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PubMed1993

The effect of testosterone aromatization on high-density lipoprotein cholesterol level and postheparin lipolytic activity.

Stanozolol, an oral 17 alpha-alkylated androgen, increases hepatic triglyceride lipase activity (HTGLA) and decreases high-density lipoprotein cholesterol (HDL-C) levels, whereas intramuscular testosterone has comparatively little effect. In the present study, we tested the hypothesis that aromatization of androgen to estrogen blunts the lipid and lipase effects of exogenous testosterone. Fourteen male weightlifters received testosterone enanthate (200 mg/wk intramuscularly), the aromatase inhibitor testolactone (250 mg four times per day), or both drugs together in a randomized cross-over design. Serum testosterone level increased during all three drug treatments, whereas estradiol level increased only with testosterone alone (+47%, P < .05), demonstrating that testolactone effectively inhibited testosterone aromatization. Testosterone decreased HDL-C(-16%, P < .05), HDL2-C(-23%, NS), and apoprotein (apo) A-I (-12%, P < .05) levels, effects that were consistently but not significantly greater with simultaneous testosterone and testolactone administration (HDL-C, -20%; HDL2-C, -30%; apo A-I, -15%; P < .05 for all). In contrast, both testosterone regimens decreased HDL3-C levels by 13% (P < .05 for both). HTGLA increased 21% during testosterone treatment and 38% during combined testosterone and testolactone treatment (P < .01 for both). Lipoprotein lipase activity (LPLA) increased only during combined testosterone and testolactone treatment (+31%, P < .01), suggesting that estrogen production may counteract the effects of testosterone on LPLA. Testolactone alone had little effect on any lipid, lipoprotein, apoprotein, or lipase concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2005

Development and validation of a simple and direct ELISA method for the determination of conjugated (glucuronide) and non-conjugated testosterone excretion in urine.

BACKGROUND: Several methods are now available to estimate urinary testosterone levels that can only be performed in established big laboratories using GC/MS techniques. In clinical practice or for research projects, an inexpensive method that does not require skilled technicians would be useful. A simple, rapid and accurate ELISA method has been developed and applied in our laboratory to measure urinary non-conjugated and total testosterone. METHODS: High affinity anti-testosterone antibody and HRP-Donkey anti-sheep IgG (Horse Radish Peroxidase) as enzyme tracer were used to develop the ELISA method. The assay was evaluated for specificity, sensitivity, parallelism, accuracy and imprecision by the established methods on samples obtained from healthy volunteers. The results from the direct ELISA were compared to those after enzyme hydrolysis plus solvent extraction and HPLC or commercial kits. RESULTS: A satisfactory standard curve for the direct testosterone ELISA has been developed with good sensitivity. Cross-reactivity values of anti-testosterone antibody with major interfering steroids were minimal except for testosterone-3-glucuronide (58.8%). The validity of urinary testosterone assay was confirmed by the good correlation between the results obtained by the direct ELISA and those after enzyme hydrolysis and solvent extraction (Y = 0.987X + 0.398, R2 = 0.97). Accuracy studies, parallelism and imprecision data were determined and all found to be satisfactory. Urinary testosterone excretion values obtained by our direct ELISA from healthy volunteers were generally in agreement with those published by other workers. Male urinary total testosterone excretion (non-conjugated and testosterone glucuronide) ranged from 177.9 to 865.3 nmol/day, which was about 3-6 times more than the range for women urinary testosterone excretion (34.5-308.8 nmol/day). CONCLUSION: A direct, reliable, easy to perform, sensitive and highly specific ELISA type assay for the measurement of total testosterone in urine samples (conjugated and non-conjugated) has been developed. The novel features of the assay are that it does not require an initial extraction step or involve time consuming procedures such as chromatography. A simple method has also been developed to measure non-conjugated urinary testosterone excretion after solvent extraction alone.

Adult↗

PubMed2006

Impact of testosterone on cardiac L-type calcium channels and Ca2+ sparks: acute actions antagonize chronic effects.

