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PubMed1985

Contrasting effects of prolactin on luteal and follicular steroidogenesis.

To determine whether prolactin affects both luteal and follicular production of testosterone and oestradiol, pseudopregnant rats, either intact or hypophysectomized on day 8, were injected daily between days 8 and 9 with 1.5 i.u. human chorionic gonadotrophin (hCG), 250 micrograms prolactin or a combination of both. Control rats were given vehicle. On day 9, blood was obtained from the ovarian vein and corpora lutea and follicles were isolated and incubated in vitro for 2 h. Administration of hCG to intact rats increased ovarian secretion of testosterone and oestradiol dramatically, but did not affect progesterone secretion. Hypophysectomy on day 8 of pseudopregnancy was followed by a drop in ovarian steroid secretion. Prolactin treatment of hypophysectomized rats markedly enhanced progesterone production but had no stimulatory effect on either testosterone or oestradiol. In contrast, hCG dramatically enhanced ovarian secretion of both testosterone and oestradiol without affecting progesterone secretion. Prolactin administered together with hCG antagonized the stimulation of both testosterone and oestradiol secretion by hCG, yet increased progesterone production. When the specific effects of hCG and prolactin administration on follicles and corpora lutea were studied separately, it was found that hCG treatment in vivo greatly stimulated testosterone and oestradiol production by both tissues in vitro. Since hCG only marginally affected aromatase activity in the follicle, had no effect on aromatase activity in luteal cells and did not increase progesterone synthesis, it appears that hCG acts to increase the formation of androgen substrate for oestradiol biosynthesis. Prolactin, administered with or without hCG, inhibited both basal and hCG-stimulated testosterone and oestradiol synthesis by the follicle. In sharp contrast to its inhibitory effect on follicular production of steroids, prolactin appears to be essential for LH stimulation of testosterone and oestradiol by the corpus luteum. In the absence of prolactin, luteal cells gradually ceased to respond to LH and decreased their output of testosterone and oestradiol. Prolactin administration to hypophysectomized rats did not affect luteal cell production of either steroid. However, corpora lutea of rats treated with prolactin responded to the hCG challenge with an increase in testosterone and oestradiol synthesis. In summary, results of this investigation demonstrate that prolactin affects follicular and luteal production of testosterone and oestradiol in opposite ways.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1996

Older males secrete luteinizing hormone and testosterone more irregularly, and jointly more asynchronously, than younger males.

New statistical perspectives on the secretory patterns of both luteinizing hormone (LH) and testosterone (T) may prove useful in further understanding the aging process, and possibly ultimately in improving the diagnosis and treatment of spermatogenetic failure and loss of sexual interest. We examined serum concentration time-series for LH and T in 14 young (21-34 years of age) and 11 aged (62-74 years of age) healthy men. For each subject, blood samples were obtained at 2.5-min intervals during a sleep period, with an average sampling duration of 7 hr. For each of LH and T, we used the model-independent statistic approximate entropy (ApEn) to quantify the irregularity of the serum concentration time-series; to quantify joint LH-T secretory asynchrony, we employed the recently introduced cross-ApEn. Although mean (and SD) LH and T concentrations were indistinguishable in the two age groups (P > 0.25), for LH, aged subjects had greater ApEn values (1.525 +/- 0.221) than younger individuals (1.207 +/- 0.252), P < 0.003, indicating more irregular secretion in the older cohort. For T, aged subjects also had greater ApEn values (1.622 +/- 0.120) than younger counterparts (1.384 +/- 0.228), P < 0.004. In young, but not older men, ApEn(T) significantly exceeded ApEn(LH), P < 0.02. Aged subjects had greater cross-ApEn values (1.961 +/- 0.121) than younger subjects (1.574 +/- 0.249), P < 10(-4), with nearly 100% sensitivity and specificity, indicating greater LH-T asynchrony in the older group. In conjunction with previous findings of greater irregularity of growth hormone release with increasing age, we propose that increased secretory irregularity with advancing age may be a widespread hormonal phenomenon. Finally, theoretically, we clarify the need for quantifications such as ApEn and cross-ApEn via a study of a "variable lag" pulsatile process, and empirically note the potential wide applicability of cross-ApEn to quantify asynchrony in interconnected (hormonal) networks.

Adult↗
PubMed1994

Effects of dietary zinc deficiency on the reproductive system of young male sheep: testicular growth and the secretion of inhibin and testosterone.

