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PubMed2005

Oral testosterone in male rats and the development of experimental autoimmune encephalomyelitis.

OBJECTIVES: Considering that sex steroids can influence the immune system, we studied the development of experimental autoimmune encephalomyelitis (EAE), a T-cell-mediated autoimmune disease of the central nervous system, and the concomitant cell-mediated immunity in gonadally intact and gonadectomized male Wistar rats given testosterone supplementation. METHODS/RESULTS: Sham-operated rats and surgically castrated animals were orally self-administered with vehicle or testosterone added in the water bottle for 20 days before EAE induction. The androgenic effect of oral testosterone self-administration was evidenced by changes in body weight, and in the weights of androgen-dependent testes and seminal vesicles. Testosterone administration reduced the incidence of clinical signs of EAE in sham-operated animals and reversed the clinical symptoms of the disease associated with castrated EAE animals. The clinical signs observed in the different groups correlated with changes in delayed-type hypersensitivity and mononuclear cell-proliferative responses to the encephalitogenic myelin basic protein. Moreover, testosterone but not cholesterol supplementation in vitro suppressed the proliferative response of mononuclear cells to myelin basic protein suggesting that testosterone may affect specific immune functions through direct actions on immune cells. Finally, self-administration of testosterone induced also elevated corticosterone levels that in sham-operated rats correlated with the low incidence of the disease and in gonadectomized animals could be involved in the remission of clinical symptoms of EAE. CONCLUSIONS: These results suggest that orally self-administered testosterone can modulate specific cellular immune responses and serum corticosterone levels leading to changes in the development of EAE.

Administration, Oral↗

PubMed2006

Failure to maintain a suppressed level of serum testosterone during long-acting depot luteinizing hormone-releasing hormone agonist therapy in patients with advanced prostate cancer.

OBJECTIVES: It was the aim of this study to analyze the failure rates in achieving or maintaining castrate levels of serum testosterone in patients with advanced prostate cancer treated with the 3-month luteinizing hormone-releasing hormone agonist (LH-RH) therapy. METHODS: Total serum testosterone was determined in 234 patients with prostate cancer in a cross-sectional study. A subset of 90 patients submitted to radical prostatectomy was used as the control group (group 1), and 144 patients with advanced prostate cancer under androgen suppression therapy were included in the study group (groups 2 and 3). The study group was divided into 93 patients (group 2) treated with 50 mg daily bicalutamide and LH-RH agonist (maximal androgen blockade, MAB) and 51 patients treated with the LH-RH agonist alone (group 3). Median follow-up after androgen suppression was 42 months. The castrate testosterone level was defined below 50 ng/dl. RESULTS: The mean serum testosterone level was 29.1 ng/dl in patients undergoing MAB (group 2) and 29.5 ng/dl in patients treated with the LH-RH agonist (group 3; p > 0.05). In group 1, the mean serum testosterone was 445.2 ng/dl (p < 0.0001). The rate of patients with a serum testosterone level higher than 50 ng/dl was 10.9% in patients undergoing androgen suppression, 10% in patients with MAB treatment and 12.5% in those with LH-RH agonist therapy (p > 0.05). In group 1, 98.9% of the patients had a serum testosterone level higher than 50 ng/dl. CONCLUSIONS: A small but clinically significant rate of patients under 3-month LH-RH agonist therapy fail to achieve or maintain castrate testosterone serum levels. This finding supports the need of monitoring testicular response during LH-RH agonist therapy.

Aged↗

PubMed1976

Effect of testosterone on hypothalamic LH-RH content.

