SEARCH · PubMed Health

Results for “testosterone”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,009 records · Page 56Linked to original sources

PubMed1988

Endocrine, seminal and peripheral effects of depot medroxyprogesterone acetate and testosterone enanthate in men.

Depot medroxyprogesterone acetate (D-MPA, 250 mg) and testosterone enanthate (TE, 200 mg) were administered twice with a 4-week interval to nine healthy men, and the levels in blood of steroids, gonadotrophins, lipoproteins, sex hormone binding globulin (SHBG) and prostaglandins (PGs) were measured, as well as steroid levels in semen and the sperm count and motility. The hormones analysed were: MPA, testosterone, androstenedione (A), dihydrotestosterone (DHT), oestradiol (E2), cortisol (C), luteinizing hormone (LH), follicle stimulating hormone (FSH) and the sulphoconjugated forms (-S) of testosterone, DHT, pregnenolone (5-P) and dehydroepiandrosterone (DHEA). Peak values of MPA (10.2 +/- 4.6 nmol/l) and testosterone (28.0 +/- 10.0) were found in the first blood samples 2 days after each injection. Thereafter the levels of MPA decreased gradually and reached the limit of detection 18-20 weeks after the second injection. Blood levels of testosterone fell sharply from the peak values and were grossly subnormal 2 weeks after each injection; levels did not return to pretreatment values during 24 weeks of follow-up. The pattern of change of DHT, A, E2 and sulphonated androgens was similar to that of testosterone. These data suggest that D-MPA and TE are absorbed at similar rates, and that the TE is metabolized rapidly. The subsequent reduction in the levels of A, testosterone-S and DHT-S was less marked and reached pretreatment values earlier than did the testosterone levels. No obvious changes were found in the levels of C, 5-P-S and DHEA-S or in the seminal plasma levels of the various steroids studied. The blood levels of LH and FSH fell precipitously 2 days after the first injection, then started to increase 4 weeks after the second injection to reach pretreatment values 12 weeks later. Of the lipoproteins studied only the levels of HDL-cholesterol and SHBG were found suppressed after treatment. Severe oligozoospermia and the complete absence of progressively motile sperm, in at least one semen sample, was observed in all subjects at 3-7 and at 5-16 weeks, respectively, after the last injection, suggesting that the men were infertile for at least 1 month after treatment. A spurious increase in the PG content of semen was also observed. In spite of the low blood testosterone levels, no subject reported changes in sexual behaviour or other signs of anabolic imbalance during or after the study. However, the increase in levels of E2 in some individuals should be kept in mind as a possible cause of side-effects.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1992

Effect of testosterone deprivation on expression of the androgen receptor in rat prostate, epididymis and testis.

Adult rats were treated with ethane dimethane sulphonate (EDS) to eliminate the Leydig cells. This treatment resulted in very low levels of testosterone in the blood and in the testis. Furthermore, histological evaluation of spermatogenesis showed no marked differences between control and EDS-treated animals. In the ventral prostate, 5 days after EDS-treatment, a 4.0 +/- 0.3-fold up-regulation of androgen receptor (AR) mRNA was observed, together with a 2.2 +/- 0.2-fold increase in actin mRNA. In the epididymis, a 2.0 +/- 0.5-fold increase in AR mRNA level was observed, without a change in actin mRNA level. In the testes of EDS-treated rats, the AR mRNA level was not changed (1.02 +/- 0.17-fold of controls), and there was also no change in actin mRNA level at 5 days after EDS-treatment. These results indicate that AR mRNA expression in the ventral prostate and epididymis is regulated differentially by testosterone when compared to regulation in the testis. Testicular androgen binding sites were assayed by Scatchard analysis of the binding of 3H-R1881 to a nuclear fraction, that was isolated by a method which involved the use of liquid nitrogen and high sucrose buffer. The number of specific binding sites per testis in EDS-treated rats with testosterone-implants, remained unaltered compared to control rats (9.1 +/- 1.4 pmol/testis). In these rats, 20% of the normal testicular testosterone level was sufficient to maintain the androgen receptor in a tight nuclear binding (transformed) form. In testes from EDS-treated rats without testosterone-implants, the AR did not fractionate into the nuclear fraction; however, the total testicular AR content in these animals was close to control levels, as measured by nuclear 3H-R1881 binding after receptor transformation through injection of a high dose of testosterone (10 mg) 2 h before killing the rats (testosterone pulse). In the different experimental groups, FSH was not required to maintain the total testicular AR content (ligand binding). Immunoprecipitation and Western blotting of the testicular AR using specific monoclonal and polyclonal antibodies indicated that the total testicular amount of immunodetectable AR protein in long-term testosterone deprived rats was very low when compared to that in control rats or rats with testosterone-implants. This is in disagreement with results obtained in the ligand binding assay, and may point to a structural modification of the AR in the testis that possibly occurs in the prolonged absence of androgens.