While androgens generally have been associated with an increased cardiovascular risk, recent studies indicate potential beneficial acute effects of testosterone. However, detailed evaluation of chronic and acute actions of testosterone on the function of cardiac I(Ca,L) and intracellular Ca2+ handling is limited. To clarify this situation we performed whole-cell and single-channel analysis of I(Ca,L), recordings of Ca2+ sparks, measurements of contractility and quantitative real-time RT-PCR in rat cardiomyocytes following testosterone pretreatment and acute testosterone application. Pretreatment with testosterone 100 nM for 24-30 h increased whole-cell I(Ca,L) from 3.8+/-0.8 pA/pF (n=10) to 10.1+/-0.31 pA/pF (n=9) at +10 mV (p<0.001). Increase of I(Ca,L) density was caused by both, increased expression levels of the alpha 1C subunit of L-type calcium channel and a pronounced increment of the single-channel activity (availability 81.8+/-3.15% versus 37.1+/-7.01%; open probability 12.8+/-3.09% versus 1.0+/-0.62%, p<0.01). Moreover, testosterone pretreatment significantly increased the frequency of Ca2+ sparks and improved myocytes contractility without altering SR Ca2+ load. All chronic effects could be inhibited by flutamide. In contrast acute testosterone administration significantly reduced I(Ca,L) density. Indeed, on the single-channel level acute testosterone application completely reversed the chronic testosterone-mediated effects, and antagonized the chronic testosterone effects on Ca2+ spark frequency, which was unaffected by flutamide. Thus, testosterone pretreatment activates I(Ca,L) via nuclear receptor-mediated pathways, while testosterone acutely blocks I(Ca,L) in a direct manner. Thus, testosterone chronically affects the basal level of intracellular Ca2+ handling, which in addition rapidly may be modulated by acute changes of hormone levels.

Animals↗

PubMed2006

Age related testosterone depletion in patients with erectile dysfunction.

PURPOSE: We assessed the pattern of age related testosterone depletion in patients with erectile dysfunction. MATERIALS AND METHODS: A total of 305 patients with erectile dysfunction who had a normal testosterone level at baseline visit and who completed the study were candidates for analysis. Erectile function was assessed using the International Index of Erectile Function. Patients underwent routine laboratory investigations plus total testosterone and prolactin assessment at the baseline visit and on a yearly basis for 4 years. RESULTS: The mean age +/- SD was significantly higher in 210 patients with decreased testosterone (55.3 +/- 7.3 years) than in 95 patients with steady testosterone (remaining within the normal range) (50.8 +/- 10.2 years). There was a significant decrease in yearly mean testosterone level throughout the study in all the age groups (determined by decades) older than 30 years. Of the study population 68.9% had decreases in testosterone levels throughout the 4 years of visits. Hypogonadism (testosterone lower than normal range) developed in 7.6% of the study population. There was a significant decrease in mean testosterone at any visit in comparison to previous visits. There were significant associations between decreased levels of testosterone and increased severity of erectile dysfunction at baseline visit, longer duration and poor metabolic control of diabetes, ischemic heart disease, hyperprolactinemia and low desire. CONCLUSIONS: This study clearly demonstrated a decrease in testosterone level throughout the 4-year followup in patients with erectile dysfunction. Patients with decreasing testosterone were older than patients with a steady testosterone level.

Adult↗

PubMed1997

The effect of parenteral testosterone replacement on prostate specific antigen in hypogonadal men with erectile dysfunction.

PURPOSE: Parenteral testosterone supplementation is a common treatment for erectile dysfunction in hypogonadal men. Despite its frequent use, the effect of testosterone on prostate specific antigen (PSA) in these patients has not been documented previously. In this study we determined the effect of parenteral testosterone replacement on PSA and PSA velocity in a group of men being treated for erectile dysfunction. MATERIALS AND METHODS: A retrospective analysis of 48 patients (mean age 65.9) was performed and 2 study groups were identified. Group 1 consisted of 27 patients with a serum PSA level before and after initiating testosterone replacement therapy, and group 2 consisted of 27 men with a minimum of 3 PSA measurements (intervals of 6 months or greater) while on testosterone replacement. Each man had erectile dysfunction, a normal digital rectal examination and a low or low-normal total serum testosterone level before initiating therapy. Testosterone replacement was discontinued if no subjective improvement in erectile function was obtained, or if prostate adenocarcinoma was suggested by digital rectal examination or PSA. RESULTS: The mean increase in PSA after initiating testosterone replacement was 0.29 ng./ml. representing a mean change of 37% from baseline (mean interval 12.8 months). The mean PSA velocity was 0.05 ng./ml. per year. Pretreatment testosterone level, age and testosterone dose did not independently alter the PSA during testosterone replacement. Eleven men required prostate biopsies during treatment. Biopsies were indicated for abnormal digital rectal examination in 10 men and an elevated PSA in 1. All biopsies were benign. CONCLUSIONS: Parenteral testosterone replacement in hypogonadal men with normal pretreatment digital rectal examination and serum PSA levels does not alter PSA or PSA velocity beyond established nontreatment norms. Thus, any significant increase in PSA or PSA velocity should not be attributed to testosterone replacement therapy and should be evaluated.

