Effects Of Testosterone Replacement Research Articles

Is Hypoandrogenemia a Component of Metabolic Syndrome in Males?

This study was done to assess testosterone deficiency in males with metabolic syndrome (MetS) and the effect of testosterone replacement on insulin resistance and biochemical parameters of this syndrome with hypogonadism. Sixty three males fulfilling the International Diabetes Federation 2005 MetS guidelines as cases and 32 healthy males as controls with the mean age of 35.29±8.16 and 34±6.76 years respectively were enrolled in the study. Fasting blood samples were collected for gonadal profile and insulin assay. Homeostasis model assessment for insulin resistance (HOMA-IR) and free testosterone index were calculated. Hypogonadism was defined when the calculated free testosterone value was <0.225 nmol/L. Total and calculated free testosterone, sex hormone binding globulin (SHBG) were lower in cases than controls (P<0.001). Hypogonadism was seen in 19 (30%) cases with MetS while 1 (3.1%) in controls. MetS cases with hypogonadism had significantly higher HOMA-IR than eugonadal cases. Hypogonadotropic hypogonadism was observed in 16 (84%) cases. Treatment with oral Testosterone 40 mg twice a day for 3 months led to significant improvement of HOMA-IR (P≤0.001) in the MetS males with hypogonadism. This study revealed that males with MetS with or without diabetes had lower serum testosterone than their age matched healthy subjects. Hypogonadism was also common in subjects with MetS. Testosterone therapy to correct hypoandrogenimia improved insulin sensitivity and other biochemical parameters except High density lipoprotein cholesterol in MetS. This emphasizes that hypogonadism in all men with MetS or MetS in all men with hypogonadism needs clinical evaluation and subsequent management.

Effects of Testosterone Replacement in Middle-Aged Men With Dysthymia

Mid-life onset male dysthymic disorder (DD) seems to be a distinct clinical condition with limited therapeutic options. Testosterone replacement is mood-enhancing and has been proposed as an antidepressant therapy, though this strategy has received limited systematic study. We therefore conducted a six-week double-blind placebo-controlled clinical trial in 23 men with DD and with low or low-normal testosterone (T) level (i.e, screening total serum testosterone <350 ng/dL). Enrolled men were randomized to receive intramuscular injections of 200 mg of testosterone cypionate or placebo every 10 days. The primary outcome measures were the Clinical Global Impression (CGI) improvement score and the 21-item Hamilton Depression Rating Scale (HDRS) score.Twenty-three patients were randomized. The mean (SD) age of the enrolled patients was 50.6 (7.0) years and that of total testosterone level was 339 (93) ng/dL. The median duration of the current dysthymic episode was 3.6 (2.3) years, and the mean (SD) HDRS was 14.0 (2.9). After the intervention, the mean HDRS score decreased significantly more in the testosterone group (7.46 [4.56]) than in the placebo group (1.8 [4.13], t21 = -3.07, P = 0.006). Remission, defined as a CGI improvement score of 1 or 2 and a final HDRS score lower than 8, was achieved by 7 (53.8%) of 13 in the testosterone group and 1 (10%) of 10 in the placebo group (P = 0.03). Testosterone replacement may be an effective antidepressant strategy for late-onset male dysthymia.

Changes in prostate specific antigen (PSA) with clomiphine citrate: preliminary data on infertile hypogonadal men