Animals↗

PubMed2006

Testosterone and erectile function in hypogonadal men unresponsive to tadalafil: results from an open-label uncontrolled study.

The study was aimed at investigating the efficacy of tadalafil (Cialis) in combination with transdermal testosterone (Testogel) for the treatment of tadalafil-refractory erectile dysfunction in hypogonadal patients. In an open-label, retrospective trial, 69 hypogonadal nonresponders to tadalafil monotherapy (mean age: 59 years, total testosterone < or =3.4 ng ml(-1)) were randomly divided into two homogeneous groups. Group I (n = 35) received Testogel (5 g containing 50 mg testosterone, daily) for 4 weeks, followed by concurrent therapy with tadalafil (20 mg, twice a week). Group II (n = 34) was assigned to treatment with Testogel (5 g containing 50 mg testosterone, daily) for a duration of 10 weeks before adjunctive therapy with tadalafil was initiated. Total testosterone levels were measured at baseline, week 4 and week 10. Sexual function was assessed employing the International Index of Erectile Function (IIEF). As an additional measure of efficacy, a questionnaire completed by the patients' partner was used. Mean testosterone levels were observed to increase from baseline to study end. Following 4 weeks of therapy, an improvement in Erectile Function (EF) from baseline was observed, which was greater in group I than in group II. The assessment after week 10 showed that EF had further increased and was quite similar now in both groups. Partners found that erectile capacity had greatly improved from baseline to study end. No adverse effects have been observed. These data suggest that combination therapy with testosterone and tadalafil is an effective means in a subset of hypogonadal patients who did not respond to tadalafil alone. We assume that testosterone-induced remodelling of penile tissue structure is one underlying reason for the observed improvement of erectile function. The results imply that this process may require a longer period of testosterone administration than 4 weeks.

Adult↗

PubMed2005

Effects of testosterone on lipid peroxidation, lipid profiles and some coagulation parameters in rabbits.

The purpose of this study was to investigate the effects of testosterone on some risk factors of atherosclerosis. Twenty-four male New Zealand white rabbits were randomly divided into three groups of eight. The first group was used as control. Second group was injected with 10 mg of testosterone propionate. Third group was castrated bilaterally. At the end of 6 weeks, lipid peroxidation (LPO), lipid profile, fibrinogen (FBN) level and coagulation parameters were evaluated. Testosterone administration decreased the level of high-density lipoprotein cholesterol (HDL-C), while castration increased this level (P < 0.05). Triglyceride (TG) and total cholesterol (TC) levels in the castration group were significantly higher (P < 0.05) than those in the testosterone group. The ratio of HDL-C:low-density lipoprotein cholesterol (LDL-C) decreased, while TC:HDL-C ratio increased (P < 0.05) in the testosterone group. No significant differences were found in the LDL-C and FBN levels among groups. However, there was a tendency for higher FBN level in the testosterone group. Testosterone administration resulted in an increase in the level of LPO (P < 0.05). Clotting time and prothrombin time prolonged in the castration group compared with testosterone group (P < 0.05). As a result, testosterone has exacerbating effect on atherosclerosis risk factors including lipid profile, LPO, FBN and coagulation system.

Animals↗

PubMed1993

Decreased postnatal testosterone surge in male rats exposed to ethanol during the last week of gestation.