Hypothalamic LH-RH content in male rats is lowered after castration. The s.c. implantation of testosterone or testosterone propionate-packed Silastic tubing (from 0.5 to 6 cm in length) in a range which encompassed the normal circulating plasma testosterone concentration, prevented this lowered LH-RH content 21 days following castration and simultaneous implantation. The temporal response to implanted testosterone was then studied: rats were killed 1,2,4,8,14 and 21 days after castration and simultaneous implantation of 3 cm testosterone-packed Silastic tubing. The hypothalamic LH-RH content began to decrease in the castrated group after 4 days and fell progressively thereafter. However, the hypothalamic LH-RH content of the castrated group maintained with constant levels of testosterone showed no such reduction at any time following castration. These experiments indicate that circulating testosterone in physiological concentrations can maintain a normal hypothalamic LH-RH content and demonstrate an action of testosterone, in physiological concentrations, in the feedback regulation of LH-RH secretion.

Animals↗

PubMed1981

Impact of social conflict between mice on testosterone binding in the central nervous system.

Adult male mice previously isolated for 14 days, were maintained in pairs as residents and intruders. They were categorized as dominant or subordinate on the basis of initiation of attacks and of wounding. After 10 days, the amount of free cytoplasmic testosterone receptors was determined in a part of the basal forebrain consisting of septum, diencephalon, corpus striatum, and amygdala. In addition, the plasma testosterone level and the activity of the adrenal tyrosine hydroxylase were measured. The adrenal tyrosine hydroxylase activity was increased in the dominant and the subordinate mice compared to isolated controls. Subordinates had higher tyrosine hydroxylase activities than dominants. The specific testosterone in brain cytosol of dominants were freed like those of 6-day castrates despite the fact that the plasma testosterone concentration of dominants (717 ng/100 ml) was not significantly decreased compared to controls (1,003 ng/100 ml). In subordinates, the plasma testosterone content fell to 265 ng/100 ml while castrated mice showed 20-43 ng/100 ml. The amount of free testosterone specific binding sites in the brain cytosol of subordinates corresponded to that of 10-day castrates. Thus, the amount of circulating total testosterone does not seem to be the only factor determining the binding of available testosterone in brain cytosol.

Aggression↗

PubMed1987

Sites at which testosterone may act as an estrogen in the brain of the male primate.

Testosterone is converted to estradiol in specific regions of the primate brain and accumulates as such in the nuclei of cells in hypothalamus, preoptic area, and amygdala. To locate more precisely those neurons in which nuclear estrogen receptors were occupied by estrogenic metabolites of testosterone, we injected 8 castrated male rhesus monkeys with [3H]-estradiol. Four were injected with oil for control purposes, and 4 were pretreated for 3 days with 2 mg/day testosterone propionate. This dose raised plasma testosterone levels into the high physiological range for intact males. After 60 min, brains were rapidly removed, the levels of [3H]-estradiol in nuclei were measured in the right halves of the brains by high-performance liquid chromatography, and labeled neurons were located in the left halves by autoradiography. Compared with the 4 control animals, nuclear levels of [3H]-estradiol in testosterone-treated males were reduced by 77% in the hypothalamus (p less than 0.001), by 93% in the preoptic area (p less than 0.001), and by 90% in the amygdala (p less than 0.05). In autoradiograms from testosterone-treated males, the labeling of neurons was reduced by 72-96% in most of the regions in which the control males showed high percentages of labeled cells. However, there were only small reductions in the number of labeled neurons in lateral septum (by 31%) and arcuate nucleus (by 23%). These two regions, therefore, contained estrogen receptors that were not blocked by pretreatment with testosterone. The simplest explanation for these results is that estrogenic metabolites of testosterone prevented the uptake of [3H]-estradiol by prior occupation of estrogen receptor sites. The rather precise neuroanatomical localization of the effects pointed to the existence of two populations of estrogen target neurons in the primate brain depending on the presence or absence of local aromatase activity.

Amygdala↗

PubMed1996

Decreased serum testosterone in men with acute ischemic stroke.

