physical changes.
Hormonal regulation of the male reproductive system : GnRH stimulates the production of FSH and LH, which act on the testes to begin spermatogenesis and to develop secondary sex characteristics in the male.
At the onset of puberty, the hypothalamus begins secreting high pulses of GnRH, or gonadotropin-releasing hormone. In response, the pituitary gland releases follicle stimulating hormone FSH and luteinizing hormone LH into the male system for the first time. FSH enters the testes, stimulating the Sertoli cells, which help to nourish the sperm cells that the testes produce, to begin facilitating spermatogenesis. LH also enters the testes, stimulating the interstitial cells, called Leydig cells, to make and release testosterone into the testes and the blood.
Testosterone, the hormone responsible for the secondary sexual characteristics that develop in the male during adolescence, stimulates spermatogenesis, or the process of sperm production in the testes.
Secondary sex characteristics include a deepening of the voice, the growth of facial, axillary, and pubic hair, and the beginnings of the sex drive. A negative feedback system occurs in the male with rising levels of testosterone acting on the hypothalamus and anterior pituitary to inhibit the release of GnRH, FSH, and LH.
The Sertoli cells produce the hormone inhibin, which is released into the blood when the sperm count is too high. The stages of the ovarian cycle in the female are regulated by hormones secreted by the hypothalamus, pituitary, and the ovaries. The control of reproduction in females is more complex than that of the male. As with the male, the hypothalamic hormone GnRH gonadotropin-releasing hormone causes the release of the hormones FSH follicle stimulating hormone and LH luteinizing hormone from the anterior pituitary.
In addition, estrogens and progesterone are released from the developing follicles, which are structures on the ovaries that contain the maturing eggs. In females, FSH stimulates the development of egg cells, called ova, which develop in structures called follicles.
Follicle cells produce the hormone inhibin, which inhibits FSH production. LH also plays a role in the development of ova, as well as in the induction of ovulation and stimulation of estradiol and progesterone production by the ovaries. Estradiol and progesterone are steroid hormones that prepare the body for pregnancy.
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