Aged↗

PubMed2006

[Evaluation of an immunoassay kit to measure free testosterone].

INTRODUCTION AND OBJECTIVES: The best indicators to the diagnosis of hypogonadism are free and bioavailable testosterone circulating levels. Free and bioavailable testosterone measurements are complex. However, simple kits for direct measurement of free testosterone by analog immunoassay are available. We examined the utility of an enzymoimmunoassay kit for free testosterone measurement. MATERIAL AND METHOD: One hundred thirty-three healthy males were included. Total testosterone, SHBG, albumin and free testosterone was measured. We used two different methods to free testosterone estimation: direct measurement by enzymoimmunoassay and mathematical calculation with Vermeulen's formula, which uses albumin concentration, total testosterone and SHBG to calculate free testosterone (method recommended by the International Society for the Study of the Aging Male). We compared the two methods means values and a linear regression study was performed. RESULTS: Mean age was 37 +/- 11 years. Mean serum concentration for total testosterone was 21.43 +/- 6.8 nm ol/L. The mean value for free testosterone measured by direct and mathematical method was 0.0508 +/- 0.0118 nmol/L and 0.474 +/- 0.123 nmol/L respectively. In linear regression study exists a positive correlation between both methods (p< 0.05), although correlation coefficient is very low (r = 0.25). CONCLUSIONS: There are significant statistical differences between the measurements of free testosterone by direct and mathematical methods. Although certain correlation is observed, this is very low. In conclusion, free testosterone measurement by enzymoimmunoassay is not reliable.

Adult↗

PubMed1996

Buccal absorption of testosterone and its esters using a bioadhesive tablet in dogs.

PURPOSE: As the oral bioavailability of testosterone is very low because of its high first pass effect, buccal administration might present a viable alternative. In this study a buccal bioadhesive tablet was used in order to sustain the delivery and bypass the liver. METHODS: Testosterone and testosterone acetate, propionate, enanthate and decanoate were investigated. The influence of the concentration of testosterone (10-50%) and testosterone esters (30%) on in vitro bioadhesion was investigated. The absolute (i.v.) and relative (oral) bioavailability of 60 mg testosterone or an equivalent amount of testosterone ester was determined in castrated male dogs. RESULTS: Both the in vitro detachment force and the work of adhesion decreased gradually with an increasing amount of testosterone and for an increasing chain length of the esters, except in the case of testosterone enanthate. The in vivo results revealed that the bioavailability of testosterone was significantly higher (p < 0.05) than that of the esters, which is probably due to the lower solubility of the esters. The mean absolute bioavailability of testosterone from the bioadhesive tablet was 14.1%, while the mean relative bioavailability was 1370%. The buccal administration of testosterone via the bioadhesive tablet allowed the maintenance of the plasma level at above 3 ng/ml for 15 to 24 h. CONCLUSIONS: Buccal absorption of testosterone was significantly higher than that of its esters.

Administration, Oral↗

PubMed2003

Significant ethnic variation in total and free testosterone concentration.