Serum levels of total and free testosterone and 17 beta-estradiol were determined in 144 men with acute ischemic stroke and 47 healthy male control subjects. Blood samples from patients were drawn a mean of 3 days after stroke onset and also 6 months after admission in a subgroup of 45 patients. Initial stroke severity was assessed on the Scandinavian Stroke Scale and infarct size by computed tomographic scan. Mean total serum testosterone was 13.8 +/- 0.5 nmol/L in stroke patients and 16.5 +/- 0.7 nmol/L in control subjects (P = .002); the respective values for free serum testosterone were 40.8 +/- 1.3 and 51.0 +/- 2.2 pmol/L (P = .0001). Both total and free testosterone were significantly inversely associated with stroke severity and 6-month mortality, and total testosterone was significantly inversely associated with infarct size. The differences in total and free testosterone levels between patients and control subjects could not be explained by 10 putative risk factors for stroke, including age, blood pressure, diabetes, ischemic heart disease, smoking, and atrial fibrillation. Total and free testosterone levels tended to normalize 6 months after the stroke. There was no difference between patients and control subjects in serum 17 beta-estradiol levels. These results support the idea that testosterone affects the pathogenesis of ischemic stroke in men.

Acute Disease↗

PubMed2001

Effect of testosterone on plaque development and androgen receptor expression in the arterial vessel wall.

BACKGROUND: -Recent studies have suggested that testosterone has a protective effect in the arterial vascular system. However, little is known about the molecular aspects of the mechanism(s) involved in these processes. The aim of the present study was to investigate the effect of testosterone on neointimal plaque development and on the expression of the vascular androgen receptor. Methods and Results-Neointimal plaque formation was induced by endothelial denudation in the aortas of male New Zealand White rabbits. Aortic ring segments were cultured for 21 days after endothelial denudation. Testosterone was applied to the culture medium in different doses. Compared with the non-hormone-treated control group, a significant inhibition of neointimal plaque development (expressed as the intima/media ratio) was found at testosterone concentrations of 10 ng/mL (P:=0.037) and 100 ng/mL (P:=0.012; intima/media ratios: median of controls, 0.25; median of 10 ng/mL testosterone group, 0.15; median of 100 ng/mL testosterone group, 0.16). Associated with this inhibitory effect on plaque size was a 50% increase of the amount of androgen receptor mRNA in the arterial segments treated with testosterone. CONCLUSION: -The beneficial effects of testosterone on postinjury plaque development underlines, at least in males, the important role of androgens in the vascular system. As our data suggest, the vascular androgen receptor is probably involved in these processes. Further studies are required to characterize the androgen receptor-dependent pathways in the vascular system.

Animals↗

PubMed1995

Testosterone increases human platelet thromboxane A2 receptor density and aggregation responses.

BACKGROUND: The incidence of thrombotic cardiovascular disease is greater in men than in premenopausal women. Testosterone has been implicated as a significant risk factor for cardiovascular disease and for acute myocardial infarctions and strokes in young male athletes who abuse anabolic steroids. Thromboxane A2 (TXA2) is a vasoconstrictor and platelet proaggregatory agent that has been implicated in the pathogenesis of cardiovascular disease. We therefore tested the hypothesis that testosterone regulates the expression of human platelet TXA2 receptors. METHODS AND RESULTS: In a double-blind, placebo-controlled, randomized, parallel-group study, we determined the effects of testosterone cypionate 200 mg IM given twice, 2 weeks apart, or saline placebo in 16 healthy men. Platelet TXA2 receptor density (Bmax) and dissociation constant (Kd) were measured by use of the TXA2 mimetic 125I-BOP. Platelet aggregation responses to I-BOP and to thrombin and plasma testosterone concentrations were measured before treatment (pretreatment phase), at 2 and 4 weeks (active phase), and again at 8 weeks (recovery phase). Treatment with testosterone was associated with an increase in the Bmax value from 0.95 +/- 0.13 to 2.10 +/- 0.4 pmol/mg protein (n = 9), with a peak effect at 4 weeks (P = .001), returning to baseline by 8 weeks. There was no significant change in Bmax values in the saline-treated group. The Kd values were unchanged. Testosterone treatment was associated with a significant increase in the maximum platelet aggregation response to I-BOP (P < .001) at 4 weeks and returned to baseline at 8 weeks. The EC50 values were not significantly changed. Platelet TXA2 receptor density was positively correlated (r = .56, P < .001, n = 32 measurements) with pretreatment (endogenous) plasma testosterone levels (range, 215 to 883 ng/dL) but not Kd. CONCLUSIONS: Testosterone regulates the expression of platelet TXA2 receptors in humans. This may contribute to the thrombogenicity of androgenic steroids.