OBJECTIVE: The effects of testosterone replacement on the initiation of prostate cancer are controversial. Hypogonadal men treated with testosterone replacement are followed with regular PSA and DRE exams during testosterone therapy. Hypogonadal infertile men or men with loss of libido in childbearing age are sometimes treated with clomiphene citrate (CC) to improve libido or sperm concentration. However, the effects of CC on the prostate and PSA are unknown. The objective of this preliminary study was to determine if short term CC therapy affects PSA levels.DESIGN: Patient charts were reviewed over the last two years in those who had PSA testing done either pre/post-CC therapy or post-CC therapy. 15 patients met the inclusion criteria.MATERIALS AND METHODS: Patients were started on CC if they were hypogonadal or had borderline normal testosterone with low/low normal FSH. Testosterone, FSH, LH, prolactin and PSA levels were recorded. PSA testing was done in some but not all cases prior to therapy and all patients post therapy. Semen analysis data were collected.RESULTS: Average pre-therapy testosterone, LH and FSH were 300, 3.34, and 4.68, respectively. PSA testing was done in all patients on an average of 4.6 months post CC therapy. All patients had minimal increases in PSA or had post-CC therapy PSA levels less than 1.8. Average post-therapy PSA was 0.74. FSH levels increased an average of 2.35 ng/dl. Testosterone increased an average of 198 ng/dl.CONCLUSIONS: There were no significant increases in PSA or post-CC therapy PSA measurements were all below 1.8 ng/dl. Preliminary data suggest that clomiphene citrate has no short term effects on PSA levels. OBJECTIVE: The effects of testosterone replacement on the initiation of prostate cancer are controversial. Hypogonadal men treated with testosterone replacement are followed with regular PSA and DRE exams during testosterone therapy. Hypogonadal infertile men or men with loss of libido in childbearing age are sometimes treated with clomiphene citrate (CC) to improve libido or sperm concentration. However, the effects of CC on the prostate and PSA are unknown. The objective of this preliminary study was to determine if short term CC therapy affects PSA levels. DESIGN: Patient charts were reviewed over the last two years in those who had PSA testing done either pre/post-CC therapy or post-CC therapy. 15 patients met the inclusion criteria. MATERIALS AND METHODS: Patients were started on CC if they were hypogonadal or had borderline normal testosterone with low/low normal FSH. Testosterone, FSH, LH, prolactin and PSA levels were recorded. PSA testing was done in some but not all cases prior to therapy and all patients post therapy. Semen analysis data were collected. RESULTS: Average pre-therapy testosterone, LH and FSH were 300, 3.34, and 4.68, respectively. PSA testing was done in all patients on an average of 4.6 months post CC therapy. All patients had minimal increases in PSA or had post-CC therapy PSA levels less than 1.8. Average post-therapy PSA was 0.74. FSH levels increased an average of 2.35 ng/dl. Testosterone increased an average of 198 ng/dl. CONCLUSIONS: There were no significant increases in PSA or post-CC therapy PSA measurements were all below 1.8 ng/dl. Preliminary data suggest that clomiphene citrate has no short term effects on PSA levels.

Effects of Testosterone Replacement and Exercise Training on Cardiac Apoptosis in Orchiectomized Rats

Effects of Testosterone Replacement and Exercise Training on Cardiac Apoptosis in Orchiectomized Rats

Effects of testosterone replacement and its pharmacogenetics on physical performance and metabolism

In men, testosterone (T) deficiency is associated with decreased physical performance, as defined by adverse traits in body composition, namely increased body fat content and reduced muscle mass. Physical abilities in androgen-deficient men are further attenuated by lower oxygen supply due to decreased hemoglobin concentrations and by poor glucose utilization. Dysthymia and a lack of necessary aggressiveness also contribute to deteriorate physical effectiveness. Substitution of T can improve lipid and insulin metabolism as well as growth of muscle fibers and decreasing fat depots, which consequently will result in changes of body composition. Increment of bone density will further contribute to increase physical fitness. The effects of T replacement therapy (TRT) are strongly influenced by age, training, and also pharmacogenetics: the CAG repeat polymorphism in exon 1 of the androgen receptor (AR) gene modulates androgen effects. In vitro, transcription of androgen-dependent target genes is attenuated with increasing length of triplet residues. Clinically, the CAG repeat polymorphism causes significant modulations of androgenicity in healthy eugonadal men as well as efficacy of TRT. Thresholds at which T treatment should be initiated, as well as androgen dosage, could be tailored according to this polymorphism.

