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PubMed2005

The effect of testosterone supplement on insulin sensitivity, glucose effectiveness, and acute insulin response after glucose load in male type 2 diabetics.

Our understanding of the effect of androgens on insulin action and glucose metabolism is incomplete. Several different models and methods have been used to study androgen effects, with some studies indicating that higher testosterone levels are associated with increased insulin resistance. In polycystic ovary syndrome, where high testosterone levels are frequently found, affected patients have a higher risk of diabetes. In contrast, increased insulin resistance was found in both hypergonadotropic and hypogonadotropic men with hypoandrogenism, patients with Klinefelter's syndrome and men with idiopathic gonadotropin deficiency. Insulin resistance is considered to be one of the cornerstones in the state that ultimately leads to clinically established type 2 diabetes mellitus. In addition, men with type 2 diabetes have relative hypogonadism. Therefore, supplementation with testosterone might play a role in improving both insulin resistance and hypogonadism. The study population consisted of 11 male patients with type 2 diabetes. Their mean age was 57.7 +/- 3.41 years, the body mass index (BMI) was 24.4 +/- 1.02 kg/m2, and the waist-to-hip ratio (W/H) was 0.91 +/- 0.05. The patients were all treated with oral hypoglycemic agents. The men received androgen injections every 3 weeks intramuscularly for 12 weeks. The injections were testosterone depot 100 mg/3 weeks. Insulin sensitivity, glucose effectiveness and area under acute insulin response were calculated from "minimal model" algorithms. There were no significant differences in the value of BMI, W/H ratios, plasma lipid concentrations, testosterone, homeostasis model assessment (HOMA) of insulin sensitivity, and beta-cell function, before and after supplementation of testosterone. Furthermore, the insulin sensitivity (SI) (1.04 +/- 0.25, 1.11 +/- 0.36 x 10(-5) min(-1/)pM; p = 0.43), glucose effectiveness (EG) (0.018 +/- 0.003, 0.017 +/- 0.002 min(-1); p = 0.29), and acute insulin response (AIR) after a glucose load (45.7 +/- 24.3, 50.1 +/- 32.5 pM; p = 0.45) did not change significantly after supplmentation with testosterone. In our study, there was no improvement of SI, EG, and AIR after 3 months of Testosterone Depot treatment in type 2 diabetes, but we believe that duration and dosage of the androgen therapy might play an important role in improving insulin sensitivity. The mechanisms by which testosterone causes insulin resistance is unknown, and larger studies on androgen treatment in type 2 diabetic patients are necessary.

Adult↗

PubMed2006

Testosterone and erectile physiology.

The role of testosterone deficiency in sexual dysfunction is an important aspect of aging, because it affects such a large proportion of men over 50 years old. A number of age-related factors can cause sexual dysfunction (in particular erectile dysfunction) and testosterone deficiency, such as chronic illness and multiple medications, and the causative link between hypogonadism and erectile dysfunction is still debated. However, studies in castrated animals have proven that addition of testosterone, and its conversion to dihydrotestosterone, can restore erectile function. It appears that testosterone achieves this by peripheral mechanisms (endothelial dependent and independent) and central mechanisms. Testosterone replacement therapy is therefore effective for erectile dysfunction in men with hypogonadism, with success rates of 35-40%. Testosterone supplementation is also important in men who fail on phosphodiesterase type-5 inhibitors, because a minimum plasma concentration of testosterone is required for the successful restoration of erectile function with these agents. Testosterone gels are now the preferred formulation for testosterone supplementation and they can be highly beneficial in a proportion of men with erectile dysfunction.

Adult↗

PubMed2000

Determinants of bone density in healthy older men with low testosterone levels.