Adult↗

PubMed1998

Testosterone effects on renal norepinephrine content and release in rats with different Y chromosomes.

The Y chromosome in spontaneously hypertensive rats (SHR) and stroke-prone rats has been shown to contain a locus that contributes to the hypertensive effect; both the sympathetic nervous system and testosterone may be involved. The objective of this study was to look at the effects of testosterone on renal norepinephrine (NE) release and content in the isolated perfused kidney in different Y chromosome backgrounds. The study involved male SHR, Wistar-Kyoto rats (WKY), and 2 consomic strains with different Y chromosomes (n=5 to 8 per group). Adult animals were castrated, and implants containing testosterone propionate were placed at the base of the neck. Blood testosterone levels were measured by radioimmunoassay 2 weeks after castration. The left kidney was isolated and perfused with oxygenated Krebs solution at a constant flow and temperature with KCl and electrical stimulation of the renal nerves. Perfusate was collected and analyzed for NE by high-performance liquid chromatography. Lactate dehydrogenase analyses were performed as a marker for potential tissue damage. Renal perfusate and renal tissue NE levels were significantly elevated by testosterone. The average NE increase with a single testosterone implant was 13.2 ng/mL, and for a double testosterone implant it was 29.8 ng/mL. The Y chromosome from the SHR produced a significant increase in renal NE release compared with the WKY Y chromosome. Significance was shown between all groups: 1 versus 2 implants, P=0.0067; 1 versus sham implants, P=0.015; 2 versus sham implants, P<0.001. In conclusion, testosterone caused an enhanced renal NE release that was strain-specific, with the Y chromosome raising renal NE content and release.

Animals↗

PubMed1967

Testosterone and androstenedione blood production rates in normal women and women with idiopathic hirsutism or polycystic ovaries.

The average plasma testosterone concentration of women with either hirsutism or polycystic ovaries and hirsutism was higher (p < 0.01) than that of normal women although the ranges overlapped. Testosterone blood production rates averaged 830 +/- 120 SE and 1,180 +/- 310 SE mug per day in the two groups of hirsute women and 230 +/- 33 SE mug per day in normal women. The ranges did not overlap. The testosterone metabolic clearance rates of hirsute women (1,090 +/- 140 SE L per day) and of men (1,240 +/- 136 SE L per day) were significantly higher than those of normal women (590 +/- 44 SE L per day). These differences persisted when the metabolic clearance rates were corrected for surface area. We suggest that testosterone metabolic clearance rates vary directly with some function of testosterone production. The mean plasma androstenedione levels (2.8 +/- 0.35 SE and 2.8 +/- 0.30 SE mug per L) and production rates (6,060 +/- 450 SE and 7,360 +/- 345 SE mug per day) of the women with hirsutism or polycystic ovaries, respectively, were significantly higher than those of normal women (1.5 +/- 0.22 SE mug per L; 3,300 +/- 830 SE mug per day). The androstenedione metabolic clearance rates were the same in each group. Plasma androstenedione was the precursor of 49% of plasma testosterone in normal women and of 26% of plasma testosterone in hirsute women. Thus, 74% of the plasma testosterone in these subjects must have been either secreted or derived from a precursor that did not enter the plasma androstenedione pool.

17-Ketosteroids↗

PubMed1969

Metabolism of testosterone and androstenedione in normal and ovariectomized women.

