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PubMed2005

Testosterone replacement-induced hyperprolactinaemia: case report and review of the literature.

Half of all men with prolactin (PRL)-producing macroadenomas present with hypogonadism, decreased libido and impotence, and therefore require testosterone replacement. However, very little is known about the effect of testosterone on prolactinomas. We report a case of an 18-year-old obese man who presented with hypogonadism and hyperprolactinaemia and underwent a transphenoidal hypophysectomy after a computer tomography scan showed the presence of a suprasellar macroadenoma. On separate occasions, we documented a rise in PRL when testosterone replacement was started and a fall in PRL when testosterone replacement was stopped (r = 0.6090, P = 0.0095). Furthermore, imaging studies suggested the possibility of tumour re-growth after testosterone therapy. We hypothesize that the exogenous testosterone was aromatized to oestradiol, which stimulated the release of PRL by the anterior pituitary. This was supported by the increase in oestradiol levels after testosterone replacement, although statistical significance was not achieved due to the availability of only a few data points. This case highlights the need to be aware of testosterone-replacement-induced hyperprolactinaemia, an under-recognized complication of androgen replacement in this setting. The use of aromatase inhibitors together with testosterone-replacement therapy or the use of non-aromatizable androgens might be indicated in such patients. Taken together, this report and previous studies show that dopamine agonists apparently do not suppress the hyperprolactinaemia induced by testosterone replacement.

Adenoma↗

PubMed2005

Effect of testosterone replacement on trabecular architecture in hypogonadal men.

UNLABELLED: We evaluated the effect of testosterone treatment on trabecular architecture by microMRI in 10 untreated severely hypogonadal men. After 2 years, microMRI parameters of trabecular connectivity improved significantly, suggesting the possibility that testosterone improves trabecular architecture. INTRODUCTION: Osteoporosis, characterized by low BMD and diminished bone quality, is a significant public health problem in men. Hypogonadal men have decreased BMD and deteriorated trabecular architecture compared with eugonadal men, and testosterone treatment improves their BMD. We tested the hypothesis that testosterone replacement in hypogonadal men would also improve their trabecular architecture. MATERIALS AND METHODS: We selected 10 untreated severely hypogonadal men and treated them with a testosterone gel for 24 months to maintain their serum testosterone concentrations within the normal range. Each subject was assessed before and after 6, 12, and 24 months of testosterone treatment by magnetic resonance microimaging (microMRI) of the distal tibia and by DXA of the spine and hip. The microMRI parameters reflect the integrity of the trabecular network and include the ratio of all surface voxels (representing plates) to curve voxels (representing rods) and the topological erosion index, a ratio of topological parameters expected to increase on trabecular deterioration to those expected to decrease. The higher the surface-to-curve ratio and the lower the topological erosion index, the more intact the trabecular network. RESULTS: Serum testosterone concentrations increased to midnormal after 3 months of treatment and remained normal thereafter. After 24 months of testosterone treatment, BMD of the spine increased 7.4% (p<0.001), and of the total hip increased 3.8% (p=0.008). Architectural parameters assessed by microMRI also changed: the surface-to-curve ratio increased 11% (p=0.004) and the topological erosion index decreased 7.5% (p=0.004). CONCLUSIONS: These results suggest the possibility that testosterone replacement of hypogonadal men improves trabecular architecture.

Adolescent↗

PubMed2003

Modulatory role of testosterone in plasma leptin turnover in rats.

We explored whether testosterone influences circulating leptin turnover in rats. Sham-operated male and female rats and 21-d gonadectomized rats treated or not treated with testosterone propionate were used. Anesthetized rats were implanted with an iv catheter, and then blood samples were drawn before and throughout a 60-min period following systemic leptin administration. Plasma testosterone, estradiol, and leptin concentrations were monitored. The results indicated that while gonadectomy blunted circulating concentrations of the homologous sex steroid, testosterone therapy, in gonadectomized rats, restored plasma testosterone concentrations to values found in normal male rats. Pharmacokinetic parameters evaluated during the test indicated the following: First, in the overall pharmacokinetic analyses, testosterone therapy in gonadectomized rats induced a more rapid disappearance of leptin from the circulation. Second, orchidectomy significantly enhanced the area under the curve (AUC) of circulating leptin, an effect fully reversed by testosterone treatment. Third, testosterone treatment in ovariectomized rats significantly decreased the AUC of leptin concentrations. Fourth, while gonadectomy alone did not modify circulating leptin half-life, conversely, testosterone therapy in gonadectomized rats decreased leptin halflife in the circulation. Finally, while orchidectomy reduced leptin body clearance, this parameter was increased by androgen therapy in gonadectomized rats. Our results strongly support that testosterone could play a main role in plasma leptin turnover by increasing leptin clearance rate and shortening plasma leptin half-life.

