Doses Of Testosterone Research Articles

Interaction between Testosterone and Growth Hormone on Whole-Body Protein Anabolism Occurs in the Liver

GH and testosterone both exert protein-anabolic effects and may act synergistically. Liver and muscle are major sites of protein metabolism. Our objective was to determine whether the site of GH and testosterone interaction on protein metabolism is primarily hepatic or extrahepatic. In this open-label randomized crossover study, the impact on whole-body protein metabolism of oral (solely hepatic testosterone exposure) and transdermal (systemic testosterone exposure) testosterone replacement in the presence or absence of GH was compared. Eleven hypopituitary men with GH and testosterone deficiency were randomized to 2-wk treatments with transdermal testosterone (10 mg) or oral testosterone (40 mg), with or without GH replacement (0.6 mg/d). The dose of testosterone administered orally achieves physiological portal testosterone concentrations without spillover into the systemic circulation. Whole-body leucine turnover was measured, from which leucine rate of appearance (LRa), an index of protein breakdown, and leucine oxidation (Lox), a measure of irreversible protein loss, were estimated at the end of each treatment. In the absence of GH, neither transdermal nor oral testosterone affected LRa or Lox. GH therapy significantly increased LRa, an effect equally reduced by transdermal and oral testosterone administration. GH replacement alone did not significantly change Lox, whereas addition of testosterone treatment reduced Lox, with the effect not significantly different between transdermal and oral testosterone. In the doses used, testosterone stimulates protein anabolism by reducing protein breakdown and oxidation only in the presence of GH. Because the net effect on protein metabolism during GH therapy is not different between systemic and solely hepatic testosterone administration, we conclude that the liver is the primary site of this hormonal interaction.

Androgens as therapy for androgen receptor-positive castration-resistant prostate cancer.

Prostate cancer is the most frequently diagnosed non-cutaneous tumor of men in Western countries. While surgery is often successful for organ-confined prostate cancer, androgen ablation therapy is the primary treatment for metastatic prostate cancer. However, this therapy is associated with several undesired side-effects, including increased risk of cardiovascular diseases. Shortening the period of androgen ablation therapy may benefit prostate cancer patients. Intermittent Androgen Deprivation therapy improves quality of life, reduces toxicity and medical costs, and delays disease progression in some patients. Cell culture and xenograft studies using androgen receptor (AR)-positive castration-resistant human prostate cancers cells (LNCaP, ARCaP, and PC-3 cells over-expressing AR) suggest that androgens may suppress the growth of AR-rich prostate cancer cells. Androgens cause growth inhibition and G1 cell cycle arrest in these cells by regulating c-Myc, Skp2, and p27Kip via AR. Higher dosages of testosterone cause greater growth inhibition of relapsed tumors. Manipulating androgen/AR signaling may therefore be a potential therapy for AR-positive advanced prostate cancer.

Evidence That Androgens Modulate Human Thymic T Cell Output

BackgroundThe thymus has long been recognized as a target for the actions of androgenic hormones, but it has only been recently recognized that alterations in circulating levels of gonadal steroids...

Efeitos dos hormônios anabólicos sobre a estrutura, metabolismo e função do músculo esquelético

This study reviewed information regarding the effects of anabolic hormones on strength gain and muscle hypertrophy, emphasizing the physiological mechanisms that may increase muscle strength. Structural, metabolic and functional aspects were analyzed and special attention was paid to the dose-response relationship. The Pubmed database was searched and studies were selected according to relevance and date of publication (last 15 years). The administration of high testosterone doses (~600 mg/week) potentiates the effects of strength training, increasing lean body mass, muscle fiber type IIA and IIB cross-sectional area, and the number of myonuclei. There is no evidence of conversion between MHC isoforms. The interaction between testosterone administration and strength training seems to modify some metabolic pathways, increasing protein synthesis, glycogen and ATP-CP muscle stores and improving fat mobilization. Changes in 17-estradiol concentration or in the ACTH-cortisol and insulin-glucagon ratios seem to be associated with these metabolic alterations. Regarding performance, testosterone administration may improve muscle strength by 5-20% depending on the dose used. On the other hand, the effects of growth hormone on the structural and functional aspects of skeletal muscle are not evident, with this hormone more affecting metabolic aspects. However, strictly controlled human studies are necessary to establish the extent of the effects of anabolic hormones on structural, metabolic and functional aspects.