Testosterone Making an Entry Into the Cardiometabolic World

Testosterone, the predominant sex hormone in men, is produced by the testes under stimulation by the gonadotrophs in the pituitary, which in turn are controlled by gonadotropin-releasing hormone neurons in the hypothalamus. A young adult man generally produces 3 to 10 mg of testosterone daily, which translates into serum values of 300 to 1000 ng/dL. The consequences of classical male hypogonadism (primary or secondary) have been long known to physicians and patients alike and include decreased libido, erectile dysfunction, osteoporosis, reduced sexual hair, and changes in body habitus. Recently, we have come to appreciate that reductions in serum testosterone resulting from aging or chronic disease have signs and symptoms similar to those seen in classical male hypogonadism, along with increased fat mass, decreased lean body mass, decreased muscle strength, and diminished quality of life.1 During the past decade, reports have been trickling in, mainly from laboratory and epidemiological studies (and a few clinical studies), linking differences in serum testosterone levels to various cardiovascular risk factors and also directly to cardiovascular disease and death. The article by Khaw et al2 in this issue of Circulation is another link to this growing chain. Article p 2694 Thirteen years ago, Phillips et al3 reported that low total and free testosterone levels were inversely linked to coronary artery disease, even after adjusting for age and adiposity. This observation still holds true, as was recently supported by a study showing that men with angiographically proven coronary artery disease had lower levels of testosterone than those of controls.4 Furthermore, testosterone levels were negatively correlated to the degree of coronary involvement. A few population-based studies have been published that relate low serum testosterone level with risk of death. A study of male veterans showed that low testosterone was associated with increased risk of …

Testosterone replacement therapy and the prostate

The major risk concern of testosterone replacement therapy in middle-aged and older men is that it may lead to an increase in the incidence and severity of symptomatic benign prostatic hyperplasia (BPH) and prostate carcinoma. While this concern is based on the role of androgens in the development and maintenance of these prostate diseases and the use of castration to treat both BPH and prostate cancer, a paucity of data from clinical trials of testosterone replacement exists to support or refute these concerns. Data from testosterone replacement therapy trials to date have demonstrated only a minor effect of testosterone therapy on parameters related to BPH, serum prostate-specific antigen levels, or the development of prostate cancer, but the study population has been highly selected and the total evaluation experience is very limited. This review article summarizes what is known to date about the effect of testosterone replacement on the prostate in adult men.

Testosterone Is Required for Delayed Cardioprotection and Enhanced Heat Shock Protein 70 Expression Induced by Preconditioning

Ischemic preconditioning fails to confer immediate cardioprotection in the absence of testosterone, indicating that the hormone is required for the process. Here we set out to determine whether testosterone is also necessary for delayed cardioprotection and, if so, how it acts. Male Sprague Dawley rats (7-8 wk) underwent sham operation or gonadectomy without (G) or with testosterone replacement (GT) for 8 wk. Isolated ventricular myocytes were preconditioned either by metabolic inhibition or with U50,488H, a kappa-opioid receptor agonist. In intact rats, U50,488H was administered systemically and 24 h later the hearts were removed. Ventricular myocytes were then subjected to metabolic inhibition and anoxia and isolated hearts to regional ischemia, followed by reperfusion to induce injury. Both types of preconditioning significantly increased the viability and decreased the lactate dehydrogenase release in ventricular myocytes from sham rats. They also activated heat shock transcription factor-1 and increased heat shock protein 70 expression. In contrast, all these effects were absent in myocytes from G rats and were restored by testosterone replacement. Parallel results were found in isolated hearts. In addition, preconditioning improved contractile functions impaired by ischemic insults in sham and rats gonadectomized with testosterone replacement but not G rats. The effects of testosterone replacement in ventricular myocytes were abolished by androgen receptor blockade. In conclusion, preconditioning requires testosterone to increase heat shock protein 70 synthesis, which mediates delayed cardioprotection in the male. These effects of testosterone are mediated by the androgen receptor.

The Sexual Effects of Testosterone Replacement in Depressed Men: Randomized, Placebo-Controlled Clinical Trial