Animals↗

PubMed1990

Testicular responsiveness to hCG during infancy measured by salivary testosterone.

To investigate the role of gonadotropins in postnatal testicular activation, testosterone responsiveness to human chorionic gonadotropin was studied in 11 male infants (aged 5-180 days). The boys were given a single im injection of 5000 IU/1.7m2 hCG, and serum and salivary testosterone responses were then measured for 7 days. The results were compared with the serum testosterone responses of 8 older prepubertal boys (aged 1.7-10.4 years) studied with the same protocol. The mean (+/- SEM) basal serum testosterone levels were 2.67 +/- 1.27 nmol/l in the infants and 0.09 +/- 0.02 nmol/l in the prepubertal boys (p less than 0.05). Both groups gave a significant response to hCG stimulation (p less than 0.001, ANOVA, one-way). The stimulated concentrations of serum testosterone were higher in the infants than in the prepubertal boys (p less than 0.001). The mean basal level of salivary testosterone was 30.5 +/- 7.0 and the mean maximal level was 97 +/- 10.3 pmol/l in the infants (p less than 0.001). No age-related changes were observed in either basal or hCG-stimulated levels. In infants the mean (+/- SEM) maximal hCG-stimulated increase was 25 +/- 10-fold in serum and 8 +/- 4-fold in saliva (p = 0.13). A clear stimulatory effect of hCG on testicular testosterone production was found, suggesting that the postnatal increase in serum testosterone concentration in male infants is gonadotropin-mediated. Salivary testosterone concentrations can be increased by hCG, indicating that measurements of salivary testosterone may provide an optional, non-invasive method for assessing gonadal function in children.

Aging↗

PubMed1983

Effect of oestradiol and tamoxifen on the testosterone response in male rats to a single injection of hCG.

A single s.c. injection of hCG (100 i.u.) produced a biphasic serum testosterone response in adult male rats, peaks being noted at 2 h (24 ng/ml) and 3 days (16 ng/ml). The levels fell to control during the intervening interval (8 ng/ml), although there were elevated levels of serum hCG. Maintenance of high oestradiol levels by a s.c. injection of 50 micrograms oestradiol benzoate given on Day 2 after the initial hCG injection failed to prolong the refractory period and the secondary peak of testosterone (16 ng/ml) occurred on Day 3. Administration of the antioestrogen, tamoxifen (2 mg or 3 micrograms), 24 h before or simultaneously with hCG did not prevent testicular refractoriness in vivo because serum testosterone levels still declined after 2 h to reach a nadir at 2 days. The basal in-vitro testosterone production by decapsulated testes from animals injected with hCG was enhanced at 2 h. Stimulation by hCG increased the amount of testosterone produced (X 1.5 that in controls). By 12 h basal production decreased and there was no further increment in testosterone in the presence of hCG. This refractoriness to further hCG stimulation prevailed until Day 3, but the total production of testosterone fell so that at 24 h and 2 days testes were producing basal amounts of testosterone. Testes recovered from refractoriness at 4 and 5 days, when basal and stimulated testosterone production were greater than in controls. Injection of 50 micrograms oestradiol benzoate at 2 days did not prolong the in-vitro refractory period and 2 mg or 3 micrograms tamoxifen had no effect on the in-vitro steroidogenic activity, since testes were still refractory to further hCG stimulation from 12 h to 3 days. The results of the present study do not support the hypothesis that oestradiol is involved in the hCG-induced refractoriness of the Leydig cell. The nadir between the peaks of serum testosterone in vivo corresponds to the period during which the testis is refractory to in-vitro stimulation by hCG.

Animals↗

PubMed1993

Maintenance of spermiogenesis by exogenous testosterone in rats treated with a GnRH antagonist: relationship with androgen-binding protein status.