OBJECTIVE: Measurement of serum testosterone is an integral part of the assessment of men presenting to endocrine clinics. Little is known about the variation of total bound or bioavailable testosterone by ethnic group. The principal determinant of testosterone bioavailability is SHBG, which itself is a marker for insulin sensitivity. Our aim was to examine variations in testosterone and SHBG levels across three ethnic groups in relation to ethnic differences in insulin sensitivity. DESIGN: Men of three ethnic groups living in Manchester, UK, were sampled randomly from population registers being of white European (n = 55), Pakistani (n = 50) and African-Caribbean (AfC) origin (n = 75). Circulating serum testosterone and SHBG concentrations were measured and free testosterone calculated. Insulin sensitivity (HOMA-S) and insulin secretory capacity (HOMA-B) were determined from fasting plasma intact insulin and glucose values. RESULTS: Testosterone levels were lower in Pakistani men (mean 14.6 nmol/l, 95% confidence interval 12.6-16.6 nmol/l) than in Europeans (18.7, 16.8-20.6 nmol/l) or AfCs (18.0, 16.4-19.6 nmol/l) (F = 4.8, P = 0.009). Despite SHBG levels also being lower in Pakistani men (22.9, 19.4-26.5 nmol/l) compared with Europeans (28.7, 25.7-31.8 nmol/l) and AfCs (26.9, 23.9-30.0 nmol/l) (F = 3.0, P < 0.05), circulating free testosterone was significantly lower in the Pakistani group (367, 326-408 pmol/l) than in Europeans (455, 416-494 pmol/l) or AfCs (458, 424-492 pmol/l) (F = 6.8, P = 0.001). Pakistani men were on average 4 cm shorter than other groups. However, the lower free testosterone persisted even when adjusted for height or waist-hip ratio. The lower SHBG in the Pakistani men was paralleled by a lower HOMA-S (0.40, 0.25-0.56) compared with Europeans (0.77, 0.61-0.93) and AfCs (0.80, 0.66-0.93) (F = 8.2, P < 0.0001). SHBG correlated positively with HOMA-S (rho = 0.28, P < 0.001) and strongly with total testosterone (rho = 0.54, P < 0.001). There was no difference in insulin secretory capacity (HOMA-B) in Pakistani men compared with Europeans and AfCs. Multiple linear regression analysis showed that total testosterone was independently and negatively related to ln fasting insulin (beta = -0.28, P < 0.001) and age (beta = -0.17, P = 0.02) and positively to ln SHBG (beta = 0.23, P < 0.001) and height (beta = 0.22, P = 0.001). There was no relationship with ethnicity or waist-hip ratio. CONCLUSION: Both total bound and calculated free testosterone were lower in Pakistani men. SHBG levels were also lower in Pakistani men, in keeping with poorer insulin sensitivity. We propose that further work is necessary to establish ethnic-specific ranges for the interpretation of total circulating and free testosterone levels in men.

Adult↗

PubMed1985

Testosterone response of cryptorchid and hypophysectomized rats to human chorionic gonadotrophin (hCG) stimulation.

The testosterone responses to a single injection of hCG (100 i.u.) in hypophysectomized (hypox.), cryptorchid or sham-operated rats were followed over a 5-day period. In sham-operated rats, hCG induced a biphasic rise in serum testosterone, peaks being observed at 2 and 72 h. Reduced testis weights, elevated FSH and LH levels and reduced serum testosterone levels were found after 4 weeks of cryptorchidism, but hCG stimulation resulted in a normal 2 h peak in serum testosterone. However, the secondary rise at 72 h in cryptorchid rats was significantly lower than sham-operated rats. Reduced testis weight and undetectable serum FSH and LH levels together with decreased testosterone levels were found 4 weeks after hypophysectomy. Serum testosterone levels rose 2 h after hCG in comparison to hypox. controls but this peak was significantly reduced compared with sham-operated rats. The second rise in serum testosterone began on day 2, peaking on day 4 at levels comparable to that seen in sham-operated rats after hCG. The in vitro basal and hCG stimulated secretion of testosterone by cryptorchid testes was greater than that secreted by normal rat testes (518.0 +/- 45.9 and 3337.6 +/- 304.1 pmol per testis per 4 h compared with 223.6 +/- 24.9 and 1312.9 +/- 141.4 pmol per testis per 4 h for normal rat testes). In cryptorchid animals a single injection of 100 i.u. hCG resulted in a pattern of in vitro refractoriness similar to normal rats, lasting from 12 h to 2 days, during which testosterone secretion was reduced to near basal levels. The in vitro basal and hCG-stimulated secretion of testosterone by hypox. rat testes was severely diminished compared with normal rat testes. The temporal pattern of in vitro secretion of testosterone from hypox. rat testes mimicked the in vivo serum testosterone pattern seen in these animals. This study demonstrates important differences in the in vivo and in vitro testosterone response to hCG after testicular damage.