BACKGROUND: Osteoporosis is a significant problem in older men, 30% of all hip fractures occur in men and the mortality rate following hip fracture exceeds that of women. Testosterone is thought to be important in the development of peak bone mass hut its role in age-related bone loss is not established. The purpose of this study was to define the predictors of bone mass ill healthy older men with low testosterone levels but without symptomatic osteoporosis. METHODS: Eighty-three community-dwelling white men, aged more than 65 years old, selected for low bioavailable testosterone levels (< or = 4.44 nmol/l) participated in a cross-sectional study located at a university general clinical research center. Sex hormone concentrations and markers of bone turnover were assayed in serum and urine. Risk factors for osteoporosis and physical activity were ascertained by physical examination and questionnaire, including the Physical Activity Scale in the Elderly (PASE) questionnaire. Bone mineral densities of the femoral neck (FN BMD), spine, and whole body were measured by dual x-ray absorptiometry. Lower extremity muscle strength (1 repetition maximum) was measured using a leg press machine. RESULTS: Mean bone mineral density values were 0.93 +/- 0.14 g/cm2 for femoral neck, 1.31 +/- 0.23 g/cm2 for spine, and 1.22 +/- 0.12 g/cm2 for whole body. Thirty-one of the 82 subjects (37%) had t scores < -1 and 12 of 82 subjects (15%) had t scores < -2.5 at the femoral neck. Multiple linear regression analysis demonstrated that bioavailable testosterone, body mass index (BMI), and PASE scores were positively correlated with, and significant predictors of, femoral neck BMD, accounting for 34.4% of the variance in FN BMD (F = 10.10, p = .001). Examining each variable independently, bioavailable testosterone accounted for 20.7%, physical activity score for 9.0%, and BMI for 6.5% of FN BMD. Using analysis of variance, mean values for FN BMD were significantly different between men grouped by tertile of bioavailable testosterone (F = 6.192, p = .003). FN BMD mean values were 0.86 +/- 0.14 g/cm2 for the lowest tertile, 0.94 +/- 0.16 for the middle tertile, and 0.99 +/- 0.14 for the highest tertile. Markers of bone turnover were inversely correlated, and strength directly correlated with BMD, but did not contribute to the multiple regression model. CONCLUSIONS: Fifty-two percent of older men with low bioavailable testosterone levels had BMD levels below the young adult normal range and are likely at an increased risk of fracture. Bioavailable testosterone, BMI, and physical activity scores were significant determinants of FN BMD in these men. These variables are potentially modifiable and, therefore, amenable to intervention. Hence, our results suggest the need for testosterone replacement and physical activity intervention trials in men at risk for osteoporotic fractures.

Absorptiometry, Photon↗

PubMed2001

Prostate-specific antigen, testosterone, sex-hormone binding globulin and androgen receptor CAG repeat polymorphisms in subfertile and normal men.

The aim of this study was to understand the androgen-related factors which may regulate concentrations of the tumour marker, prostate-specific antigen (PSA). We therefore measured the serum concentrations of total and free testosterone and of sex hormone-binding globulin (SHBG) and determined the androgen receptor (AR) gene CAG repeat length, then compared these values to total and free PSA concentrations in 91 subjects with proven fertility, and 112 subfertile men with defective spermatogenesis. Concentrations of free testosterone and total testosterone, adjusted for SHBG, were 17-20% lower in subfertile men compared with those in their fertile counterparts. This subtle, but highly significant (P < 0.001), difference in testosterone between fertile and subfertile men was accentuated by the positive correlation between testosterone and AR gene CAG repeat length in fertile, but not subfertile, subjects. In subfertile subjects, testosterone strongly correlated (r = 0.354, P < 0.001) with PSA concentrations, and independent of testosterone, total PSA negatively correlated (r = -0.229, P = 0.011) with AR CAG length. Overall our data suggest that, firstly, PSA correlates with testosterone only in an environment of relatively low androgenicity, such as in subfertile men. Secondly, in such a low androgenic environment, short CAG tracts (associated with high AR activity) correlate positively with PSA concentrations. These results suggest that interpretation of PSA is best made in conjunction with testosterone concentrations and AR CAG length.

Adult↗

PubMed1998

Effects of testosterone on glomerular growth after uninephrectomy.