The relationship of the testicular distribution and [3H]dihydrotestosterone-binding capacity of androgen-binding protein (ABP) to the completion of spermiogenesis was examined in mature rats given daily injections of 25 or 250 micrograms kg-1 body weight of GnRH antagonist (GnRH-A; Ac-D(2), Nal1, 4Cl-D, Phe2, D-Trp3, D-Arg6, D-Ala10) for two weeks with or without subcutaneous implantation of 10 cm testosterone capsules. GnRH-A administration resulted in a dose-dependent suppression of serum FSH, which was partially prevented in the 250 micrograms GnRH-A kg-1 group by exogenous testosterone. The total testicular testosterone content and concentration of testosterone in seminiferous tubular fluid were equally suppressed in both groups of rats treated with GnRH-A and receiving the testosterone supplement. ABP concentrations in interstitial and seminiferous tubular fluid were normal in rats given the 25 micrograms GnRH-A kg-1 dose, and were increased (P < 0.05) by concomitant testosterone treatment. In contrast, ABP concentrations in interstitial and seminiferous tubular fluid were increased in rats given the 250 micrograms GnRH-A kg-1 dose. This effect was attenuated when exogenous testosterone was given. Although binding of [3H]dihydrotestosterone by ABP in seminiferous tubular fluid was not affected by GnRH-A treatment, with or without exogenous testosterone, it was reduced in interstitial fluid by GnRH-A in a dose-dependent manner, and partially restored by testosterone administration. While complete spermatogenesis was maintained in rats given 25 micrograms GnRH-A kg-1, the number of step 7 and step 19 spermatids were both reduced by 35%, and were not affected by testosterone implants.(ABSTRACT TRUNCATED AT 250 WORDS)

Androgen-Binding Protein↗

PubMed1993

Seasonal patterns of basal and GnRH-induced LH, FSH and testosterone secretion in Eld's deer stags (Cervus eldi thamin).

Plasma LH, FSH and testosterone were measured in blood samples collected via remote catheterization from six adult Eld's deer stags every 10 min for 8 h before and 2 h after GnRH (1 microgram kg-1, i.v.) administration. Blood samples were collected within 2 weeks of the summer solstice (21 June), autumn equinox (22 September), winter solstice (21 December) and spring equinox (20 March). Marked seasonal variations in basal LH, FSH and testosterone concentrations were observed. From autumn, well-defined LH pulses were temporally associated with small, but detectable pulses in testosterone. During the winter transition into the breeding season, episodic LH pulses were also temporally associated with corresponding testosterone surges that lasted 2-3 h. High amplitude, low frequency testosterone surges were also observed during the spring, but often in the absence of detectable LH pulses. Basal LH and testosterone concentrations decreased during the summer and, although LH pulses were detected, associated testosterone pulses were absent. Only 37% of LH pulses occurred coincidentally with FSH pulses, and FSH pulses were generally less prominent. The increases in LH and FSH above basal concentrations after GnRH treatment were significant (P < 0.05) for all seasons. Increases in testosterone after GnRH treatment were greatest during the winter and spring, but testosterone also increased to a lesser extent during the autumn (P < 0.05). In contrast, testosterone concentrations were not different before and after GnRH treatment during summer.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Effect of active immunization against testosterone on plasma gonadotrophin concentrations, spermatogenic function, testicular blood flow, epididymis mass and mating behaviour in adult rams.

The long-term effects of active immunization against testosterone were studied in rams, with particular reference to blood concentrations of gonadotrophin and testosterone, spermatogenesis, testis blood flow and mating behaviour. Ten 18-month-old Merino rams, kept on pasture, were studied for 1 year. Every 2 months, five rams received injections of BSA in Freund's adjuvant and five other rams were treated with testosterone-3(o-carboxymethyl)oxime-BSA as immunogen. Anti-testosterone antibodies (mean titre: 1:4484 +/- 582, after boosters) were maintained in the circulation, with the help of regular booster injections. In time, immunization reduced live mass in testosterone-immunized rams; however, there was no effect on testicular volume throughout the whole study. In testosterone-immunized rams, significantly higher concentrations of gonadotrophins were found in jugular venous plasma, as well as increased concentrations of total plasma testosterone. LH pulse frequency, amplitude and nadir were increased significantly in testosterone-immunized rams. After 12 months of immunization, no differences were found in the number of spermatozoa per ejaculate, in daily sperm production or in testis mass between the two groups of rams; however, testicular blood flow (per testis) and epididymis mass were significantly reduced in testosterone-immunized rams. Testosterone immuno-neutralization also resulted in a significant reduction in the number of mounts culminating in ejaculation performed during a 10 min trial carried out on a number of occasions during the experiment. Additional information on these rams was collected 3 months after castration. However, there were no significant differences in mean plasma LH and FSH concentrations, either before, or after, a single GnRH injection between the two groups of rams at this time.