Beneficial effects of testosterone therapy in women measured by the validated Menopause Rating Scale (MRS)

Objectives This study was designed to measure the beneficial effects of continuous testosterone therapy, delivered by subcutaneous implant, in the relief of somatic, psychological and urogenital symptoms in both pre- and post-menopausal patients, utilizing the validated Health Related Quality of Life (HRQOL), Menopause Rating Scale (MRS). Study design 300 pre- and post-menopausal women with symptoms of relative androgen deficiency, were asked to self-administer the 11-item MRS, at baseline and 3 months after their first insertion of the subcutaneous testosterone implant. Baseline hormone measurements, menopausal status and BMI, were assessed to determine correlation with symptoms and clinical outcome. Main outcome measurements Changes related to therapy were determined. Total MRS scores as well as psychological, somatic and urogenital subscale scores were compared prior to therapy and following testosterone implant therapy. Results Pre-menopausal and post-menopausal females reported similar hormone deficiency symptoms. Both groups demonstrated similar improvement in total score, as well as psychological, somatic and urogenital subscale scores with testosterone therapy. Better effect was noted in women with more severe complaints. Higher doses of testosterone correlated with greater improvement in symptoms. Conclusion Continuous testosterone alone, delivered by subcutaneous implant, was effective for the relief of hormone deficiency symptoms in both pre- and post-menopausal patients. The validated, HRQOL questionnaire, Menopause Rating Scale (MRS), proved a valuable tool in the measurement of the beneficial effects of testosterone therapy in both cohorts.

GPRC6A Mediates the Non-genomic Effects of Steroids

The identity of the putative G-protein coupled receptor (GPCR) that mediates the non-genomic effects of androgens is unknown. We present in vitro and in vivo evidence that the orphan GPRC6A receptor, a widely expressed calcium and amino acid sensing GPCR, transduces the non-genomic effects of testosterone and other steroids. Overexpression of GPRC6A imparts the ability of extracellular testosterone to illicit a rapid, non-genomic signaling response in HEK-293 cells lacking the androgen receptor. Conversely, testosterone-stimulated rapid signaling and phosphorylation of ERK is attenuated in bone marrow stromal cells derived from GPRC6A(-/-) mice and in 22Rv1 prostate cancer cells after siRNA-mediated knockdown of GPRC6A. Compared with wild-type controls, GPRC6A(-/-) null mice exhibit significantly less ERK activation and Egr-1 expression in both bone marrow and testis in response to pharmacological doses of testosterone in vivo. In addition, testosterone administration results in suppression of luteinizing hormone in wild-type male mice, but paradoxically stimulates serum luteinizing hormone levels in GPRC6A(-/-) null mice. These results suggest that GPRC6A is functionally important in regulating non-genomic effects of androgens in multiple tissues.

Testosterone manipulation postcastration does not alter cloacal gland growth differences in male quail selected for divergent plasma corticosterone stress response

Japanese quail selected for reduced (low-stress, LS) rather than exaggerated (high-stress, HS) plasma corticosterone response to brief restraint have consistently shown greater cloacal gland (CG) development, an androgen-dependent trait. In this study, the effects of testosterone implants on levels of plasma testosterone and CG development in castrated LS and HS quail were determined. Stress-line males were castrated and randomly allocated to 1 of 3 testosterone treatments: the empty testosterone (ET), low testosterone (LT), or high testosterone (HT) implant group. Cloacal gland volume was determined at 4 weekly intervals that represented ranges of 1 to 9 d, 8 to 17 d, 15 to 24 d, and 22 to 31 d after castration and testosterone implantation. Levels of plasma testosterone were also assessed at the end of the study. Development of the CG was affected by quail line (LS > HS), testosterone treatment (HT > LT > ET), and time of measurement (1 to 9 d < 8 to 17 d < 15 to 24 d = 22 to 31 d after castration and testosterone implantation). A significant interaction between testosterone treatment and time of measurement on CG volume was also detected (with CG volume generally increasing with time in LT- and HT-treated quail, but not in ET-treated quail). However, even though HT implant treatments induced higher CG development than did LT treatments beyond the first interval of CG volume measurement, and despite the finding of greater CG volumes in LS than HS quail during the last 2 measurement intervals within each of the LT and HT groups, no interaction was observed between testosterone implant dosages and quail stress line on CG volume. Thus, by the end of the study, regardless of testosterone dose, CG volume was consistently greater in LS quail than in their HS counterparts. In addition, although, as expected, the testosterone implant treatment significantly altered levels of plasma testosterone (HT > LT > ET), neither quail line nor its interaction with testosterone treatment affected plasma testosterone. The present findings suggest that the often-observed depressed CG development in the HS line may be independent of testosterone effects.