BACKGROUND: Renal functional prognosis is consistently more adverse in male individuals with renal disease. Male animals develop more marked proteinuria and glomerulosclerosis in several models of renal damage. Renal and glomerular growth are important permissive factors for progression of renal failure. PURPOSE OF THE STUDY: To investigate the influence of testosterone on renal and glomerular growth. DESIGN: Renal compensatory growth after uninephrectomy (UNX) was chosen as a model of renal growth. The effect of testosterone was assessed in control male, in orchidectomized (OX) male, and in ovariectomized (OV) female SD rats. Observation time was 10 months. MEASUREMENTS: Albuminuria by nephelometry; glomerular diameter, glomerular tuft area, renal zonal analysis by quantitative stereology. Testosterone and dihydroxytestosterone by gas chromatography and RIA. RESULTS: In sham-operated male rats, testosterone administration did not change the (left) kidney:body-weight ratio after uninephrectomy. In contrast, in OX male rats, testosterone administration caused a significant increase in kidney:body-weight ratio and in albuminuria. In these animals, glomerular diameter and outer stripe width were significantly lower in OX rats than in sham-operated controls. Glomerular volume and outer stripe width in OX animals were significantly higher after uninephrectomy (UNX) and were further increased in OX-UNX animals by administration of testosterone. Similar effects on glomerular diameter, cortical width (single) kidney:body-weight ratio were seen when OV female rats were treated with testosterone. CONCLUSION: After gonadal ablation, administration of testosterone amplifies compensatory glomerular and tubular growth in uninephrectomized male and female rats, i.e. testosterone is a permissive factor. Stimulation of glomerular growth may favour development of glomerulosclerosis.

Adaptation, Physiological↗

PubMed1997

Longitudinal relation between endogenous testosterone and cardiovascular disease risk factors in middle-aged men. A 13-year follow-up of former Multiple Risk Factor Intervention Trial participants.

The present study examined lifestyle and behavioral correlates of the change in total testosterone over 13 years in 66 men aged 41-61 years who were former participants of the Multiple Risk Factor Intervention Trial (MRFIT) at the Pittsburgh, Pennsylvania, center. The authors also determined in these men if changes in total testosterone are related to changes in cardiovascular disease risk factors. The mean total testosterone level was 751 (standard deviation, 248) ng/dl at baseline and decreased by 41 (standard deviation, 314) ng/dl during follow-up. The correlation between measures was r = 0.44 (p < 0.001). In multivariate analysis, higher type A coronary-prone behavior score, greater pack-years of cigarette smoking, and the MRFIT special intervention group were associated with larger decreases in total testosterone. Age, body weight, weight change, leisure time activity level, and alcohol intake were not related to the change in total testosterone. The decrease in endogenous testosterone was associated with an increase in triglycerides and a decrease in high density lipoprotein cholesterol in multivariate analysis controlling for obesity and other lifestyle covariates. There was little relation between change in testosterone and change in total and low density lipoprotein cholesterol or blood pressure. This longitudinal study confirms a gradual decline in total testosterone levels with advancing age in older men and provides evidence that lifestyle and psychosocial factors are related to this decline. Decreases in endogenous testosterone levels with age in men are associated with potentially unfavorable changes in triglycerides and high density lipoprotein cholesterol.

Adult↗

PubMed2005

Caponization and testosterone implantation effects on blood lipid and lipoprotein profile in male chickens.