Animals↗

PubMed1998

Effect of testosterone and cortisol administration on the reproductive tract of male Antechinus stuartii (Marsupialia).

The life history of Antechinus stuartii, a marsupial, is highly synchronized and culminates in a brief mating period that is followed by complete male mortality. The accessory reproductive tracts of male A. stuartii enlarge in association with testosterone and cortisol hormone concentrations, but this appears to be unrelated to the spermatogenic cycle. The present study examined the effects of testosterone and cortisol on the male reproductive tract. Four groups of adult males from May (when plasma testosterone and cortisol concentrations are low) were given depot injections of testosterone esters or synthetic cortisol in doses that mimic concentrations found in males in the breeding period (August). Males were given either saline, testosterone only, cortisol only, or testosterone plus cortisol. Experimental groups did not differ in the seminiferous tubule morphology. However, the cells from the caudal end of the epididymides of both testosterone groups were considerably hypertrophied compared with males treated with saline or cortisol only. Testosterone treatment significantly increased prostate and bulbourethral gland mass, although addition of cortisol to the testosterone administration diminished this effect. The morphology of the accessory reproductive tract of males treated with either saline or cortisol only was similar to that of untreated males at the same time of year, and the morphology of the accessory reproductive tract of males treated with testosterone plus cortisol was similar to that of untreated males in the breeding season. Like some other marsupials, the spermatogenic cycle in A. stuartii is apparently not correlated with androgen activity, while the accessory reproductive tract is affected by androgens.

Analysis of Variance↗

PubMed1985

Differential effects of gonadectomy on sensitivity to testosterone of brain centres associated with gonadotrophin negative feedback and with mating behaviour in rams.

Castrated sheep were used to study the effects of gonadectomy on sensitivity to testosterone of brain centres associated with gonadotrophin negative feedback and with mating behaviour. In the first experiment serum LH and FSH concentrations were determined in intact rams, recently castrated (2 days and 3 weeks) and long-term castrated animals (greater than 2 years, wethers) during intravenous testosterone infusion at physiological and supraphysiological levels. In intact rams, testosterone infusions effectively suppressed serum LH whilst FSH levels were suppressed only after prolonged infusion at the supraphysiological dose. Recently castrated sheep, which had higher gonadotrophin levels than intact rams, were less sensitive to testosterone feedback. Neither rate of testosterone infusion had any effect on the raised gonadotrophin levels in wethers. In a second experiment gonadotrophin concentrations and mating behaviour were determined in wethers bearing subdermal polydimethylsiloxane implants of testosterone, dihydrotestosterone and oestradiol. Testosterone implants stimulated mating behaviour in all wethers but suppressed gonadotrophins in only a proportion (three out of seven) of the animals. Both oestradiol and dihydrotestosterone suppressed LH and FSH in all wethers, whilst oestradiol, but not dihydrotestosterone, also stimulated mating behaviour. The present findings indicate that testosterone imposes continuing negative feedback on gonadotrophin secretion and that changes in the gonadotrophin regulatory system, which lead eventually to a loss in sensitivity to testosterone feedback, develop soon after gonadectomy. The results also provide the first direct evidence that longterm gonadectomy in male sheep has differential effects on sensitivity to testosterone of brain centres associated with gonadotrophin negative feedback and with mating behaviour.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

A testosterone-independent reduction in net photoperiodic drive triggers photorefractoriness in male tree sparrows (Spizella arborea).

