Male hypogonadism--current concepts and trends.
Important advances have been made recently in our knowledge of hypothalamic-pituitary-testicular functions. Current understanding of the hypothalamic control of pituitary gonadotrophin secretion and the mechanisms of testicular feedback is beginning to yield benefits in the clinical management of certain reproductive disorders. But much remains to be learned about the neuroendocrine control of hypothalamic GnRH secretion--an area which encompasses the mechanisms regulating the onset of puberty. Spermatogenesis is a highly complex process involving subtle interactions between endocrine, paracrine and autocrine regulators acting on different cell populations within and without the testis. Until basic research can advance the very limited knowledge in this area, we cannot expect to improve the currently unsatisfactory management of infertile men. It is not surprising that only limited information can accrue from conventional semen analysis and measurement of systemic hormones. Nor is it unexpected that empirical or seemingly rational treatments for male infertility are of dubious benefit. In future, assessment of the infertile man should be improved by studying sperm functional capacities and testicular synthesis and metabolism of gonadal steroids and by the definition of representative markers of Sertoli cell and epididymal functions. Reversible male contraception is another objective that remains beyond our reach at present. Hormonal disruption of spermatogenesis is often incomplete and invariably suppresses Leydig cell function, so that androgen replacement for sustaining sexual function is mandatory. Alternative approaches to male contraception aimed at the epididymis and sperm-egg interaction seem more promising avenues for future exploration.
D000375:Aging; D000728:Androgens / Q000378:metabolism / Q000494:pharmacology; D005298:Fertility / Q000187:drug effects; D005640:Follicle Stimulating Hormone / Q000502:physiology; D006801:Humans; D006966:Hyperprolactinemia / Q000503:physiopathology; D007006:Hypogonadism / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D007031:Hypothalamus / Q000502:physiology; D007248:Infertility, Male / Q000209:etiology / Q000276:immunology / Q000628:therapy; D007265:Inhibins / Q000502:physiology; D007985:Leydig Cells / Q000502:physiology; D007986:Luteinizing Hormone / Q000502:physiology; D008297:Male; D011628:Puberty, Delayed / Q000503:physiopathology; D012708:Sertoli Cells / Q000502:physiology; D012727:Sex Characteristics; D013091:Spermatogenesis; D013739:Testosterone / Q000032:analysis
D000728:Androgens; D013739:Testosterone; D007265:Inhibins; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone