About: Androgen-binding protein is a research topic. Over the lifetime, 328 publications have been published within this topic receiving 13647 citations. The topic is also known as: Sex hormone-binding globulin.
TL;DR: The observations identify the perinatal period, when the Sertoli cell population is established, as critical for development of quantitatively normal spermatogenesis in the adult, and indicates that production of normal numbers of germ cells in adults depends, at least in part, on the size of the Sergio cell population.
Abstract: To probe the relationship between the size of the Sertoli cell population, established during perinatal development, and production of germ cells in the adult testis, a Sertoli cell-depleted rat model was developed. This was accomplished by delivering an antimitotic drug, cytosine arabinoside (araC), directly to the testis of newborn pups. Initial studies of these araC-treated neonates indicated that 1) the drug is cleared rapidly from the testis; 2) it substantially reduces the level of Sertoli cell proliferation; 3) Sertoli cell division ceases at a normal time in spite of the previous drug treatment; and 4) araC itself has no residual effect on germ cell proliferation, which begins several days after the injection. Pups given araC were allowed to reach maturity, and their testes were perfuse-fixed for light microscopic morphometry. When the numbers of Sertoli cells in adult rats given araC as were compared with those in normal littermates, a 54% decrease in the size of the Sertoli cell population was detected in treated rats, now referred to as Sertoli cell-depleted. Moreover, when round spermatids were quantified and compared in normal and Sertoli cell-depleted adults, testes of the latter were found to contain 55% fewer round spermatids. Since, in the araC-treated group, the decrease in Sertoli cell population size was paralleled by a reduction in spermatid production of equal magnitude, the number of round spermatids per Sertoli cell was essentially identical in normal and Sertoli cell-depleted animals. Measurements of serum androgen-binding protein (ABP) and FSH in both groups indicated that the circulating level of ABP in Sertoli cell-depleted rats was approximately half, and the concentration of FSH approximately twice, that in normal animals. Thus, even though FSH is elevated in Sertoli cell-depleted rats, the production of ABP per Sertoli cell is unchanged. In addition, collective volume of Leydig cells and ventral prostate weights were normal in the Sertoli cell-depleted group, suggesting that Leydig cell function in these rats is normal. In summary, a Sertoli cell-depleted rat model has been produced by interfering specifically with Sertoli cell proliferation early in postnatal life, before onset of germ cell division. Moreover, our findings with this model indicate that production of normal numbers of germ cells in adults depends, at least in part, on the size of the Sertoli cell population. Thus, our observations identify the perinatal period, when the Sertoli cell population is established, as critical for development of quantitatively normal spermatogenesis in the adult.
TL;DR: Treatment of an infertile man with testosterone does improve spermatogenesis, since exogenous administrated testosterone and its metabolite estrogen will suppress both GnRH production by the hypothalamus and Luteinising hormoneproduction by the pituitary gland and subsequently suppress testicular testosterone production.
Abstract: Androgens play a crucial role in the development of male reproductive organs such as the epididymis, vas deferens, seminal vesicle, prostate and the penis. Furthermore, androgens are needed for puberty, male fertility and male sexual function. High levels of intratesticular testosterone, secreted by the leydig cells, are necessary for spermatogenesis. Intratesticular testosterone is mainly bound to androgen binding protein and secreted into the seminiferous tubules. Inside the sertoli cells, testosterone is selectively bound to the androgen receptor and activation of the receptor will result in initiation and maintenance of the spermatogenic process and inhibition of germ cell apoptosis. The androgen receptor is found in all male reproductive organs and can be stimulated by either testosterone or its more potential metabolite dihydrotestosterone. Severe defects of the androgen receptor may result in abnormal male sexual development. More subtle modulations can be a potential cause of male infertility. Treatment of an infertile man with testosterone does improve spermatogenesis, since exogenous administrated testosterone and its metabolite estrogen will suppress both GnRH production by the hypothalamus and Luteinising hormone production by the pituitary gland and subsequently suppress testicular testosterone production. Also, high levels of testosterone are needed inside the testis and this can never be accomplished by oral or parenteral administration of androgens. Suppression of testosterone production by the leydig cells will result in a deficient spermatogenesis, as can be seen in men taking anabolic-androgenic steroids. Suppression of spermatogenesis by testosterone administration is also the basis for the development of a male contraceptive. During cytotoxic treatment or irradiation suppression of intratesticular testosterone production cells may prevent irreversible damage to the spermotogonial stem cells.
TL;DR: Examination of morphological and functional changes in adult seminiferous tubules associated with PTU-induced increases in testicular size and sperm production demonstrates that increases in Sertoli cell numbers result in increased sperm production and supports the idea that SERToli cells are the major regulators of the magnitude of sperm production.
Abstract: Our previous studies have shown that transient neonatal hypothyroidism, induced by treatment with the reversible goitrogen 6-propyl-2-thiouracil (PTU), increases testicular size and daily sperm production in the adult rat by up to 82% and 136%, respectively The objective of the present study was to examine morphological and functional changes in adult seminiferous tubules associated with PTU-induced increases in testicular size and sperm production Sprague-Dawley rats were treated with PTU from birth to day 25 or left untreated; for morphometry, all testes were fixed by vascular perfusion at 90 days of age Although testicular weight was increased 62% in treated rats, gross pathological changes were not evident in these organs, and spermatogenesis appeared morphologically normal The percent area of testis occupied by seminiferous tubules was equal in control and treated testes, but mean seminiferous tubule diameter and length were increased in the PTU-treated testis The adult number of Sertoli cells in treated testes was increased by 157%, and the numbers of leptotene spermatocytes and round spermatids were increased 84% and 93%, respectively These results demonstrate that increases in Sertoli cell numbers result in increased sperm production and support the idea that Sertoli cells are the major regulators of the magnitude of sperm production Although the round spermatid to Sertoli cell ratio was reduced by nearly 30%, the number of round spermatids per g testis was increased by 14% This increased efficiency of sperm production was accomplished by an increased density of Sertoli cells along the basement membrane and an increased height of the seminiferous epithelium Despite the large increase in Sertoli cell numbers in treated rats, Northern blot analysis using Sertoli cell-specific cDNA probes for transferrin and androgen-binding protein indicated that relative steady state levels of mRNAs per Sertoli cell for these two secretory proteins were similar in control and treated rats at 90 days of age
TL;DR: The extracellular transport and intracellular receptor mechanisms for androgen are described, which influence spermatogenesis and sperm maturation.
Abstract: Spermatogenesis is an androgen dependent process which can be maintained in hypophysectomized rats by the administration of either testosterone (1) or 5α-dihydrostestosterone (2). Gonadotrophins may exert their effects on spermatogenesis indirectly by way of androgens. The sole action of LH appears to result from the stimulation of testosterone synthesis by the interstitial cells of Leydig. FSH is necessary for the full maintenance of spermatogenesis, but its effects can be mimicked by androgen and blocked by the anti-androgen, cyproterone, indicating that its action is linked in series with androgen (1) or that androgen is the mediator of FSH action.
TL;DR: An androgen-binding protein (ABP) was detected in 105,000 × g supernatants of rat testis homogenates after removal of endogenous steroids by charcoal extraction and it was suggested that a major portion of ABP is found in caput supernatant.
Abstract: An androgen-binding protein (ABP) was detected in 105,000 × g supernatants of rat testis homogenates after removal of endogenous steroids by charcoal extraction. The ABP was identical to that previously demonstrated in highspeed supernatants of epididymis homogenates. When the exocrine secretion of the testis was blocked by ligation of efferent ducts, ABP increased in testis supernatant in proportion to the retention of testicular fluid while at the same time it disappeared from epididymis supernatant, first from the caput and later from the cauda. Treatment with large doses of testosterone did not alter the disappearance from epididymis. ABP disappeared almost completely from caput supernatant within three days after efferent duct ligation. When efferent ducts and corpus epididymidis were ligated simultaneously to block the flow of luminal fluid into and out of the caput, the disappearance of ABP from caput supernatant was only partially prevented. This finding suggested that a major portion of ABP is ei...