An experiment was performed to determine whether photorefractoriness in male tree sparrows is triggered by a testosterone-independent reduction in net photoperiodic drive or by a photoperiod-induced hypersensitivity of the hypothalamic-pituitary axis to testosterone negative feedback. Photosensitive male tree sparrows were transferred from 8 h light:16 h darkness (8L:16D) to 20L:4D. Birds were castrated bilaterally on day 28 of photostimulation. Beginning on day 33 and weekly thereafter until day 54, birds were given replacement testosterone (0-1.49 mumol) in s.c. polydimethylsiloxane capsules. Plasma samples collected on days 36, 43, 50 and 57 were assayed for LH. Plasma LH concentrations in birds without replacement testosterone were regarded as reflecting net photoperiodic drive in the absence of testosterone feedback, and the slopes of curves relating the logarithm of plasma LH concentration to dose of replacement testosterone were taken as quantitative measures of testosterone feedback sensitivity. The results showed that a testosterone-independent reduction in net photoperiodic drive beginning between days 43 and 50 preceded any change in sensitivity to testosterone negative feedback. Such results provide compelling evidence that a testosterone-independent mechanism triggers the photorefractory state in male tree sparrows.

Animals↗

PubMed1986

Testosterone metabolites do not participate in the control of hypothalamic LH-releasing hormone.

To determine whether the ability of testosterone to increase intrahypothalamic LH-releasing hormone (LHRH) in orchidectomized rats might be explained by the conversion of the hormone into either its 5 alpha-reduced or oestrogenic metabolites, testosterone, 5 alpha-androstan-17 beta-ol-3-one (DHT), 5 alpha-androstane-3 alpha,17 beta-diol (3 alpha-diol) and 5 alpha-androstane-3 beta,17 beta-diol (3 beta-diol) (2 mg/rat per day for 6 days) and oestradiol (0.1, 0.5, 1.0 and 5.0 micrograms/rat per day for 6 days) were injected into castrated male rats. After 6 days the rats were killed and serum LH levels and intrahypothalamic LHRH stores measured using specific radioimmunoassay procedures. Testosterone and its 5 alpha-reduced metabolites were used in either the free alcohol or the propionate form (dipropionates in the case of the diols); oestradiol was used as oestradiol-17 beta or in the benzoate form. Treatment with testosterone, DHT, 3 alpha-diol and 3 beta-diol resulted in a significant decrease in serum LH levels; all the 5 alpha-reduced testosterone derivatives were more effective than testosterone in this respect. Testosterone and DHT propionates suppressed LH release following orchidectomy totally; 3 alpha-diol and 3 beta-diol dipropionates were less effective. Testosterone increased intrahypothalamic LHRH stores, this effect being much higher after testosterone propionate, i.e. when intrahypothalamic LHRH stores were restored to pre-castration levels. None of the 5 alpha-reduced steroids was capable of modifying the low intrahypothalamic levels of LHRH found following orchidectomy; only 3 alpha-diol dipropionate exhibited some activity, but this was much lower than that of testosterone propionate. Oestradiol-17 beta was totally ineffective in decreasing serum LH in orchidectomized animals; in contrast, oestradiol benzoate progressively decreased serum LH.(ABSTRACT TRUNCATED AT 250 WORDS)

Androstane-3,17-diol↗

PubMed1996

Ontogeny of growth hormone, insulin-like growth factor-I, estradiol and cortisol in the growing lamb: effect of testosterone.

Exogenous sex steroids have altered growth hormone secretion in some domestic species. This study examined whether different physiological concentrations of testosterone alter muscle growth in sheep through modification of the somatotropic axis. The effects of testosterone on growth hormone (GH), insulin-like growth factor-I (IGF-I), estradiol (E2) and cortisol concentrations in growing lambs were evaluated in 20 rams, 20 wethers and 20 wethers receiving subcutaneous testosterone replacement therapy. Two animals from each of the three testosterone status groups were slaughtered at 14-day intervals from 49 to 133 days of age, and then at 28-day intervals until 217 days of age for a total of 10 slaughter ages. Animals were sampled every 10 min for an 8-h period 1 day prior to slaughter to characterize the episodic patterns of GH and testosterone. Immediately after slaughter, the semitendinosus, splenius and triceps brachii muscles were removed, trimmed of adhering fat and connective tissue, and weighed. Testosterone increased the combined muscle weight. GH concentrations decreased during the course of the experiment. However, there was no effect of testosterone on GH mean, baseline, amplitude or GH pulse frequency measured by PULSAR. IGF-I concentrations increased in response to testosterone treatment. Testosterone had no effect on cortisol levels while E2 levels were increased after 133 days. Increased muscle growth due to testosterone appeared to be caused either by a direct effect or by increased levels of IGF-I independent of circulating GH concentrations.