The effects of dietary zinc deficiency on testicular development in young Merino rams (initial live mass, 22 kg) were tested. Four groups of five rams were fed ad libitum with diets containing 4, 10, 17 or 27 micrograms Zn g-1. To control the effects of loss of appetite caused by zinc deficiency, a fifth group (pair-fed control) was fed the diet containing 27 micrograms Zn g-1, but the amount of feed offered was restricted to that eaten voluntarily by the zinc deficient (4 micrograms Zn g-1) rams they were paired with. After 96 days on the diets, epididymal and testicular masses did not differ significantly between the animals fed 10, 17 or 27 micrograms Zn g-1 ad libitum, but were significantly lower in pair-fed controls, and lowest in the zinc-deficient animals. Testicular responsiveness to LH, as measured by testosterone production, increased substantially in most rams as the experiment progressed, the only exception being the zinc-deficient group, in which the response to LH was lower than in any of the other groups. Testicular concentrations of zinc and testosterone were lower in the zinc-deficient animals than in all the other groups. Plasma inhibin concentrations fell as the experiment progressed in rams fed 17 and 27 micrograms Zn g-1 ad libitum, but not in the other groups. The pair-fed control rams had smaller seminiferous tubules and less lumen development than did the controls fed ad libitum (27 micrograms Zn g-1), which were similar to the animals fed 10 or 17 micrograms Zn g-1. In zinc-deficient rams, the tubule development was further retarded and the interstitial regions were more extensive than in the other groups. We conclude that the overall effect of zinc deficiency on testicular development is due to a combination of a non-specific effect (low gonadotrophin concentrations caused by the low feed intake) and a specific effect due to the lack of zinc. The zinc-specific effect is localized within the testis where it reduces the development of the capacity to produce testosterone, leading to low intratesticular concentrations of testosterone, a critical factor for the growth, development and function of the seminiferous tubules.

Animals↗
PubMed1985

Steroid secretion by cumulus cells isolated from human preovulatory follicles.

The secretion of progesterone, testosterone, and oestradiol by intact human oocyte-cumulus complexes in vitro was examined in incubations lasting 6-24 h. The complexes were aspirated from preovulatory follicles in 32 women who, due to tubal disease, were participating in an in vitro fertilization program. In 12 of the women follicular maturation was induced with clomiphene and human chorionic gonadotrophin (hCG), in 13 women with human menopausal gonadotrophin (hMG) and hCG and in 7 women with a combination of clomiphene-hMG plus hCG. The net secretion of steroids into the fertilization medium was studied before (0-6 h) and after (6-24 h) the addition of sperm, by RIA of aliquots removed at specific times. A high and sustained secretion of progesterone was found both before and after insemination. Testosterone secretion remained at a low and constant level while a net release of oestradiol was found mainly during the first hours of incubation. The release of steroids, particularly progesterone, varied according to the mode of hormonal stimulation in vivo and was highest in complexes from clomiphene-hMG-treated women, probably reflecting different maturity of the aspirated follicles. In a second series of experiments the dispersed cumulus cells were recovered after fertilization and cultured as monolayers for 2-4 days. The cells underwent spontaneous luteinization and secreted high amounts of progesterone. These results extend previous work in animals showing that also in the human the periovulatory cumulus cells are steroidogenically active. The results also suggest a functional difference in the cumulus cells related to the mode of ovulation induction.

Cell Count↗
PubMed1987

Decrease of serum testosterone by cyproterone acetate accompanied by an unexpected increase of calcitonin secretion capacity.

The interaction between testosterone and calcitonin secretion capacity was studied in 9 patients with prostatic cancer. Treatment with the antiandrogenic agent cyproterone acetate resulted in an expected decrease in serum testosterone but an unexpected and unexplained increase in calcitonin secretion capacity. The previous statement that a positive correlation between sex hormones and calcitonin secretion capacity can be recognized probably requires revision. This unexpected effect of cyproterone acetate had possible additive beneficial advantages for treatment, such as bone mass sparing and its analgesic effect.

Aged↗
PubMed1984

Ontogeny of hypothalamo-adenohypophyseal-gonadal (HAG) interrelationships in the chick embryo.