Prenatal alcohol exposure in the rat is known to interfere with the neurobehavioral sexual differentiation of the male brain. Because normal sexual differentiation of the male brain requires adequate levels of perinatal testosterone, we examined the effect of prenatal ethanol exposure on (1) the postnatal surge of testosterone and (2) the in vitro secretion of testosterone in response to luteinizing hormone (LH) stimulation of testes from fetal alcohol exposed (FAE) animals and controls. Sprague-Dawley dams were administered a fortified liquid diet containing 35% ethanol-derived calories, a pair-fed (PF) isocaloric liquid diet, or given ad libitum access to dry lab chow (CF). Dams were administered the liquid diets from days 7 or 14 through parturition. The postnatal surge of testosterone in FAE males was studied only in animals exposed to ethanol from day 14 through parturition. In the first experiment, FAE and PF males and females were delivered by cesarean section on day 22 of gestation (E22) and trunk blood collected at 0, 60, 120, and 240 min after parturition. Experiment 2 measured plasma testosterone in male pups that were killed at 0, 60, 120, 240, 360, and 480 min after delivery. Results showed that the postnatal testosterone surge of FAE males in both experiments was significantly attenuated compared with PF controls. No effect of prenatal ethanol was observed in female offspring. Female testosterone levels were several fold lower than male littermates, and no evidence of a postnatal testosterone surge was observed. Production of testosterone from testes was studied using an automated perifusion system.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Low serum testosterone and myocardial infarction in geriatric male inpatients.

A survey of serum testosterone levels and a range of medical and behavioral factors was conducted on 71 males aged 46 to 89 years in an extended care medical facility. Histories of myocardial infarction or heavy drinking were separately associated with diminished testosterone levels (P less than .002 and P less than .006, respectively). No other factor was associated with testosterone level, including age and mobility. A testosterone level of no more than 438 ng/dl best discriminated patients with myocardial infarction (P less than .005, sensitivity 86.2%, and selectivity 50%). Increased incidence of myocardial infarction appeared to be influenced by testosterone in a threshold manner, since the incidence did not rise further with lesser testosterone levels once the level was below 438 ng/dl. The incidence of myocardial infarction among patients with testosterone levels below this threshold was unaffected by their exposure to alcohol. Among the 21 formerly heavy drinkers, many (62%) showed testosterone levels less than or equal to 300 ng/dl. Formerly heavy drinkers should be routinely considered for serum testosterone determination.

Age Factors↗

PubMed1978

Relationship between haemoglobin and serum testosterone in normal children and adolescents and in boys with delayed puberty.

The concentrations of haemoglobin and of serum testosterone were measured in 215 normal children and adolescents aged 7--20 years, and in 8 boys with constitutional delayed puberty. From the age of 14 years onward haemoglobin and testosterone rose in normal boys and differed significantly from the stable levels observed in prepubertal children and pubertal girls. In the entire series of normal boys (n = 118, age 7--20 years) concentrations of haemoglobin and testosterone were found to be closely correlated (r = 0.73, p less than 0.001). These results provide further evidence for a major role of testosterone in the control of erythropoiesis. Therefore, this correlation suggests the use of serum testosterone determination for the proper selection of haemoglobin reference ranges in boys. The respective reference ranges of haemoglobin corresponding to testosterone levels at 0 and 30 nmol/l were 120.5--148.5 and 143.5--171.5 g/l (95% confidence limits). Boys with delayed puberty were found to have significantly reduced median values of haemoglobin and testosterone for their chronological age, and 6 of the 8 boys investigated were truly anaemic on this background. Nevertheless, their haemoglobin concentration did appear appropriate as judged from their testosterone levels. This observation supports the idea that the selection of the relevant reference range for haemoglobin in boys should depend on the state of physical development as expressed by serum testosterone.

Adolescent↗

PubMed2005

Testosterone therapy in erectile dysfunction and hypogonadism.

INTRODUCTION: Laboratory experiments indicate that the nitric oxide erectile pathway is testosterone-dependent. Castration induces erectile dysfunction (ED) and reduction in nitric oxide synthase and in phosphodiesterase type 5 (PDE5) in the erectile tissue. Furthermore, castration causes apoptosis adversely affecting smooth muscle content and penile hemodynamics leading to veno-occlusive dysfunction. Testosterone therapy reverses these structural, biochemical, and physiological changes. In humans, testosterone therapy improves erectile function in men with hypogonadism. However, the efficacy of testosterone monotherapy may not be adequate because of the multifactorial nature of the pathophysiology of ED. METHODS: Preliminary data from a number of studies have been reviewed. RESULTS: There are emerging evidence-based benefits to using the combination of testoterone and PDE5 inhibitors. A recently published multicenter, randomized, placebo-controlled study evaluated the safety and efficacy of testosterone gel 1% plus sildenafil vs. placebo gel plus sildenafil, in producing an erectile response in hypogonadal men who had failed prior sildenafil alone for ED. Screening yielded a prevalence of hypogonadism in ED patients who failed prior sildenafil. Following randomization, the double-blinded treatment phase was 12 weeks. Testosterone therapy with testosterone gel significantly improved erectile function in response to sildenafil. In addition, it significantly improved orgasmic function and patient satisfaction. CONCLUSION: It is important to screen all men with ED for hypogonadism, especially those with a history of inadequate response to prior PDE5 inhibitors. The combination of testosterone plus PDE5 inhibitors may be considered for the treatment of ED in men with low to low-normal testosterone levels, who had inadequate response to prior treatment with PDE5 inhibitors alone.