Symptoms of male hypogonadism such as low libido and erectile dysfunction (ED) respond to testosterone (T) replacement. In hypogonadal men with major depressive disorder (MDD), the extent to which T replacement alleviates sexual symptoms of hypogonadism is not known. We conducted 6 week double-blind placebo-controlled clinical trial in men with low and low-normal T levels (i.e., total T ≤ 350 ng/dl) and MDD. Men were randomized to receive weekly intramuscular injections of either T enanthate 200 mg or sesame-seed oil (placebo). The primary outcome measure was self-reported sexual functioning. We randomized 30 patients. The mean age was 52(SD ± 8) years, mean T level 262.5(SD ± 8) ng/dl, and mean baseline Hamilton Rating Scale for Depression (HAM-D) score 21(SD ± 8). At baseline, sexual function was low, with the majority reporting having had normal erectile and orgasmic functioning 0–1 time in the preceding month. All patients who received T achieved normalization of their T levels. The HAM-D scores decreased significantly in both T and placebo groups, and there were no significant between-group differences: reduction in mean HAM-D score from baseline to endpoint was 10.1 in patients who received T and 10.5 in those who received placebo. Self-reported sexual functioning improved slightly in both groups; a between-group difference was not detected. Both T replacement and placebo were associated with improvement in sexual function and mood, but differences between T and placebo were not distinguishable.

Effects of Testosterone Replacement in Androgen-Deficient Women with Hypopituitarism: A Randomized, Double-Blind, Placebo-Controlled Study

Hypopituitarism in women is characterized by profound androgen deficiency due to a loss of adrenal and/or ovarian function. The effects of testosterone replacement in this population have not been reported. The objective of the study was to determine whether physiologic testosterone replacement improves bone density, body composition, and/or neurobehavioral function in women with severe androgen deficiency secondary to hypopituitarism. This was a 12-month randomized, placebo-controlled study. The study was conducted at a general clinical research center. Fifty-one women of reproductive age with androgen deficiency due to hypopituitarism participated. Physiologic testosterone administration using a patch that delivers 300 microg daily or placebo was administered. Bone density, fat-free mass, and fat mass were measured by dual x-ray absorptiometry. Thigh muscle and abdominal cross-sectional area were measured by computed tomography scan. Mood, sexual function, quality of life, and cognitive function were assessed using self-administered questionnaires. Mean free testosterone increased into the normal range during testosterone administration. Mean hip (P = 0.023) and radius (P = 0.007), but not posteroanterior spine, bone mineral density increased in the group receiving testosterone, compared with placebo, as did mean fat-free mass (P = 0.040) and thigh muscle area (P = 0.038), but there was no change in fat mass. Mood (P = 0.029) and sexual function (P = 0.044) improved, as did some aspects of quality of life, but not cognitive function. Testosterone at physiologic replacement levels was well tolerated, with few side effects. This is the first randomized, double-blind, placebo-controlled study to show a positive effect of testosterone on bone density, body composition, and neurobehavioral function in women with severe androgen deficiency due to hypopituitarism.

The Effects on Visceral Fat and Cardiovascular Risk Factors of Testosterone Replacement in Secondary Hypogonadal Men

Background: Increased body fat, abdominal obesity and insulin resistance are important clinical features in hypogonadal men. Several studies have demonstrated that a low testosterone concentration in men is associated with coronary heart disease, visceral obesity and insulin resistance. In this study, the effects of testosterone replacement therapy on the abdominal visceral fat and cardiovas cular risk factors in hypogonadal men were investigated. Methods: We selected 26 men with secondary hypogonadism (mean serum testosterone ± SD 0.39 ± 0.57 ng/mL), who were then treated with testosterone for 12 months. We measured the body composition, including the abdominal visceral fat area by abdominal CT at the L4 level, both before and 12 months after treatment, and the lipid profile, fasting plasma insulin, HOMA-IR and the serum homocysteine, CRP and IL-6 before and 6, 12 months after treatment. Results: With respect to the body composition, the lean body mass had significantly increased 12 months after treatment (P = 0.002), but there were no significant changes in the body fat mass and abdominal visceral fat area. There was a trend toward a decreased fasting plasma insulin and HOMA-IR, but this did not reach statistical significance. The total cholesterol had decreased significantly at 12 months (P =0 .04) and the HDL cholesterol decreased significantly over the course of study (P = 0.02). There were no significant changes in the serum homocysteine, CRP and IL-6 after treatment. Conclusions: After 12 months testosterone replacement therapy in the 26 men with hypogonadism, the lean body mass had increased significantly, but there was no significant change on the abdominal visceral fat during the treatment period. Testosterone replacement had deleterious effect on HDL cholesterol, but not significant effects on insulin resistance and the serum homocysteine, CRP a nd IL-6. These results suggest that testosterone replacement therapy may have a few adverse effects on cardiovascular diseases in hypogonadal men. However, it will be necessary to examine the long-term effects of testosterone replacement on the incidence of cardiovascular events as well as the cardiovascular risk factors in men with hypogonadism (J Kor Soc Endocrinol 20:252～260, 2005).