To understand the role of lipid metabolism in increasing body fat accumulation after caponization of male chickens, trials were conducted to determine the effects of levels of testosterone implantation on lipoprotein composition. Male chickens were caponized at 12 wk and selected at 16 wk for a 10-wk feeding experiment. Fifteen male and 15 caponized (capon) chickens were used in trial 1. Ten sham operated chickens (sham) and 40 capons were randomly divided among 4 treatments in trial 2; the treatments were as follows: implantation of cholesterol (1.62 mm i.d. x 3.16 mm o.d., 9.24+/-0.36 mg) or implantation of testosterone at low (1 mm i.d. x 3 mm, o.d., 5.88+/-0.23 mg), medium (1.62 mm i.d. x 3.16 mm, o.d., 9.81+/-0.17 mg), or high (2 mm i.d. x 4 mm, o.d., 16.7+/-0.24 mg) dose. The results of trial 1 showed that caponization decreased (P < 0.05) blood testosterone concentrations and increased (P < 0.05) abdominal fat weight and relative abdominal fat weight in capons. Caponization also increased low density lipoprotein (LDL), high density lipoprotein (HDL), LDL protein, and HDL protein and decreased LDL-free cholesterol (LDL-FC), HDL-FC, and HDL-phospholipid (HDL-PL) percentages (P < 0.05). In trial 2 capons implanted with increasing testosterone levels exhibited proportional increases in blood testosterone concentration, although blood testosterone concentration in implanted capons were not fully restored to those of the sham group. High dose testosterone implantation inhibited abdominal fat accumulation and increased glucose and glycerol concentrations compared with the cholesterol implantation. Caponization of male chickens decreased the androgen level and increased the blood triacylglyceride content. Caponization also changed the lipoprotein profiles, which resulted in increased lipid storage capacity. The testosterone concentration, therefore, must achieve threshold concentrations to inhibit lipid accumulation in the testosterone implanted capon.

Animals↗

PubMed1983

Influence of testosterone and/or luteinizing hormone releasing hormone analogue on precocious sexual development in the juvenile rainbow trout.

The influence of testosterone, luteinizing hormone releasing hormone (LHRH) agonist and combinations of these hormones on gonadotropic hormone (GtH) levels in the sexually immature trout was investigated. Both the steroid and releasing hormone preparations, testosterone in Silastic capsules and cholesterol-pelleted LHRH-A, were formulated for sustained release and long-term biological action following a single hormone implantation. Marked increases in pituitary GtH followed testosterone and/or testosterone and LHRH analogue treatment combined, but the low pituitary GtH level in controls remained unchanged after LHRH analogue administration alone. Plasma GtH titers increased with time after testosterone treatment, indicating a positive steroid feedback effect by androgen on GtH in the juvenile rainbow trout. When combined with testosterone treatment, LHRH analogue augmented plasma GtH levels compared to fish receiving testosterone treatment alone. In males the elevated plasma GtH levels were associated with testes stimulation and onset of spermatogenesis; in females, however, no significant stimulation of the ovaries was observed. It can be concluded from these studies that the testosterone stimulus is sufficient to induce onset of sexual development in immature males but not females. Whereas LHRH analogue releases GtH from the testosterone-primed trout pituitary, LHRH treatment alone under these conditions fails to stimulate the juvenile trout reproductive system.

Animals↗

PubMed2002

Pulmonary vasodilatory action of testosterone: evidence of a calcium antagonistic action.

Recent evidence supports a beneficial effect of testosterone on the cardiovascular system. Testosterone acts as a coronary vasodilator and reduces myocardial ischemia in men with coronary heart disease. The aim of the current study was to determine whether testosterone has a similar vasodilatory action in the pulmonary circulation and to characterize the underlying mechanism of action. The vasodilatory action of testosterone was studied in pulmonary arteries (n = 132, mean internal diameter = 344 +/- 8 microm) isolated from male rats (n = 48, mass = 396 +/- 7 g) mounted in a small vessel wire myograph and loaded to a tension equivalent to 17.5 mm Hg. Micromolar concentrations of testosterone induced dilatation in pulmonary arteries preconstricted with prostaglandin F2alpha (100 microM) within seconds of application. Dilatation to testosterone was similar in vessels treated with N-gamma-nitro-l-arginine methyl ester (l-NAME) (10 microM) or vehicle (5 microl distilled water), -38.2 +/- 2.9%, and -38.1 +/- 3.4%, respectively, and in vessels treated with indomethacin (10 microM), flutamide (10 microM), or vehicle (5 microl ethanol), -35.5 +/- 2.8%, -43.2 +/- 3.6%, and -35.7 +/- 4.6%, respectively (all p > 0.05). Maximal dilatation to testosterone occurred following preconstriction with agents that activated voltage-gated calcium channels such as prostaglandin F2alpha (-34.6 +/- 5.0%), BAY K8644 (-32.9 +/- 8.7), or potassium chloride (-26.7 +/- 1.5%), compared with calcium-independent protein kinase C activation by phorbol dibutyrate (-14.7 +/- 1.6%) or capacitative calcium entry via thapsigargin (-5.1 +/- 0.9%). This study demonstrates that testosterone induces pulmonary dilatation via a mechanism that is independent of the classic androgen receptor and also of the release of nitric oxide or dilator prostaglandins. The data support a calcium antagonistic action for testosterone in the pulmonary circulation, primarily against voltage-gated calcium channels.