In the male chick embryo the components of the hypothalamo-adenohypophyseal-testicular axis initially function independently of each other. It is not until days 12.5-13.5 that the adenohypophysis begins to regulate testosterone synthesis and secretion; on day 13.5 plasma testosterone reaches a maximum embryonic level. This feed forward regulation of the pituitary-testicular unit appears to involve a cause and effect relation between a statistically significant increase in the number of testicular interstitial cell LH receptors on days 12.5 and 13.0 and an increase in plasma LH levels on day 13.5 (up-regulation). Subsequently, events occur that are interpreted as indicative of the feedback phase of this endocrine axis. Plasma LH levels decrease after day 13.5. Also on day 13.5 and all subsequent embryonic days, there is a significant decline in the volume density of testicular LH receptor-positive interstitial cells (IC) associated with an internalization of the LH receptor complexes and a marked decline in plasma testosterone levels (down-regulation). It is strongly suggested that the decline in the number of LH receptor-positive ICs and the internalization of the LH receptor complexes is indicative of a "desensitization" of the ICs followed by a decrease in testosterone synthesis and secretion. Comparable events that occur in the female embryo with respect to the development of the hypothalamo-adenohypophyseal-ovarian axis are also discussed in this minireview.

Animals↗
PubMed1991

Naloxone does not reverse the suppressive effects of testosterone infusion on luteinizing hormone secretion in pubertal boys.

In this study we wished to test whether, and if so when, the suppressive effects of testosterone on LH and, by inference, GnRH secretion are mediated via endogenous opioid pathways during male pubertal maturation. As a preliminary study, we evaluated the acute effects of a 24-h infusion of testosterone (T) in eight pubertal boys with constitutional delay of growth in order to determine the optimal time for administration of naloxone. Eight additional pubertal boys received a saline infusion, followed 1 week later by a similar T infusion starting at 1000 h and lasting for 33 h. After 2 h of infusion (both saline and T), four iv boluses of saline were given hourly, and after 26 h of infusion, four hourly iv boluses of naloxone were given. Blood was obtained every 15 min for LH and every 30 min for T measurements. T infusion increased the mean T concentration by 3.8-fold (P less than 0.001). Mean LH and LH pulse frequency were suppressed (P less than 0.01), and the sleep-associated increase in LH secretion was abolished. Naloxone administration during the infusion of T did not reverse the suppression of LH secretion. Compared to the saline control period, mean LH was significantly lower during T infusion during the time naloxone boluses were given (4.5 +/- 0.9 vs. 5.9 +/- 1.1 IU/L, T infusion and naloxone boluses vs. saline respectively, P less than 0.01). Although the suppression of LH pulse frequency remained significantly lower than that during the saline control period (0.23 +/- 0.04 pulses/boy.h during T infusion and saline boluses; 0.33 +/- 0.04 pulses/boy.h during T infusion plus naloxone boluses; 0.44 +/- 0.06 pulses/boy.h during saline infusion and saline boluses). Naloxone increased mean LH and LH pulse frequency only in the four older, more mature boys during the infusion of saline. Pituitary responsiveness to exogenous GnRH was not altered by infusion of T. We conclude that acute administration of T suppresses LH secretion and, by inference, GnRH secretion at all stages of pubertal maturation in boys. These negative feedback effects, however, cannot be reversed by coadministration of naloxone, even in mid- to late pubertal boys who respond to naloxone with increased pulsatile secretion of LH. These studies suggest that during pubertal maturation in boys, endogenous opioid pathways do not play a major role in the regulation of the negative feedback effects of T.

Adolescent↗
PubMed1976

Seasonal variation in the episodic secretion of luteinizing hormone and testosterone in the ram.

Rams of an ancient breed of domestic sheep (Soay) were housed under artificial lighting conditions to study the way in which the secretion of LH and testosterone changes in relation to the mating season. Conspicuous changes were found in the short-term fluctuations in plasma LH concentrations related to the cycle of testis growth and regression; serial blood samples collected at short intervals revealed episodic peaks in plasma LH at all times, but there were changes in the frequency (lowest when the testes were regressed and highest when fully active), amplitude (lowest at the peak of testis activity, and highest during the developing phase), and duration of the peaks (shortest when the testes were regressed). In addition, the basal levels changed from being lowest in the regressed phase of the testis cycle, and highest when the gonads were most active. Plasma testosterone concentrations changed in parallel with the cycle of testis size and were correlated with the fluctuating levels of LH. Each episodic peak in plasma LH was associated with an increase in the levels of testosterone, beginning after 0-30 min and rising to a peak at 60-90 min; the speed and magnitude of the response being greatest when the testes were largest, but was not correlated with the magnitude of the LH change. Injections of LH releasing hormone (5 mug) stimulated an increase in plasma LH and testosterone proportional to the endogenous fluctuations in the hormones at the various stages of the seasonal cycle; LH concentrations were raised to supra-physiological levels after the injections, while testosterone concentrations seldom exceeded the normal peak values at any stage. These observations are used to discuss the role of the hypothalamus in the control of male seasonality with emphasis on the dynamic interplay between the hypothalamus, pituitary and testis.

Animals↗