Effect of testosterone replacement or duration of castration on baroreflex bradycardia in conscious rats

BackgroundIn this study, we tested the hypothesis that 17β-estradiol contributes to testosterone-mediated restoration of baroreflex-mediated bradycardia in short-term (3 weeks) castrated rats. Further, a reported increase in serum testosterone after long-term (6 weeks) castration constituted a basis for testing the hypothesis that a spontaneous increase in serum testosterone or androstenedione in this model causes a commensurate increase in baroreflex-mediated bradycardia.ResultsTestosterone (1 week) replacement enhanced baroreflex-mediated bradycardia in short-term castrated rats without changing 17β-estradiol level. A spontaneous recovery of baroreflex-mediated bradycardia occurred following long-term castration, although circulating testosterone and androstenedione remained suppressed.ConclusionThe data suggest: 1) 17β-Estradiol does not contribute to testosterone restoration of the baroreflex-mediated bradycardia in short-term castrated rats. 2) The long-term modulation of baroreflex-mediated bradycardia occurs independent of androgens, or the baroreflex mechanism may become adapted to low levels of circulating androgens.

Effects of Testosterone Replacement in Human Immunodeficiency Virus-Infected Women with Weight Loss

The objective of this study was to determine whether physiological testosterone replacement increases fat-free mass (FFM) and muscle strength and contributes to weight maintenance in HIV-infected women with relative androgen deficiency and weight loss. Fifty-two HIV-infected, medically stable women, 18-50 yr of age, with more than 5% weight loss over 6 months and testosterone levels below 33 ng/dl were randomized into this double-blind, placebo-controlled trial of 24-wk duration. Subjects in the testosterone group applied testosterone patches twice weekly to achieve a nominal delivery of 300 mug testosterone over 24 h. Data were evaluable for 44 women. Serum average total and peak testosterone levels increased significantly in the testosterone group, but did not change in the placebo group. However, there were no significant changes in FFM (testosterone, 0.7 +/- 0.4 kg; placebo, 0.3 +/- 0.4 kg), fat mass (testosterone, 0.3 +/- 0.7 kg; placebo, 0.6 +/- 0.7 kg), or body weight (testosterone, 1.0 +/- 0.9 kg; placebo, 0.9 +/- 0.8 kg) between the two treatment groups. There were no significant changes in leg press strength, leg power, or muscle fatigability in either group. Changes in quality of life, sexual function, cognitive function, and Karnofsky performance scores did not differ significantly between the two groups. High-density lipoprotein cholesterol levels decreased significantly in the testosterone group. The patches were well tolerated. We conclude that physiological testosterone replacement was safe and effective in raising testosterone levels into the mid to high normal range, but did not significantly increase FFM, body weight, or muscle performance in HIV-infected women with low testosterone levels and mild weight loss. Additional studies are needed to fully explore the role of androgens in the regulation of body composition in women.

The Effect of Testosterone Replacement on Endogenous Inflammatory Cytokines and Lipid Profiles in Hypogonadal Men

Testosterone has immune-modulating properties, and current in vitro evidence suggests that testosterone may suppress the expression of the proinflammatory cytokines TNFalpha, IL-1beta, and IL-6 and potentiate the expression of the antiinflammatory cytokine IL-10. We report a randomized, single-blind, placebo-controlled, crossover study of testosterone replacement (Sustanon 100) vs. placebo in 27 men (age, 62 +/- 9 yr) with symptomatic androgen deficiency (total testosterone, 4.4 +/- 1.2 nmol/liter; bioavailable testosterone, 2.4 +/- 1.1 nmol/liter). Compared with placebo, testosterone induced reductions in TNFalpha (-3.1 +/- 8.3 vs. 1.3 +/- 5.2 pg/ml; P = 0.01) and IL-1beta (-0.14 +/- 0.32 vs. 0.18 +/- 0.55 pg/ml; P = 0.08) and an increase in IL-10 (0.33 +/- 1.8 vs. -1.1 +/- 3.0 pg/ml; P = 0.01); the reductions of TNFalpha and IL-1beta were positively correlated (r(S) = 0.588; P = 0.003). In addition, a significant reduction in total cholesterol was recorded with testosterone therapy (-0.25 +/- 0.4 vs. -0.004 +/- 0.4 mmol/liter; P = 0.04). In conclusion, testosterone replacement shifts the cytokine balance to a state of reduced inflammation and lowers total cholesterol. Twenty of these men had established coronary disease, and because total cholesterol is a cardiovascular risk factor, and proinflammatory cytokines mediate the development and complications associated with atheromatous plaque, these properties may have particular relevance in men with overt vascular disease.