Metabolic clearance rates of testosterone (MCR(T)) and androstenedione (MCR(A)) were determined twice during the same cycle in six normal women, using a constant infusion of testosterone-(3)H and androstenedione-(14)C. Nonlabeled steroids served as internal standards. Plasma concentrations of testosterone (i(T)) and androstenedione (i(A)) were measured, and the blood production of testosterone (P(B) (T)) and of androstenedione (P(B) (A)) were calculated. The interconversions of these two steroids were also estimated. Six ovariectomized women were studied in the same manner. For testosterone, the mean i(T) in the normal women was not significantly different from that in the ovariectomized subjects, whereas the MCR(T) and P(B) (T) were significantly lower in the ovariectomized subjects. For androstenedione, the mean MCR(A) values of the two groups of subjects were not different, whereas the i(A) and P(B) (A) in the normal women were about double those in the ovariectomized subjects. In comparing the follicular and luteal phases of the menstrual cycle in four of six subjects there was no difference in i(T), MCR(T), or P(B) (T), whereas i(A), MCR(A), and P(B) (A) were increased in the luteal phase. In one ovariectomized woman infused with testosterone and androstenedione at physiologic levels, MCR(T) doubled but MCR(A) remained the same. After six wk on estrogen, the same subject did not show any change in MCR(T) after infusion of testosterone. It is suggested that MCR(T) depends on P(B) (T) and on plasma binding of testosterone which is partly estrogen dependent.

Adult↗

PubMed1999

Bloodspot testosterone assay suitable for study of neonates and monitoring of children with congenital adrenal hyperplasia.

A bloodspot assay for testosterone has been developed using an antiserum raised against testosterone-3-carboxymethyloxime-bovine serum albumin (T-3 CMO-BSA) conjugate and 125I-T-3CMO-histamine tracer. The method has a detection limit of 0.4 nmol/L with between-batch precision of less than 15% for testosterone values between 0.9 and 2.0 nmol/L and less than 10% for values greater than 2.0 nmol/L. Recovery of 4 nmol/L testosterone spiked into whole blood samples from 16 women (with unspiked bloodspot testosterone concentrations ranging from 0.4 to 3.7 nmol/L) was 100.9%. Bloodspot testosterone concentration was measured in thirty 6-9 day old infants (19 boys, 11 girls) with an absolute range in boys of < 0.4-2.3 nmol/L and in girls of < 0.4 nmol/L. In preterm infants (12 boys, 12 girls) of varying birth gestation and postnatal age, levels were higher than in term infants, with boys showing a rise with increasing postnatal age. Daytime bloodspot profiles in four children on replacement therapy for congenital adrenal hyperplasia demonstrated consistently low testosterone levels in the presence of moderately elevated early morning 17-hydroxyprogesterone concentrations, thus indicating adequate treatment. The bloodspot testosterone assay can be applied to the study of androgen physiology in preterm neonates as well as for monitoring treatment in disorders such as congenital adrenal hyperplasia.

Adrenal Hyperplasia, Congenital↗

PubMed2005

Pharmacokinetics and acute safety of inhaled testosterone in postmenopausal women.

This was a preliminary feasibility study to assess the pharmacokinetics and acute safety of a single dose of orally inhaled testosterone via the AERx system, a novel handheld aerosol delivery system in postmenopausal women. Twelve postmenopausal women stabilized on oral estrogen therapy were treated with a single dose of testosterone (0.1, 0.2, or 0.3 mg) by inhalation. Plasma concentrations of sex steroids were measured between 1 and 360 minutes. Pulmonary and cardiovascular adverse events were monitored. Inhaled testosterone produced a dose-dependent increase in plasma total and free testosterone. At the highest dose (0.3 mg), total and free testosterone increased from baseline (mean +/- SD, 0.6 +/- 0.3 nmol/L, 2.5 +/- 1.0 pmol/L) to maximum levels of 62.6 +/- 20.4 nmol/L (total) and 168.2 +/- 50.2 pmol/L(free), occurring 1 to 2 minutes after dosing. A 2-compartment model best described the free and total testosterone pharmacokinetic profile. Dihydrotestosterone levels were higher than baseline at 60 minutes (P < .0002). Estradiol did not vary, but sex hormone binding globulin and albumin fell. There were no adverse events related to the treatment. Administration of inhaled testosterone is safe and achieves a supraphysiologic "pulse" kinetic profile of total and free testosterone with a rapid return to pretreatment levels.