Animals↗

PubMed2002

Pharmacokinetics, safety and tolerability of three dosage regimens of buccal adhesive testosterone tablets in healthy men suppressed with leuprorelin.

We used a randomised, double-blind, crossover design to evaluate the pharmacokinetics, safety and tolerability of three doses of buccal adhesive testosterone tablets (BATT). Twenty-four healthy men, whose endogenous testosterone was suppressed to </=5.38 nmol/l with leuprorelin acetate, took BATT (10, 20 or 30 mg) daily for 10 days. There was a 4-day washout between treatments. Substantial testosterone absorption occurred from BATT, and mean serum testosterone, free testosterone and dihydrotestosterone (DHT) concentrations over 24 h showed circadian variation. Steady state was reached by day 5. Average 24-h concentrations for the three BATT doses were within the normal range for eugonadal men: testosterone 11.67-14.57 nmol/l, free testosterone 0.026-0.33 nmol/l and DHT 1.66-2.03 nmol/l. On all three doses, peak testosterone and free testosterone was reached 8-9 h after tablet application; DHT peaked about 1-2 h later, and declined more slowly. Hormone concentrations increased with BATT dose, but increases were less than dose-proportional. There was no evidence of testosterone accumulation. BATT was well tolerated.

Administration, Buccal↗

PubMed2006

Feedback inhibition of gonadotropins by testosterone in men with hypogonadotropic hypogonadism: comparison to the intact pituitary-testicular axis in primary hypogonadism.

Men with hypogonadotropic hypogonadism (HH) due to hypothalamic-pituitary disease present with low serum testosterone levels combined with undetectable, low, or normal gonadotropin levels. Treatment consists of testosterone replacement to reverse the symptoms of androgen deficiency. The aim of this study was to examine the dynamics and feedback inhibition of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) in relation to testosterone in 38 men with HH treated with testosterone. Findings were compared with 11 men with primary hypergonadism (PH). Testosterone replacement led to a suppression of FSH levels from 2.8 IU/L at baseline to 1.1 IU/L and to a suppression of LH levels from 2.3 to 0.8 IU/L. There was a linear correlation between levels of FSH and LH (after natural log transformation for both) and testosterone levels in both the HH and PH groups. However, the differences in intercepts and slopes between the groups were significant. To determine whether nonsuppressed FSH or LH during testosterone replacement reduces the probability of eugonadism, as reflected by normal testosterone levels, gonadotropin levels were measured and categorized as low (<0.5 IU/L), medium (0.5-2 IU/L), and high levels (>2 IU/L). The higher FSH or LH levels were found to significantly decrease the chance for achieving eugonadism. In conclusion, in men with HH due to hypothalamic-pituitary disease or injury, the pituitary-testicular hormonal axis maintains its physiological negative feedback between testosterone and gonadotropins. Thus, gonadotropin levels in men with HH might be useful, together with testosterone concentrations, for assessing the adequacy of androgen replacement.

Adolescent↗

PubMed2000

Testosterone: its role in development of prostate cancer and potential risk from use as hormone replacement therapy.

Evidence from studies in patients with prostate cancer of intermittent hormone therapy combined with results from rechallenge of hormone resistant patients with testosterone demonstrate that the majority of prostate cancers retain a similar degree of dependence on male sex hormone milieu as normal prostate cells. Yet there has so far been no conclusive evidence, despite 34 studies, that levels of circulating testosterone in individuals developing prostate cancer are higher than in controls. The aim of this article was to critically evaluate this evidence and seek clues to other mechanisms whereby sex hormones could influence the development of prostate cancer. Additionally, epidemiological data were examined to investigate the interplay between sex hormone levels and environmental factors to help understand the development of prostate cancer and identify a safe way to provide hormone replacement therapy (HRT). Three overviews provide similar evidence that there is no significant difference in mean testosterone levels between patients and controls. However in the most recent review of studies, though there was no difference in means between cases and controls, there was a significant risk (adjusted odds ratio 2.34) for individuals identified by comparing incidence of prostate cancer in men in the upper and lower quartile of testosterone level. This report, taken with epidemiological data demonstrating that prostate cancer risk is increased by early age of onset of sexual activity and multiple nonspecific sexually transmitted diseases (STDs), has led to the hypothesis that the link between sex hormones and prostate cancer is indirect. Those individuals with high testosterone levels were more at risk of acquisition of multiple nonspecific STDs. This promotes transformation of prostate cells and damage to Leydig cells in the testis leading to there being no difference in testosterone compared with controls by the time the tumour is diagnosed. Because of the observed relationship between testosterone and prostate cancer development there has been anxiety about marketing HRT for men. Two observations support the view that the prostate cancer risks from use of testosterone hormone replacement may not be as great as first feared. Firstly, prostate cancers arising in men with low serum testosterone levels are more malignant and frequently nonresponsive to hormones. Secondly, breast cancers diagnosed in women on HRT though increased in number are less malignant possibly because of enhanced sensitivity to hormone therapy, and the situation may prove to be analogous with prostate cancer and testosterone replacement.