Animals↗

PubMed1986

Suppression of testosterone-estradiol binding globulin by medroxyprogesterone acetate in polycystic ovary syndrome.

Serum androgen binding capacity is decreased in hirsute women and normal women receiving medroxyprogesterone acetate. A sensitive radioimmunoassay was used to measure the main androgen binding protein, testosterone-estradiol-binding globulin, in 13 patients with hirsutism and the polycystic ovary syndrome. Testosterone-estradiol-binding globulin concentrations were determined before, during, and after treatment with medroxyprogesterone acetate. Testosterone-estradiol-binding globulin was lower in untreated polycystic ovary syndrome patients than in normal controls (21.9 +/- 3.7 versus 64 +/- 4 nmol/L, P less than .01). Administration of medroxyprogesterone acetate (400 mg intramuscularly every 15 days for nine months) to polycystic ovary syndrome patients caused a decrease of serum testosterone and further lowering of testosterone-estradiol-binding globulin (7.6 +/- 1.9 nmol/L, P less than .01). In two patients the concentration of testosterone-estradiol-binding globulin reached values as low as 0.9 and 0.8 nmol/L, approximately 1/60 and 1/70 of the normal level. Testosterone-estradiol-binding globulin returned to basal levels (15.1 +/- 1.3 nmol/L) between one and two years after discontinuation of medroxyprogesterone acetate. Corticosteroid binding globulin levels were normal in polycystic ovary syndrome and did not change with medroxyprogesterone acetate. It was concluded that: medroxyprogesterone acetate causes marked lowering of plasma testosterone-estradiol-binding globulin; the effect is not mediated by sex hormone levels; and the decrease in testosterone-estradiol-binding globulin offsets, at least partially, the beneficial action of medroxyprogesterone acetate.

Female↗

PubMedDate not supplied

Administration of testosterone undecanoate in postmenopausal women: effects on androgens, estradiol, and gonadotrophins.

OBJECTIVE: To investigate serum androgens, estradiol, and gonadotrophins after treatment with testosterone undecanoate 40 mg daily in postmenopausal women. DESIGN: Ten postmenopausal women received 40 mg testosterone undecanoate orally every day for 4 days. Blood samples were drawn before and 2, 4, 6, and 8 hours after administration on the first day and then at 24, 48, 72, and 96 hours after administration of the first dose. Serum concentrations of testosterone, dihydrotestosterone, androstenedione, estradiol, sex hormone-binding globulin, follicle-stimulating hormone, and luteinizing hormone were analyzed. RESULTS: A rapid absorption of testosterone undecanoate was found with the highest concentrations of testosterone, dihydrotestosterone, and androstenedione 2-4 hours after administration. Significant increases from basal values were found for serum testosterone, dihydrotestosterone, androstenedione, and estradiol and a slight but significant decrease for sex hormone-binding globulin. Serum follicle-stimulating and luteinizing hormone levels were unchanged. Median levels of 3.2 nmol/L for testosterone and 3.6 nmol/L for dihydrotestosterone were recorded after the first day. CONCLUSIONS: Testosterone undecanoate displayed a rapid absorption and turnover and may offer an alternative for androgen treatment in women. Expanded pharmacokinetic studies in larger and more homogeneous groups of postmenopausal women should be performed. The individual variations were considerable, and regular monitoring of testosterone serum levels to avoid overtreatment is recommended.

Aged↗

PubMed1996

Changes in lipoprotein-lipid levels in normal men following administration of increasing doses of testosterone cypionate.