Administration, Inhalation↗

PubMed2003

Testosterone suppresses circadian responsiveness to social cues in the diurnal rodent Octodon degus.

The diurnal, social rodent Octodon degus displays a robust sex difference in the ability to use social cues to facilitate reentrainment following a phase advance of the light cycle. Adult females housed with a female social cue donor reentrained 25% to 40% faster than did females reentraining alone. However, reentrainment rates of males were unaffected by exposure to female social cues during reentrainment. The authors hypothesized that males were less sensitive to the reentrainment-enhancing effects of social cues and that their higher threshold to the stimuli could be overcome if the social cues were either increased in strength or salience. Housing a male with two females significantly shortened the time to reentrain following a 9-h phase advance (p = 0.002). Housing with a sister had no effect on reentrainment. Therefore, male degus are able to respond to social cues but require the stimulus to be stronger than that for females. The effect of testosterone was tested by comparing reentrainment rates of castrated males before and after testosterone replacement both with and without a female social cue donor. Castrated males responded to a single female social cue donor, reentraining 35% faster than when housed alone (p = 0.006), whereas the time to reentrainment of intact males and males with testosterone capsule implants did not differ. Intact females were also implanted with testosterone and phase shifted with and without donors. Testosterone treatment eliminated the increase in reentrainment rates in the presence of social cues. The authors conclude that the rate of recovery from odor-enhanced phase shifts is modulated by activational effects of testosterone in male degus. Testosterone is also effective in suppressing social cue responsiveness in females, suggesting that testosterone's effects on responsiveness are not sexually dimorphic. This hormonal effect likely occurs by altering sensory system functions or CNS response to sensory information.

Animals↗

PubMed1998

Induction of circadian rhythm of feeding activity by testosterone implantations in arrhythmic Japanese quail males.

Studies in vertebrates have shown that hormones can influence circadian rhythms of behavior. We investigated whether testosterone could induce rhythmicity in arrhythmic Japanese quail, kept in DD. The animals used were 3 1/2-week-old castrated males from a line of quail selected for the lack of the circadian rhythm of feeding activity. After 3 weeks in DD, 8 birds were implanted with an empty implant and 16 others with a testosterone implant. Two weeks later, the operation was repeated. After implantation, we noticed that 15 out of 16 testosterone-treated birds showed a circadian rhythm of feeding activity, in contrast to the control birds, which remained arrhythmic. The clarity of this rhythm increased significantly after each implantation. A positive correlation was found between the indexes of clarity of the rhythm (autocorrelation coefficient ratio and area of the peak of spectrum) and the plasma testosterone level. The period of the induced free-running rhythm was identical to the specific value of the endogenous circadian rhythm in immature quail. The circadian period showed a significant lengthening with the second implantation. This lengthening looks like the variation previously observed in maturing rhythmic or implanted quail. So, it would appear that testosterone can act on rhythmicity on at least two levels: by inducing the circadian rhythm and increasing its clarity and by modulating its period. To explain these results, several hypotheses can be considered. First, the observed arrhythmy may be the consequence of an internal desynchronization of oscillators, responsible for generating the circadian rhythm of feeding activity, and testosterone could play a role in the coupling of these oscillators. Alternatively, we suggest that testosterone could act on the transcription of genes implicated in the control of the rhythmicity or may regulate by rapid signals the cellular rhythmic activity. The possible functional values of the enhancing of circadian rhythmicity by testosterone at different stages of the bird's life were discussed.

Aging↗

PubMed2005

Testosterone, sexual offense recidivism, and treatment effect among adult male sex offenders.