Animals↗

PubMed2004

Clinical experiences with testosterone therapy: prostate safety.

Due to a decrease in Leydig cell function, a considerable proportion of men over 50 years of age will develop hypogonadism. Consequently, loss of libido and several other testosterone-dependent symptoms may become evident. When decreased levels of biologically available testosterone are found, and corresponding symptoms are present, these men could be eligible for testosterone substitution therapy. Testosterone treatment in testosterone-deprived men has been shown to improve general well-being, osteoporosis, muscle atrophy, libido and--if present--anemia. Despite these positive effects, testosterone treatment has to be performed with caution. Although it has not been proven that elevation of the serum testosterone level to the normal range results in a greater risk of developing prostate cancer, the effects of testosterone on a prostate cancer already present are well established. Several studies have demonstrated that testosterone treatment does not result in a significant increase in serum levels of prostate-specific antigen (PSA) or prostate volume. The long-term effects, however, are currently unknown. For these reasons, testosterone treatment should be performed only when the presence of prostate cancer is unlikely; i.e. when PSA levels are within normal limits and digital rectal examination does not reveal any suspicious findings. These examinations may still miss some small prostate cancers that could be promoted by testosterone treatment. The determination of PSA levels under testosterone treatment is necessary every 3 months, at least for the first year. Steadily rising PSA levels require immediate cessation of testosterone administration and the initiation of further diagnostic procedures (prostate biopsy), to rule out prostate cancer.

Androgens↗

PubMed2004

Effects of testosterone on behavior, depression, and cognitive function in older men with mild cognitive loss.

BACKGROUND: The role of sex hormones in the prevention of cognitive decline is uncertain. Animal studies suggest mechanisms for sex hormones including testosterone to maintain optimal cognitive function. But, there are studies to suggest that endogenous testosterone levels are associated with aggression in men with cognitive impairment. METHODS: In this pilot study, 11 men (mean age 80 +/- 5 years, range 73-87 years) with early cognitive decline and bioavailable testosterone levels below 128 ng/dl (lower limit for adult normal range) were randomized to receive intramuscular testosterone (200 mg every 3 weeks) or placebo for 12 weeks. Outcome measures included sex hormones (testosterone, bioavailable testosterone, sex hormone binding globulin, estradiol, and estrone), Behave AD Questionnaire, Katz Activities of Daily Living, Geriatric Depression Scale, Digit Span, Clock Face Drawing, Clock Face Perception, Verbal Fluency, Trail-Making B, and International Prostate Symptom Score at baseline, 4 weeks, and 10 weeks. RESULTS: All men completed the study. Total and bioavailable testosterone, estrone, and estradiol levels increased in men receiving testosterone, but no changes were detected in men receiving placebo. No significant changes were found in behavior following testosterone supplementation, nor was there evidence of change in depression or activities of daily living. No discernable changes were found in any of the cognitive tests. Symptoms of prostate hyperplasia remained unchanged in the testosterone (6.6 + 5.8 to 5.2 + 3.6; p =.39) and placebo (8.8 + 6.4 to 6.4 + 3.8; p =.15) groups, and prostate-specific antigen levels did not change significantly. CONCLUSION: No significant changes in behavior, function, depression, or cognitive performance occurred following 12 weeks of testosterone replacement in men with low testosterone levels and early-to-moderate cognitive impairment. This pilot work suggests that testosterone can be given to men with early cognitive impairment without significant concern about worsening aggressive or unwanted behaviors.

Aged↗

PubMed1983

Phenotypic variation in testosterone and luteinizing hormone production among boars: differential response to gonadotropin releasing hormone and adrenocorticotropic hormone.

Variation in ability of boars to produce testosterone and luteinizing hormone (LH) in response to both gonadotropin releasing hormone (GnRH) and adrenocorticotropic hormone (ACTH) stimulation, as well as quantitative relationships between pretreatment and posttreatment responses, were assessed in a population of 38 boars of similar age and breeding. Peripheral testosterone concentrations following either GnRH or ACTH increased (P less than 0.01) to peak circulating levels of 7.16 +/- 0.62 and 8.42 +/- 0.81 ng/ml by 120 and 45 min, respectively. Post-GnRH testosterone area varied from 7.44 to 50.84 ng/ml X h (CV = 47.44%) and post-ACTH testosterone area ranged from 3.05 to 28.78 ng/ml X h (CV = 46.09%). GnRH-induced increases in testosterone were preceded by elevations (P less than 0.01) in peripheral LH concentrations but ACTH had no effect upon LH levels. Post-GnRH area varied from 7.07 to 125.45 ng/ml X h (CV = 76.61%). Significant (P less than 0.01) correlations were obtained between pre-GnRH and post-GnRH testosterone areas (r = 0.58) and between pre-ACTH and post-ACTH testosterone areas (r = 0.67). Nonsignificant (P greater than 0.10) correlations were obtained between post-GnRH and post-ACTH testosterone areas (r = 0.006) and between post-GnRH testosterone and LH areas (r = 0.09). The testosterone producing ability of boars was highly variable and their innate ability to produce testosterone influenced their response to GnRH and ACTH. Additionally, the mechanisms by which GnRH and ACTH influence testosterone production in boars appear to differ. Variation in the ability of boars to produce testosterone could not be explained on the basis of differences in circulating levels of LH.

Adrenocorticotropic Hormone↗

PubMed2004

Testosterone action on skeletal muscle.

PURPOSE OF REVIEW: To highlight recent data demonstrating direct anabolic effects of androgens on the mammalian skeletal muscle and review the mechanisms by which testosterone regulates body composition. RECENT FINDINGS: Testosterone increases lean body mass and decreases fat mass in young men; the magnitude of the changes induced by testosterone in lean and fat mass are correlated with testosterone dose and the prevalent testosterone concentrations. Older men are as responsive to the anabolic effects of testosterone on the muscle as young men, but have increased frequency of adverse events with higher testosterone doses. This reciprocal change in lean and fat mass induced by androgens is best explained by the hypothesis that androgens promote the commitment of mesenchymal pluripotent cells into myogenic lineage and inhibit adipogenesis through an androgen receptor mediated pathway. Resident muscle satellite cells increase in number with testosterone administration forming myoblasts leading to greater numbers of myonuclei in larger myofibers. Testosterone administration is associated with increased size of motor neurons. The roles of 5-alpha reduction and aromatization of testosterone into dihydrotestosterone and estradiol, respectively, in mediating testosterone effects on body composition are poorly understood. SUMMARY: Testosterone induces skeletal muscle hypertrophy by multiple mechanisms, including its effects in modulating the commitment of pluripotent mesenchymal cells. These changes in skeletal muscle lead to improved muscle strength and leg power; however, further studies are needed to determine the effects of testosterone on physical function and health-related outcomes in sarcopenia associated with aging and chronic illness.

Aging↗

PubMed1992

Serum levels of free and bound testosterone in hyperthyroidism.

OBJECTIVE: The aim of this study was to improve knowledge about the relationships between free and bound forms of testosterone in serum and the major testosterone-binding proteins during hyperthyroidism. DESIGN: Nine men and 11 women were studied when hyperthyroid due to Graves' disease and again after at least 3 months of euthyroidism. MEASUREMENTS: The serum concentrations of free T3, free T4, TSH, sex hormone-binding globulin (SHBG), LH, progesterone and free, non-SHBG bound and total testosterone were determined. RESULTS: For both sexes, hyperthyroidism was associated with significant elevations of the mean total testosterone and sex hormone-binding globulin (SHBG) levels and significant depressions of the mean percentage and concentration of non-SHBG-bound testosterone and the mean percentage of free testosterone. For women, the mean free testosterone concentration was significantly lower during hyperthyroidism than during euthyroidism; no significant difference in mean free testosterone concentration was observed between hyperthyroid and euthyroid men. When the experimentally derived data were analysed according to a model based on the binding constants of testosterone with SHBG and albumin, the simulated results for each patient when hyperthyroid and euthyroid paralleled the actual results. However, the model consistently overestimated the actual amounts of non-SHBG-bound testosterone. There was a significant correlation between SHBG concentration and the severity of thyrotoxicosis as measured by the change in thyroid hormone levels between euthyroidism and hyperthyroidism. CONCLUSIONS: Our results support the following pathogenetic sequence: thyrotoxicosis leads to a rise in serum SHBG concentration which is accompanied by an increase in testosterone concentration, a fall in the concentration of non-SHBG-bound testosterone and little or no change in the concentration of free testosterone.

Adolescent↗

PubMed1993

The relationship between endogenous testosterone and gonadotrophin secretion.

OBJECTIVE: The secretion of luteinizing hormone (LH), follicle stimulating hormone (FSH) and testosterone in the adult male was studied by means of 48-hour profiles. The aim of the study was to examine the effects of the endogenous circadian variation in serum testosterone concentration on LH pulsatility, and to determine the temporal relationships between FSH and LH, and between LH and testosterone by cross-correlation, and the pulse frequency of these hormones by spectral analysis, as revealed by extended sampling periods. DESIGN: Hormone profiles were obtained by 20-minute sampling over 48 hours. SUBJECTS: Six healthy adult males, aged between 21 and 23 years. MEASUREMENTS: LH and FSH were measured using an immunoradiometric assay and testosterone with a solid-phase radioimmunoassay. RESULTS: The profiles showed pulsatile secretion of all three hormones, and a circadian rhythm with levels highest between 0200 and 0600 h. Cross-correlation analysis: There was a significant relationship between LH and FSH (r = 0.5; P = 0.001) at 0 minutes (i.e. no time lag). A pulse of testosterone followed on average 60 minutes after a pulse of LH (r = 0.26; P = 0.001). Fourier transformation: Spectral analysis showed the dominant period for LH and FSH pulsatility to be 200 minutes. The dominant period for testosterone pulsatility was 400 minutes. The effect of endogenous variations in serum testosterone concentrations: The LH profiles were divided into periods when the serum testosterone concentration was high or low, and Fourier transformation carried out on these shorter periods. These transforms showed that the dominant period during high serum testosterone concentration was 180 minutes, and during low serum testosterone was 120 minutes (P < or = 0.025). CONCLUSIONS: FSH and LH are co-secreted, and a pulse of testosterone follows a pulse of LH by 60 minutes. The physiological changes in serum testosterone concentration that occur during the day result in changes in the pulse frequency of LH. Testosterone concentrations thus have rapidly acting feedback activity at hypothalamic level.

Adult↗

PubMed2004

Testosterone replacement therapy--perceptions of recipients and partners.

BACKGROUND: The androgenic hormones are important determinants of sexual behaviour in men. Testosterone replacement is important treatment for pituitary disease to maintain normal functioning. Although the physical effects of testosterone replacement have been well documented, little is known about the effects on relationships, particularly from the point of view of the sexual partners of men receiving testosterone replacement. AIMS: This paper reports a study exploring the perceptions of testosterone replacement on well-being and sexual functioning. METHODS: Semi-structured interviews were conducted with five men receiving testosterone implants (recipients), their permanent partners, and five recipients without partners. Recipient serum testosterone concentration was measured at 0, 1 and 4 months after testosterone implantation. RESULTS: The three groups reported similar effects of testosterone on well-being and sexual functioning. Recipient and partner ratings were also similar. Strength was less affected by decreasing testosterone concentration than energy in men with partners, but both strength and energy declined in men without partners. Decreased testosterone levels had a statistically significantly different effect on libido at time zero between men with and without partners (P < 0.015) and on ability to sustain an erection, but the ability to achieve an erection persisted over the 6 months in both male groups. Intercourse frequency increased from once per week at time 0 to > or =3 per week between 1 and 4 months after implant in men with partners. There were important effects of testosterone deficiency on general and sexual relationships, and these differed between men with partners and those without. CONCLUSIONS: Testosterone has important physical and psychological benefits that may be related to the age at which testosterone replacement commences and the indications for its use. The small sample size may limit the ability to generalize the findings outside the study.

Adult↗

PubMed2004

Low testosterone is associated with decreased function and increased mortality risk: a preliminary study of men in a geriatric rehabilitation unit.