OBJECTIVE: The objective of this study was to examine the relationship between anabolic--androgenic steroids and lipoprotein levels in men receiving weekly injections of gradually escalating doses of up to 600 mg/week of testosterone cypionate. DESIGN: The design was a placebo-controlled, double-blind, 24-week cross-over design in which subjects were randomized to one of two treatment sequences: (a) weekly testosterone cypionate injections for 6 weeks, no treatment for 6 weeks, weekly placebo injections for 6 weeks, and then again no treatment for 6 weeks; or (b) placebo, no treatment, testosterone, and then no treatment, with each interval also lasting 6 weeks as in the first sequence. SETTING: The setting was a private hospital. PARTICIPANTS: Participants were normal male volunteers. INTERVENTIONS: Testosterone cypionate injections were given in gradually increasing doses of 150 mg/week for 2 weeks, 300 mg/week for 2 weeks, and 600 mg/week for 2 weeks. Eight subjects received testosterone injections during the first injection phase and placebo during the second injection phase, and the remaining eight subjects received placebo first and testosterone second. RESULTS: We found a 21% depression of high-density lipoprotein cholesterol (HDL-C) levels following the first 300-mg testosterone dose. This depression remained unchanged after the two 600-mg doses. In contrast, we did not find any changes in low-density lipoprotein or total cholesterol levels at any of the time points studied. Subjects' total cholesterol/HDL-C ratios were significantly elevated during testosterone administration and even 4 weeks following the last injection. CONCLUSION: Our findings suggest that testosterone cypionate adversely affects cholesterol fractions, that this effect reaches its full magnitude even at very modestly supraphysiologic doses, and that this effect persists for several weeks after discontinuation of the drug.

Adult↗

PubMed2003

Pretreatment total testosterone level predicts pathological stage in patients with localized prostate cancer treated with radical prostatectomy.

PURPOSE: In the last decade numerous groups have shown that low levels of pretreatment serum total testosterone consistently predict more aggressive disease, worse prognosis and worse treatment response in patients with metastatic prostate cancer. Prior studies have not demonstrated this same correlation in patients with known localized disease. We rigorously tested pretreatment total testosterone levels as a potential staging and prognostic marker in a large cohort of 879 patients with localized cancer treated with radical prostatectomy. MATERIALS AND METHODS: We retrospectively reviewed the clinical records of 879 patients treated with radical prostatectomy between January 1, 1986 and June 30, 2002 from 9 hospital sites. Nonparametric tests were used to compare the relationship of pretreatment testosterone to other variables. Multivariate logistic regression analysis was used to assess clinical predictors of extraprostatic disease. Kaplan-Meier survival methods and Cox regression analysis were used to assess predictors of biochemical recurrence. RESULTS: Patients with non-organ confined prostate cancer (pT3-T4) showed significantly lower pretreatment total testosterone levels than those with organ confined cancer (pT1-T2) (nonparametric p = 0.041). In multivariate analysis pretreatment total testosterone emerged as a significant independent predictor of extraprostatic disease (p = 0.046). Total testosterone was not a significant predictor of biochemical (prostate specific antigen) recurrence (p = 0.467). CONCLUSIONS: Pretreatment total testosterone was an independent predictor of extraprostatic disease in patients with localized prostate cancer. As testosterone decreases patients have an increased likelihood of non-organ confined disease. Low testosterone was not predictive of biochemical recurrence, although trends observed dictate study in larger cohorts with mature followup.

Aged↗

PubMed2005

Effectiveness of cyproterone acetate in achieving castration and preventing luteinizing hormone releasing hormone analogue induced testosterone surge in patients with prostate cancer.