L-prostaglandin D synthase expression and regulation in mouse testis and epididymis during sexual maturation and testosterone treatment after castration.

Lipocalin-type prostaglandin D synthase (L-PGDS) is highly expressed in the adult testis and epididymis of many mammals. The present study was to investigate L-PGDS expression in mouse testis and epididymis during sexual maturation, and the effects of testosterone replacement on L-PGDS expression in epididymis by in situ hybridization and immunohistochemistry. Both L-PGDS mRNA and protein were highly expressed in the interstitial tissue of adult testis. L-PGDS mRNA was first detected on d 30 after birth and exhibited an abundant signal in adult caput and cauda epididymis. L-PGDS immunostaining was first observed on d 30 after birth. There was a strong level of L-PGDS immunostaining in adult epididymis. Castrated male mice were treated with either vehicle or testosterone propionate following 3 d postcastration. L-PGDS expression steadily declined in a time-dependent fashion in control groups. No L-PGDS mRNA expression or immunostaining was detected in the controls for 12 d. When the castrated mice were treated with testosterone propionate for 5 or 12 d, L-PGDS expression was significantly increased in the whole epididymis. These data suggest that L-PGDS expression in mouse epididymis gradually declined in parallel to the declining concentration of endogenous androgen after castration and increased with the treatment of exogenous testosterone, indicating that L-PGDS expression in mouse epididymis was modulated by androgen levels. However, differential expression in different areas of the epididymis may also be influenced by factors derived from the testis.

Involvement of calcitonin gene-related peptide in elevation of skin temperature in castrated male rats

Objectives To assess the involvement of calcitonin gene-related peptide (CGRP) in the occurrence of hot flashes in men after castration for treatment of prostate cancer, we investigated the effects of CGRP on skin temperature in surgically and medically castrated male rats. Methods Changes in skin temperature of the hind paws after intravenous injection of 10 μg/kg of CGRP and CGRP family peptides (adrenomedullin and amylin) were measured at 5-minute intervals for 120 minutes, 3 weeks after bilateral orchiectomy or 2 weeks after subcutaneous injection of a gonadotropin-releasing hormone analogue (1.0 mg/kg Leuplin) in male rats. Antagonism with CGRP 8-37 (1000 μg/kg intravenously), a CGRP 1 receptor antagonist, to the CGRP-induced response was examined by injecting it 10 minutes before injection of CGRP. The effect of testosterone replacement on castration was evaluated in each castrated rat by the administration of testosterone (1.0 mg/kg subcutaneously once a day) for 14 days before the day of the temperature analysis. Results CGRP, but not adrenomedullin and amylin, elevated the skin temperature in surgical or medical castration-induced testosterone-deficient rats more than in the sham-treated rats. The difference was statistically significant. The CGRP-induced potentiation in the castrated rats was inhibited by pretreating with CGRP 8-37 or by supplying testosterone. Conclusions CGRP is the most potent peptide in a family that elevates the skin temperature in male rats. The elevation of the skin temperature was more affected by the testosterone deficiency resulting from castration. These results suggest that CGRP is involved in the mechanism underlying hot flashes in men.