OBJECTIVES: To evaluate whether low testosterone levels are associated with greater depression or poorer function in a geriatric rehabilitation unit. DESIGN: Retrospective review. SETTING: Geriatric rehabilitation unit. MEASUREMENTS: Low testosterone levels were defined as total testosterone of 3.0 ng/mL or less or free testosterone of 9.0 pg/mL or less. Age, ethnicity, weight, depression, ambulation, length of rehabilitation, and 6-month rehospitalization and mortality rates were obtained. Overall illness severity was determined using the Cumulative Illness Rating Scale for Geriatrics. RESULTS: Low testosterone levels were present in 29 of 44 (65.9%) men. There were no significant differences between men with low and normal testosterone levels in ethnicity, age, weight, depression, and overall illness severity. Lower testosterone levels were correlated with decreased ability to ambulate and transfer (Spearman P>.34; P<.05). There were no significant differences between men with low and normal testosterone in length of stay on the rehabilitation unit (mean+/-standard deviation= 19.6+/-11.6 vs 17.7+/-17.5 days, P=.68) or rehospitalization rates (41.4% vs 26.7%; P=.34). Men with low testosterone had a trend toward increased 6-month mortality (31.0% vs 6.7%; chi(2)=3.3, P=.07) and shorter survival time (log rank=3.2; df 1, P=.07). After entering testosterone and variables with potential prognostic significance for mortality in a stepwise manner in a Cox regression analysis, there was a significant mortality risk associated with low testosterone (hazard ratio=27.9, 95% confidence interval=2.0-384.0; P=.01). CONCLUSION: Low testosterone levels were correlated with decreased physical function and increased risk for 6-month mortality. Prospective studies with larger sample sizes and better standardized testosterone measures are needed to confirm these findings.

Activities of Daily Living↗

PubMed2002

Testosterone-induced increase in muscle size in healthy young men is associated with muscle fiber hypertrophy.

Administration of replacement doses of testosterone to healthy hypogonadal men and supraphysiological doses to eugonadal men increases muscle size. To determine whether testosterone-induced increase in muscle size is due to muscle fiber hypertrophy, 61 healthy men, 18-35 yr of age, received monthly injections of a long-acting gonadotropin-releasing hormone (GnRH) agonist to suppress endogenous testosterone secretion and weekly injections of 25, 50, 125, 300, or 600 mg testosterone enanthate (TE) for 20 wk. Thigh muscle volume was measured by magnetic resonance imaging (MRI) scan, and muscle biopsies were obtained from vastus lateralis muscle in 39 men before and after 20 wk of combined treatment with GnRH agonist and testosterone. Administration of GnRH agonist plus TE resulted in mean nadir testosterone concentrations of 234, 289, 695, 1,344, and 2,435 ng/dl at the 25-, 50-, 125-, 300-, and 600-mg doses, respectively. Graded doses of testosterone administration were associated with testosterone dose and concentration-dependent increase in muscle volume measured by MRI (changes in vastus lateralis volume, -4, +7, +15, +32, and +48 ml at 25-, 50-, 125-, 300-, and 600-mg doses, respectively). Changes in cross-sectional areas of both type I and II fibers were dependent on testosterone dose and significantly correlated with total (r = 0.35, and 0.44, P < 0.0001 for type I and II fibers, respectively) and free (r = 0.34 and 0.35, P < 0.005) testosterone concentrations during treatment. The men receiving 300 and 600 mg of TE weekly experienced significant increases from baseline in areas of type I (baseline vs. 20 wk, 3,176 +/- 186 vs. 4,201 +/- 252 microm(2), P < 0.05 at 300-mg dose, and 3,347 +/- 253 vs. 4,984 +/- 374 microm(2), P = 0.006 at 600-mg dose) muscle fibers; the men in the 600-mg group also had significant increments in cross-sectional area of type II (4,060 +/- 401 vs. 5,526 +/- 544 microm(2), P = 0.03) fibers. The relative proportions of type I and type II fibers did not change significantly after treatment in any group. The myonuclear number per fiber increased significantly in men receiving the 300- and 600-mg doses of TE and was significantly correlated with testosterone concentration and muscle fiber cross-sectional area. In conclusion, the increases in muscle volume in healthy eugonadal men treated with graded doses of testosterone are associated with concentration-dependent increases in cross-sectional areas of both type I and type II muscle fibers and myonuclear number. We conclude that the testosterone induced increase in muscle volume is due to muscle fiber hypertrophy.

Adolescent↗