Androgens↗

PubMed1994

Testosterone increases thromboxane A2 receptor density and responsiveness in rat aortas and platelets.

Testosterone has been implicated as a risk factor for cardiovascular diseases. Thromboxane (Tx) A2 is an important pathophysiological mediator for thrombotic vascular diseases. This study investigated the effects of testosterone on platelet and vascular TxA2 receptors. Male rats were treated with either testosterone cypionate for 2 wk, sham operated, castrated, or castrated and treated with testosterone cypionate for 2 wk. Treatment of intact rats with testosterone significantly (P < 0.001) increased the TxA2 receptor density in platelets from 25.4 +/- 3.2 to 42.9 +/- 4.2 fmol/mg protein (P < 0.005, n = 17) and in aortic membranes from 48.7 +/- 1.7 to 86.1 +/- 6.1 fmol/mg protein, n = 9. The threshold concentration of the TxA2 mimetic, [1S-(1 alpha, 2 beta(5Z),3 alpha(1E,3R*)4 alpha)]-7-[3-(3-hydroxy-4- (4'-iodophenoxy)-1-butenyl)-7-oxabicyclo[2.21]heptan-2-yl]-5 -heptenoic acid (I-BOP), to induce platelet aggregation was significantly (P < 0.01) decreased from 0.45 +/- 0.16 nM, n = 7, in the control rats to 0.07 +/- 0.01 nM, n = 13, in the testosterone-treated rats. Testosterone treatment resulted in a significantly (P < 0.05) greater maximum aortic contractile response to the TxA2 mimetic, U-46619, compared with intact rats. Castration resulted in a significant (P < 0.01) decrease in aortic TxA2 receptor density from 51.7 +/- 3.7 to 27.3 +/- 5.3 fmol/mg protein, which was significantly reversed by testosterone treatment (89.2 +/- 7.1 fmol/mg protein; n = 4). Castration resulted in a significantly (P < 0.05) lower maximal aortic contractile response that was reversed by treatment with testosterone. Castration did not significantly change platelet TxA2 receptor density.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2001

Prenatal exposure of testosterone prevents SDN-POA neurons of postnatal male rats from apoptosis through NMDA receptor.

The role of N-methyl-D-aspartate (NMDA) receptor in mediating the effect of testosterone exposure prenatally on neuronal apoptosis in the sexual dimorphic nucleus of the preoptic area (SDN-POA) of rats was studied. The endogenous testosterone was diminished by prenatal stress (PNS) or simulated by testosterone exposure (TE) to understand the effect of testosterone on NR(1) (a functional subunit protein of NMDA receptor) expression and neuronal apoptosis. To further study whether the testosterone, after being converted into estradiol, modulates NR(1) expression, 4-androstein-4-ol-3,17-dione (ATD; an aromatase inhibitor) was used to block the conversion of estradiol from testosterone. The expressions of the NR(1) mRNA and NR(1) subunit protein were quantified by RT-PCR and western blotting analysis, respectively. In addition, a noncompetitive antagonist of NMDA receptor, MK-801, was used to find out whether blockage of NMDA receptor affects the naturally occurring apoptosis in SDN-POA. The results showed the following. 1) Expression of perinatal NR(1) subunit protein in the central part of the medial preoptic area of male rats was significantly higher than that of females, especially on postnatal days 1 and 3. 2) The testosterone level of male fetuses on embryonic day 18 was significantly higher than that of females, while the testosterone level of TE females or PNS males was similar to that of intact males or intact females, respectively. 3) The apoptotic incidence of intact male rats was significantly less than that of females, and the apoptosis was stimulated by PNS in male or inhibited by TE in female. 4) The expression of NR(1) subunit protein could be inhibited by PNS or ATD-treatment in male, while stimulated by TE in female. 5) NR(1) mRNA showed no significant difference among intact male, PNS male, ATD-treated male, TE female and intact female rats. 6) The low apoptotic incidence of male rats was significantly increased when NMDA receptor was blocked by MK-801. These results suggest that testosterone, after being converted to estradiol, may prevent the SDN-POA neurons of male rats from apoptosis through enhancing the expression of NR(1) at the posttranscriptional level.