PURPOSE: To our knowledge this study represents the first analysis monitoring the efficacy of cyproterone acetate (CPA) monotherapy for achieving castrate testosterone levels prior to administering a luteinizing hormone-releasing analogue (LHRHA) for treating prostate cancer in the prostate specific antigen (PSA) era. MATERIALS AND METHODS: Patients with untreated locally advanced or metastatic prostate cancer were recruited prospectively. Treatment involved a 28-day course of oral cyproterone acetate and LHRHA depot injection on day 14. Patients had serum PSA, luteinizing hormone and testosterone monitored at intervals during a 56-day period. RESULTS: A total of 15 patients with a mean age of 74 years completed the study. Near castrate serum testosterone was achieved on day 7 (mean +/- 95% CI 83.38 +/- 17.87 ng/dl). There was a significant testosterone increase after LHRHA administration on day 14 compared with the level of 160.23 +/- 36.60 ng/dl on day 16 (p <0.01). Serum luteinizing hormone mirrored testosterone, increasing from a mean of 4.93 +/- 0.61 to 15.4 +/- 6.12 nmol/l after LHRHA administration (p <0.01). Mean serum PSA demonstrated a decrease from 199.25 +/- 6.12 microg/l at day 0 to 43.77 +/- 33.08 microg/l by day 56. There was no increase in serum PSA after LHRHA administration. CONCLUSIONS: Two weeks of priming with CPA does not eliminate the surge in serum testosterone (testosterone flare) upon LHRHA administration but the testosterone increase does not exceed pretreatment levels. Furthermore, 2 weeks of CPA may not offer a benefit over 1 week in lowering serum testosterone. Finally, there is no increase in serum PSA when LHRHA is administered after priming with CPA.

Aged↗

PubMed2005

Prostate cancer in men using testosterone supplementation.

PURPOSE: Although an association between testosterone supplementation and the development of prostate cancer is unproven, a recent increase in the use of this therapy has reopened the debate about its safety in men at risk for prostate cancer. To increase awareness of this risk, we report on a series of patients in whom clinically significant prostate cancer developed and was presumed to be related to exogenous testosterone use. MATERIALS AND METHODS: The medical records of 6 urology practices were reviewed to identify men undergoing testosterone supplementation for sexual dysfunction or "rejuvenation " who were found to have prostate cancer after initiation of exogenous testosterone supplementation. Cases were analyzed to determine clinical and pathological parameters characterizing the presentation of prostate cancer. RESULTS: A total of 20 men were diagnosed with prostate cancer after initiation of testosterone therapy. Prostate cancer was detected within 2 years of testosterone initiation in 11 men (55%) and from 28 months to 8 years in the remainder. The tumors were of moderate and high grade, being Gleason sum 6, 7 and 8 to 10 in 9 (45%), 6 (30%) and 5 (25%) men, respectively. Median serum prostate specific antigen (PSA) concentration at diagnosis tended to be low at 5.1 ng/ml (range 1.1 to 329.0) and digital rectal examination generally proved more sensitive than PSA assays in detecting the cancer. Patients seen by nonurologist physicians were monitored less often for prostate cancer during testosterone use than those followed by urologists. CONCLUSIONS: Prostate cancer may become clinically apparent within months to a few years after the initiation of testosterone treatment. Digital rectal examination is particularly important in the detection of these cancers. Physicians prescribing testosterone supplementation and patients receiving it should be cognizant of this risk, and serum PSA testing and digital rectal examination should be performed frequently during treatment.

Aged↗

PubMed2003

Second to fourth digit ratio, testosterone and perceived male dominance.

Previous studies have shown that male faces with extreme features associated with testosterone are perceived as dominant and masculine. Women have been reported to prefer more masculinized male faces as they may consider testosterone markers to be an 'honest' indication of good health, and such considerations may underlie their aesthetic preferences. However, pronounced testosterone facial markers are also associated with dominance, and several negative personality traits. This suggests that female aesthetic preferences may be an adaptive compromise between positive attributes associated with higher than average testosterone, and negative attributes associated with more extreme masculinization. This current study attempts to clarify the role of hormone markers in female perceptions of dominance, masculinity and attractiveness, in male facial images. Recent evidence suggests that the relative length of the 2nd to 4th finger (2D : 4D ratio) is a pointer to prenatal testosterone levels and may thus serve as a window to the prenatal hormonal environment. We measured 2D : 4D in a sample of male college students and took salivary samples to analyse circulating levels of testosterone. Women rated facial images of these males for dominance, masculinity and attractiveness. Our results show that male 2D : 4D was significantly negatively related to perceived dominance and masculinity but not attractiveness. Circulating testosterone levels were not related to dominance, masculinity or attractiveness. These findings suggest that: (i) high prenatal levels of testosterone serve to 'organize' male facial features to subsequently reflect dominance and masculine characteristics presumably activated during puberty; and (ii) attractiveness is not directly related to testosterone levels. We conclude that facial dominance and masculinity reflect a male's perceived status rather than his physical attraction to women.