The relationship between serum testosterone and sexual violence was examined in a sample of 501 convicted adult male sex offenders attending an intensive in-hospital group psychotherapy treatment program. It was found that men with higher testosterone tended to have committed the most invasive sexual crimes (p < .001, two-tailed). Further, a positive partial correlation (controlling for age) between testosterone and sexual offense recidivism over a lengthy follow-up period (mean = 8.9 years) was found. When the sample was separated into one group that completed treatment and one group that did not, an important ameliorating treatment effect was observed. Although controlling for age, serum testosterone remained significantly predictive of sexual recidivism for the treatment noncompleter group (p < .05, two-tailed). For those who completed treatment testosterone was no longer predictive of sexual reoffense (p > .05, two-tailed). Among convicted sex offenders, higher serum testosterone appears to be associated with greater likelihood of further sexual violence. Effective therapy, however, appears able to intercede in the influence of testosterone on sexually deviant behavior. It is suggested that serum testosterone may be an informative static risk factor and completion of intensive treatment should be accorded significance in future actuarially based risk prediction instruments.

Adult↗

PubMed2004

Testosterone as a modulator of vascular behavior.

Male sex is an acknowledged risk factor for many forms of cardiovascular disease, and vascular disease prevalence patterns appear to be different in men versus women. The vascular properties of the principal mammalian androgen, testosterone, are complex and linked to dose, duration of exposure, presence of underlying vascular disease, and, possibly, biological sex. Data from isolated vessels and animal models suggest that pharmacological doses of testosterone, or its potent intracellular metabolite dihydrotestosterone, produce vasodilation. Testosterone's major effect on vascular beds at physiologic concentrations remains unclear, with documentation of both vasodilatory and vasoconstrictive actions. Results of various studies suggest that testosterone can alter vascular tone through both endothelium-dependent and endothelium-independent mechanisms in a variety of vascular beds and vessel types. Testosterone's endothelium-dependent effects are likely mediated at least in part through nitric oxide (NO) elaboration, whereas mechanisms of endothelium-independent effects involve 1 or more types of smooth muscle ion conductance channels. Data from clinical studies indicate that, in men, androgen replacement may provide beneficial effects when coronary artery disease is present. Conversely, in women, testosterone may augment existing hypertension, increase risk for cardiovascular events, or promote atherogenesis. However, it should be emphasized that most of these observations are anecdotal or come from small-scale clinical studies, and limited information is available in women. New research is required to understand the potential efficacy of androgen therapy, or lack thereof. This review focuses on current understanding of testosterone's physiological effects on vascular behavior and of testosterone's putative role in vascular health and disease.

Adult↗

PubMed1983

Longitudinal relationships among endogenous testosterone, estradiol, and Quetelet index with high and low density lipoprotein cholesterols in adolescent boys.

In a 1-year longitudinal study of 19 adolescent boys, our major aim was to assess whether, and to what degree, testosterone, estradiol, Quetelet index, and their interactions related to concentrations of high and low density lipoprotein cholesterol (HDLC, LDLC). During the 1-year followup, mean HDLC and estradiol levels fell and triglycerides, LDLC, Quetelet index, and testosterone levels rose. For large decreases in estradiol, increases in testosterone were associated with decreases in HDLC. These decreases in HDLC were moderated by small decreases in Quetelet index. For boys with small decreases in estradiol, as the changes in testosterone increased, the change in HDLC varied from an increase to a decrease, except in those boys who also had a small decrease in Quetelet index, for whom the change in HDLC was positive. The greatest increases in LDLC were observed in boys having the largest increase in Quetelet index and a small decrease in estradiol; however, as the decrease in estradiol became large, the positive association of Quetelet with LDLC was moderated or nullified. For boys having large decreases in estradiol, the LDLC/HDLC ratio changed from small increments to substantial decrements as testosterone increased. As the decreases in estradiol became smaller, increases in the change of testosterone moderated the decreases in the LDLC/HDLC ratio, and large increases in Quetelet index tended to diminish this moderation. As the change in testosterone increased, the change in triglyceride increased, unless the decrease in estradiol was small. The overall pattern of change of HDLC and LDLC during sexual maturation in boys can be associated with changes in testosterone, estradiol, and Quetelet index.

Adipose Tissue↗