Animals↗

PubMed1999

Effect of short-term testosterone treatment on leptin concentrations in boys with pubertal delay.

Testosterone administration increases growth hormone (GH) secretion and decreases the plasma leptin concentration in men. We evaluated the effect of increased GH secretion due to short-term testosterone treatment on leptin concentrations. Ten boys aged 14.8 +/- 0.2 (mean +/- SE) years with transient GH deficiency caused by pubertal delay were evaluated before and after (3 months) 4 intramuscular injections of 100 mg testosterone heptylate, given at 15-day intervals. The leptin concentration decreased from 5.4 +/- 1.3 to 3. 6 +/- 1.1 microgram/l (p < 0.001), despite a weight gain of 3.4 +/- 0.5 kg. There were significant increases in body mass index (BMI), from -0.2 +/- 0.5 to 0.2 +/- 0.5 SD, p < 0.005, in GH peak after stimulation test, from 6.3 +/- 0.5 to 21.7 +/- 2.9 microgram/l, p < 0. 0003, in plasma testosterone, from 0.6 +/- 0.1 to 6.5 +/- 1.3 microgram/l, p < 0.001, in insulin-like growth factor-I (IGF-I), from 152 +/- 21 to 330 +/- 30 microgram/l, p < 0.0001, and in IGF-binding protein-3 (IGFBP-3), from 4.2 +/- 0.5 to 5.4 +/- 0.4 mg/l, p < 0.01. But there were no changes in blood glucose (4.7 +/- 0.1 and 4.8 +/- 0.1 mmol/l), or plasma fasting insulin (9.0 +/- 1.2 and 8.1 +/- 1.3 mIU/l). The leptin concentrations were positively correlated with the BMI before (p < 0.03) and after (p < 0.04) testosterone, but not with the GH peak after stimulation, or with plasma testosterone, IGF-I or IGFBP-3. The leptin and insulin concentrations after testosterone treatment were positively correlated (p < 0.04). Thus, short-term testosterone treatment of boys with pubertal delay decreases their leptin concentrations. The lack of correlation with GH secretion or with its changes, despite the dramatic increase in GH secretion, and the lack of change in insulin are additional features suggesting that testosterone increases the leptin concentration mainly by an effect on adipose tissue.

Adolescent↗

PubMed1989

Testosterone and dihydrotestosterone, but not estradiol, selectively maintain pituitary and serum follicle-stimulating hormone in gonadotropin-releasing hormone antagonist treated male rats.

Recently it has been found that testosterone can maintain and restimulate serum and pituitary follicle-stimulating hormone (FSH) in the gonadotropin-releasing hormone (GnRH) antagonist treated adult male rat. The present investigation was undertaken to determine (1) which metabolite of testosterone, dihydrotestosterone (DHT), or estradiol accounts for the effects of testosterone in GnRH antagonist suppressed rats and (2) whether these effects of testosterone are influenced by other testicular factors. Eight groups of 6-8 adult male Sprague-Dawley rats were subjected to the following treatments: vehicle, GnRH antagonist (75 micrograms/day s.c.), testosterone-filled Silastic implants (3 x 5 cm, s.c.), DHT-filled Silastic implants (3 x 5 cm, s.c.), estradiol benzoate (15 micrograms/day s.c.), and combined administration of GnRH antagonist with either steroid. In addition, the GnRH antagonist/testosterone treatment regimen was applied to rats orchidectomized 72 h prior to initiation of treatments. After 3 weeks of treatment, serum was analyzed for concentrations of luteinizing-hormone (LH), FSH, testosterone, DHT, and estradiol. Pituitary extracts were analyzed for LH and FSH content. Except for the vehicle-treated groups, serum and pituitary LH concentrations were markedly suppressed by all treatments. In intact rats treated with GnRH antagonist alone and/or estradiol, the pituitary FSH level was reduced by more than 70% relative to controls, while both testosterone and DHT maintained pituitary FSH. Similarly, testosterone and DHT, but not estradiol, delayed the decline of serum FSH induced with GnRH antagonist alone. In orchidectomized animals, testosterone was also capable of preventing a reduction of pituitary FSH despite concomitant GnRH antagonist administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Castration-induced decrease in the activity of medial preoptic and tuberoinfundibular GABAergic neurons is prevented by testosterone.