Adolescent↗

PubMed1983

Testosterone and delta 4-androstenedione in the saliva of patients with Klinefelter's syndrome.

This study compares salivary and total plasma levels of testosterone and androstenedione in healthy controls and chromatin positive patients with Klinefelter's syndrome. The mean plasma testosterone level in fifteen Klinefelter patients was significantly lower than in ten control subjects, but the mean androstenedione levels were similar. Saliva of the normal men and patients with Klinefelter's syndrome did not differ significantly in binding potency for testosterone or androstenedione. The mean salivary testosterone level in the Klinefelter patients was significantly lower than in the controls but again salivary androstenedione levels were similar. Although testosterone as well as androstenedione showed a fair correlation between the salivary and plasma concentrations, preliminary data suggested that salivary testosterone levels better characterize the clinical state of androgenicity than do plasma levels. When salivary testosterone and androstenedione were expressed as a percentage of total steroid levels in plasma, the ratios for both steroids were similar in Klinefelter patients and healthy controls and closely approximated to the reported percentages of free steroid levels in plasma. The absolute salivary testosterone concentrations also were almost identical to the reported free plasma hormone levels. Together the data provide indirect evidence that in Klinefelter patients testosterone and androstenedione binding in plasma and saliva does not differ from that in normal men, and measurement of salivary steroids, by reflecting their free hormone concentration in plasma, may be useful in evaluating endocrine function in both health and disease.

Adult↗

PubMed1987

Enhancement of Leydig cell testosterone secretion by isolated seminiferous tubules during co-perifusion in vitro: comparison with static co-culture systems.

The aim of this study was to identify an in-vitro test system for the reproducible demonstration of a modulatory effect of isolated seminiferous tubules (s-tubules) on testosterone production by purified rat Leydig cells. Co-incubation of s-tubules with various numbers of Leydig cells had no significant effect on basal and hCG-stimulated testosterone production over 4-24 h incubation. In contrast, addition of s-tubule conditioned medium (STCM) to Leydig cells enhanced both basal and hCG-stimulated testosterone production over 5 h, but this effect was variable in magnitude and was not completely reproducible. Co-perifusion of isolated s-tubules with Percoll-purified Leydig cells for 6 h produced significant and consistent increases in Leydig cell testosterone secretion compared with Leydig cells perifused on their own. In six experiments, s-tubules enhanced Leydig cell testosterone secretion by 26 +/- 5% (P less than 0.001) in the absence of LH stimulation and by 48 +/- 11% following pulsatile stimulation with 1 ng/ml ovine LH (oLH). The presence of s-tubules enhanced (P less than 0.01-0.001) testosterone secretion by Leydig cells in response to pulses of oLH at doses ranging from 0.1 to 10 ng/ml, but the magnitude of enhancement was greatest with 0.1 and 1 ng/ml doses. These stimulatory effects were not explained by Leydig cell contamination or by testosterone leakage from the isolated s-tubules. Co-perifusion of Leydig cells with isolated epididymal tubules as a control tissue had no significant effect on LH-stimulated Leydig cell testosterone production. Stimulatory effects of s-tubules on Leydig cell testosterone secretion were observed at a 'physiological' ratio of s-tubules to Leydig cells (200 cm tubules/3 million cells) and was mediated by a humoural agent(s), since perifusion of s-tubules and Leydig cells in series gave similar results to co-perifusion of these tissues. This system proved to be robust and, in contrast to static culture systems, gave highly reproducible results, which should allow detailed investigation of the dynamic interactions between s-tubules and Leydig cells and the hormonal control of these events.

Animals↗