Effects of Testosterone Replacement and/or Resistance Training on Interleukin-6, Tumor Necrosis Factor Alpha, and Leptin in Elderly Men Ingesting Megestrol Acetate: A Randomized Controlled Trial

Megestrol acetate (MA) has been used to stimulate weight gain in elderly populations with the majority of the gain being adipose tissue. Significant inverse correlations have been reported between weight gain with MA and reductions in circulating the tumor necrosis factor (TNF) alpha receptors. In addition, MA has been shown to reduce circulating interleukin 6 (IL-6) concentrations. We attempted to increase gains in fat-free mass with MA using resistance training and/or testosterone replacement and examined the effects on circulating IL-6, TNF alpha, and leptin in elderly men. All subjects received MA and were randomly assigned to one of these four groups: placebo (P) injections; resistance training and P (RT+P); weekly injections of testosterone (T; 100 mg/wk); or RT and T (RT+T). Cytokines were measured by enzyme-linked immunosorbent assay Preinterventions, Midinterventions, and after 12 weeks of the interventions (Post). IL-6 decreased ( p =.03) over time for the T and P groups when compared to the RT+T and RT+P groups. A time effect ( p =.013) was observed for TNF alpha with Mid and Post both being lower than Pre. A hormone by time interaction ( p =.03) was observed for plasma leptin with individuals not on T exhibiting higher concentrations Post than those individuals on T. A positive correlation was observed (r =.60; p <.05) between changes in fat mass and the change in leptin. IL-6 was reduced by MA except when RT was undertaken; TNF alpha was reduced over time regardless of group; leptin was higher in individuals not on T than those on T; and the change in plasma leptin was correlated with the change in fat mass.

A Causative Factor of Copulatory Disorder in Rats Following Social Stress

We investigated the causative role of testosterone in copulatory disorder and the expression of c-fos messenger (m)RNA in the medial preoptic area in rats after social stress. To generate copulatory disorder rats in the experimental defeated group were attacked by residents for 10 minutes daily for 7 consecutive days (social stress). We then investigated the effect of repeat defeat on the frequency of mounting behavior and plasma testosterone levels. The effects of testosterone replacement and/or apomorphine (100 microg./kg. subcutaneously), a dopamine receptor agonist, on the frequency of mounting behavior were also studied. After experiencing social stress the brain area within the medial preoptic area was removed for analysis of c-fos and androgen receptor mRNA expression. Real-time reverse transcription-polymerase chain reaction was done to analyze gene expression. Rats in the defeated group showed a reduced frequency of mounting behavior and a decrease in plasma testosterone levels compared with values in control rats (p <0.01). After testosterone replacement the frequency of mounting behavior became significantly higher than that of socially stressed rat (p <0.05) but did not achieve control levels. The frequency of mounting behavior by socially stressed rats after apomorphine treatment was significantly higher than that of vehicle treated rats (p <0.05) but the frequency produced by the combination of testosterone replacement and apomorphine injection did not achieve control levels. After the social stress experience c-fos mRNA expression was significantly increased compared with that in control rats (p <0.05). The expression of androgen receptor mRNA was not affected by social stress. Testosterone replacement significantly reduced the expression of c-fos mRNA in the medial preoptic area (p <0.05). Our results indicate that a reduction in plasma testosterone may have a causative role in copulatory disorder induced by social stress. Changes in c-fos mRNA expression in the medial preoptic area correlated with copulatory disorder and, thus, they are suitable for monitoring that disorder.

Effects of Testosterone Replacement and/or Resistance Exercise on the Composition of Megestrol Acetate Stimulated Weight Gain in Elderly Men: A Randomized Controlled Trial

Effects of Testosterone Replacement and/or Resistance Exercise on the Composition of Megestrol Acetate Stimulated Weight Gain in Elderly Men: A Randomized Controlled Trial

Effects of Testosterone Replacement on a Male Professional Singer

Testosterone has been known to play an important role in the development of the postpubertal male voice for many centuries. In fact, the prevention of pubertal development of the voice by castrating young male singers was a well-known practice, especially in Italy beginning in the sixteenth century. The “castrati” were well known for their clear, high-pitched voices. Because of the resulting small larynx and vocal folds, castrati apparently produced a distinctive resonance as well as the high pitch, which cannot be matched even by the counter tenors of today. Busy voice labs occasionally see males with sex hormone deficiencies secondary to chromosomal or gonadal problems. This is a presentation of an unusual patient who was a trained tenor singer and was found to have hypogonadism on a premarital health examination. Administration of replacement testosterone resulted in significant vocal register and voice quality changes.