We recently determined that castration specifically decreased GABA turnover in discrete rostral and mediobasal hypothalamic structures. This study aimed to investigate whether testosterone could stimulate GABAergic neuronal activity in these hypothalamic GABAergic neurons in the castrate rat, and to compare the effects of episodic testosterone replacement with the constant levels provided by subcutaneous testosterone implants. Animals were divided into 4 experimental groups: intact, 48 h castrate, 48 h castrate+testosterone capsules (2 x 30 mm Silastic implants, 1.57 mm ID, 3.18 mm OD) and 48 h castrate+testosterone injections (100 micrograms/injection s.c., every 8 h). GABA concentrations were measured in 4 microdissected brain regions either before or 60 min after inhibition of the GABA degrading enzyme, GABA transaminase, by injection of aminooxyacetic acid (AOAA, 100 mg/kg i.p.). The rate of GABA accumulation in the tissue following injection of AOAA was used as an index of GABAergic neuronal activity. Castration resulted in a 10-fold increase in serum LH concentrations compared with intact rats. Either mode of testosterone administration completely prevented this castration-induced LH rise. In the diagonal band of Broca at the level of the organum vasculosum of the lamina terminalis, the medial preoptic nucleus and in the median eminence, GABA turnover was significantly reduced by castration to approximately 50% that of intact rats. Either testosterone implants or testosterone injections prevented this castration-induced decrease in GABA turnover, such that the turnover rates were not significantly different from intact rats. There was no effect of castration with or without testosterone replacement in the cingulate cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1997

Testosterone does not eliminate the attenuating effect of estrogen on progressive glomerular injury in estrogen-treated hypercholesterolemic male Imai rats.

Hypercholesterolemic Imai rats spontaneously develop proteinuria and glomerulosclerosis, especially males. Estrogen attenuates the progressive glomerular injury in these male rats. To clarify whether this attenuating effect of estrogen depends on a reduction of testosterone and/or a reduction of the sex-related factors, we investigated whether testosterone administration eliminates the attenuating effect of estrogen on the development of glomerular injury in estrogen-treated male Imai rats. Estrogen significantly reduced sex-related low molecular weight protein excretion to undetectable levels; and treatment with estrogen and testosterone failed to increase these levels. Unexpectedly, treatment with estrogen and testosterone attenuated glomerular injury more than treatment with estrogen only. Estrogen significantly increased both levels of estrogen and growth hormone (GH), whereas it suppressed testosterone levels. Testosterone administration resulted in an increase in serum testosterone levels of about fivefold above the control levels, but reduced the elevated serum GH to the levels of the controls. These results suggest that estrogen appears to play a protective role by itself or in association with sex-related factors, independent of the levels of serum testosterone, and that testosterone does not exert its effect on augmenting glomerular injury and rather may act to attenuate glomerular injury associated with a reduction of GH levels.

Aging↗

PubMed1976

Bioavailability and LH-suppressing effect of different testosterone preparations in normal and hypogonadal men.

The therapeutic effectiveness of intramuscularly administered testosterone esters and free testosterone in suppositories was investigated by the measurement of plasma testosterone and LH levels after administration to normal and hypogonadal men. Testosterone levels were elevated above the lower physiological limit for 1 day after 25 mg testosterone one propionate, for 2 days after 50 mg testosterone propionate and for 14 days after 250 mg testosterone oenanthate. LH levels were suppressed for the corresponding periods. Elevated plasma testosterone and suppressed LH levels were maintained by testosterone suppositories (3 x 20 mg for 5 days).

Adult↗

PubMed1989

Binding of levonorgestrel, norethisterone and desogestrel to human sex hormone binding globulin and influence on free testosterone levels.