Animals↗

PubMedDate not supplied

The relationship between serum testosterone level and visuomotor learning in right-handed young men.

The relationship between serum testosterone level and visuomotor of learning of hand skill was studied in right-handed young men. Hand skill was assessed by a peg moving task. Peg moving times for the right and left hands linearly decreased at each successive trial (visuomotor learning). The peg moving times for the right and left hands were found to be negatively linearly related to serum testosterone levels: there was a direct relationship between hand skill and testosterone, which was more prominent for the right than the left hand. The slopes of the learning curves for the right hand were found to be equal in subjects with low, normal, and high testosterone. The intercepts of these curves exhibited a shift toward a better hand skill from low- to high-testosterone subjects. The visuomotor learning for the left hand was found to be better in subjects with normal and high testosterone than those with low testosterone. It was concluded that testosterone would favor the visuomotor development especially of the left cerebral hemisphere, probably at puberty; the motor learning of this hemisphere does not seem to be associated with testosterone. Testosterone seems to be advantageous for the visuomotor performance as well as for the motor learning of the right cerebral hemisphere.

Adolescent↗

PubMed1977

Metabolism of testosterone in the human prostate and seminal vesicles.

Tissue from the normal, hyperplastic and the cancerous human prostate as well as tissue from the human seminal vesicles are capable of metabolizing testosterone in vitro. By incubating minced tissue with 3H-testosterone for 2 hours at 37 degrees C the following radioactive metabolites were identified: testosterone (17 beta-hydroxyl-4-androsten-3-one), androstenedione (4-androstene-3,17-dione), androstanedione (5alpha-androstane-3,17-dione), 5alpha-dihydrostestosterone (17 beta-hydroxy-5alpha-androstane-3-one, DHT), 3alpha-androstanediol (5alpha-androstane-3alpha,17beta-diol), 3beta-androstanediol (5alpha-androstane-3beta-17beta-diol) and androsterone (3alpha-hydroxy-5alpha-androstane-17-one). When normal human prostatic tissue was incubated with 3H-testosterone approximately 40% of the hormone was metabolized and 30-35% of the metabolites were identified as DHT. There were apparently no differences in testosterone metabolism between the dorsal and lateral prostatic lobes. A much lower conversion of 3H-testosterone was observed in the seminal vesicles (24%). The same metabolites were formed by prostatic carcinoma tissue, although distinctive quantitative differences from the normal prostate were observed. Thus, only 23% of the testosterone was metabolized by cancerous tissue of which 15% was present as DHT. The formation of 17-keto metabolites and androstanediols in the prostatic carcinoma tissue was approximately the same as in the normal prostatic tissue. The most extensive metabolism of testosterone was found by incubation of tissue from benign nodular prostatic hyperplasia. About 65% of the testosterone was metabolized, and 40% of the metabolites were identified as DHT. Hyperplastic prostatic tissue also showed a significantly higher formation of 5alpha-androstanedoils and the other tissues examined. The high formation of DHT and 5alpha-androstanediols in benign nodular prostatic hyperplasia in comparison with normal and cancerous prostatic tissue and seminal vesicle tissue might indicate that these metabolites should be studied more closely as possible aetiological factors for prostatic hyperplasia. The very low metabolism of testosterone in prostatic carcinoma tissue should be examined further in relation to tumour differentiation and clinical effect of endocrine therapy.

Adenocarcinoma↗