The progestogens desogestrel, levonorgestrel, lynestrenol and norethisterone are known to display certain androgenic effects. Apart from direct androgen receptor interaction, binding to sex hormone binding globulin (SHBG) and displacement of testosterone could lead to an increase in free, metabolically active testosterone. The affinities for SHBG binding of some progestogens including levonorgestrel, norethisterone and the active metabolite of desogestrel, 3-keto-desogestrel, were compared using an equilibrium partition method, and the distribution between free and protein-bound testosterone during progestogen therapy was calculated with the use of a computer program. During treatment with desogestrel, levonorgestrel and norethisterone alone, testosterone displacement could account for a slight increase in free testosterone, though the decrease in serum SHBG following treatment was found to be more important in this respect. Also during treatment with combinations of ethinyl estradiol and levonorgestrel for oral contraception, testosterone displacement could theoretically have a slight influence on free testosterone levels. Combinations with ethinyl estradiol and desogestrel or norethisterone, on the other hand, cause an increase in SHBG concentration and as a result a fall in free testosterone which could not be compensated via testosterone displacement.

Binding, Competitive↗

PubMedDate not supplied

Relation of serum testosterone levels to high density lipoprotein cholesterol and other characteristics in men.

Although levels of high density lipoprotein (HDL) cholesterol in males decrease during adolescence and after treatment with testosterone derivatives, several studies have reported that levels of HDL cholesterol are positively associated with endogenous levels of testosterone in men. This association was further examined using data collected during 1985 and 1986 from 3,562 white and 500 black men who ranged in age from 31 to 45 years. Black men had higher mean levels of both HDL cholesterol (8 mg/dl) and total testosterone (33 ng/dl) than white men, and positive associations were observed between testosterone and HDL cholesterol levels (r = 0.22, whites; r = 0.26, blacks). In addition, levels of testosterone were related positively to alcohol consumption and cigarette smoking and negatively to age, Quetelet index, and use of beta-blockers. We used stratification and regression analyses to determine if any of these characteristics could account for the positive association between levels of HDL cholesterol and total testosterone. Although controlling for most factors had little influence, adjusting for Quetelet index reduced the strength of the association between levels of testosterone and HDL cholesterol by approximately 30%. These findings suggest that the positive association between levels of testosterone and HDL cholesterol may not be causal. Multivariable analyses that control for obesity and other potentially confounding characteristics should be used in studies that assess the relation of testosterone levels to coronary heart disease.

Adult↗

PubMed1999

Effects of testosterone on coronary vasomotor regulation in men with coronary heart disease.

BACKGROUND: The increased incidence of coronary artery disease in men compared with premenopausal women suggests a detrimental role of male hormones on the cardiovascular system. However, testosterone has direct relaxing effects on coronary arteries in animals, as shown both in vitro and in vivo. The effect of testosterone on the human coronary circulation remains unknown. METHODS AND RESULTS: We studied 13 men (aged 61+/-11 years) with coronary artery disease. They underwent measurement of coronary artery diameter and blood flow after a 3-minute intracoronary infusion of vehicle control (ethanol) followed by 2-minute intracoronary infusions of acetylcholine (10(-7) to 10(-5) mol/L) until peak velocity response. A dose-response curve to 3-minute infusions of testosterone (10(-10) to 10(-7) mol/L) was then determined, and the acetylcholine infusions were repeated. Finally, an intracoronary bolus of isosorbide dinitrate (1000 microgram) was given. Coronary blood flow was calculated from measurements of blood flow velocity using intracoronary Doppler and coronary artery diameter using quantitative coronary angiography. Testosterone significantly increased coronary artery diameter compared with baseline (2.78+/-0. 74 mm versus 2.86+/-0.72 mm [P=0.05], 2.87+/-0.71 mm [P=0.038], and 2.90+/-0.75 mm [P=0.005] for baseline versus testosterone 10(-9) to 10(-7) mol/L, respectively). A significant increase in coronary blood flow occurred at all concentrations of testosterone compared with baseline (geometric mean [95% CI]: 32 [25, 42] versus 36.3 [27, 48] (P=0.006), 35.3 [26, 47] (P=0.029), 36.8 [28, 49] (P=0.002), and 37 [28, 48] (P=0.002), mL/min for baseline versus testosterone 10(-10) to 10(-7) mol/L, respectively). No differences existed in coronary diameter or blood flow responses to acetylcholine before versus after testosterone. CONCLUSIONS: Short-term intracoronary administration of testosterone, at physiological concentrations, induces coronary artery dilatation and increases coronary blood flow in men with established coronary artery disease.

Acetylcholine↗