Safety of Physiological Testosterone Therapy in Women: Lessons from Female-to-Male Transsexuals (FMT) Treated with Pharmacological Testosterone Therapy

The safety of long-term physiological doses of testosterone (T) therapy in women with sexual dysfunction is a contentious issue, in part, because of fear of adverse effects, such as breast cancer, vascular disease, and excessive virilization. This unsubstantiated fear has hampered progress in treating women with sexual dysfunction using T therapy in physiological doses to achieve circulating levels in the normal range. To examine evidence derived from studies in female-to-male transsexuals (FMT) treated with supraphysiological (pharmacological) doses of T for long periods of time with no apparent major adverse effects. A comprehensive literature search of relevant articles published between 1980 and 2010 pertaining to the topic of T in FMTs was performed using PubMed. The following key words were used: female-to-male transsexuals; testosterone; virilization; gender re-assignment; and androgen therapy in women. Relevant articles were retrieved, reviewed, and the information was analyzed and evaluated for study methodology and major findings. Data from peer-reviewed publications were critically analyzed and the information was summarized. The data from the studies reported in the literature to date strongly suggest that treatment of FMTs with supra-physiological doses of T had minimal adverse effects. No increase in mortality, breast cancer, vascular disease, or other major health problems were reported. No significant serious adverse effects were reported in FMTs treated with pharmacological doses of T. In light of the findings with supraphysiological doses of T, we suggest that treatment with T at doses producing physiological levels in women with sexual dysfunction are expected to produce limited and minimal adverse effects.

Male Hypogonadism: Childhood Diagnosis and Future Therapies

Male hypogonadism results from inadequate testicular function manifested by the impairment of both testosterone secretion and spermatogenesis. Hypogonadism has several etiologies. Hypogonadotropic hypogonadism (HH) results from hypothalamic–pituitary disorders leading to a complete or partial deficiency in gonadotropin-releasing hormone (GnRH) secretion from hypothalamic neurons, or gonadotropin secretion from anterior pituitary, or defects in GnRH receptor at the pituitary. All situations result in low or normal serum gonadotropin levels and low serum testosterone levels. Congenital HH can occur isolated (idiopathic HH) or in association with olfactory dysfunction (Kallmann’s syndrome). Gonadotropin deficiency can also occur with other pituitary hormone deficiencies. Most of the congenital isolated HH are still idiopathic. However, defects in more than ten genetic loci with multiple modes of inheritance, accounting for monogenic and occasionally oligogenic presentations were found in approximately 30% of cases. Acquired HH results from a hypothalamic–pituitary structural lesion as well as from tumors, trauma, autoimmunity or radiation. Hypergonadotropic hypogonadism is characterized by elevated serum gonadotropin levels due to testicular disorders, chromosomal abnormalities (Klinefelter syndrome), genetic syndromes as well as acquired conditions (autoimmunity, chemotherapy or radiation therapy). The main clinical feature of a male infant with hypogonadism is micropenis associated with or without cryptorchidism. The diagnosis of HH at childhood is difficult and usually postponed until adult age. At pubertal age, the differential diagnosis between the constitutional delay of growth and puberty, and HH is tricky and no hormonal test can consistently distinguish between these two disorders with 100% sensitivity and specificity; therefore, clinical follow-up is essential. Optimal management of male hypogonadism depends of the underlying etiology. Genetic tests are now available to detect genetic mutations in candidate genes essential for hypothalamic–pituitary axis function. Infants with micropenis require testosterone or dihydrotestosterone therapy to increase penile length. The first-line therapy for cryptorchidism is orchiopexy. Puberty should be induced with a low dose of testosterone and fertility could be achieved with chorionic gonadotropin hormone, recombinant luteinizing hormone and follicle stimulating hormone preparations or pulsatile GnRH injection. A small subset of HH patients may have a reversible phenotype enabling the withdrawal of medication in up to 10% of cases.

Androgen Receptor-Dependent and Independent Atheroprotection by Testosterone in Male Mice

The atheroprotective effect of testosterone is thought to require aromatization of testosterone to estradiol, but no study has adequately addressed the role of the androgen receptor (AR), the major pathway for the physiological effects of testosterone. We used AR knockout (ARKO) mice on apolipoprotein E-deficient background to study the role of the AR in testosterone atheroprotection in male mice. Because ARKO mice are testosterone deficient, we sham operated or orchiectomized (Orx) the mice before puberty, and Orx mice were supplemented with placebo or a physiological testosterone dose. From 8 to 16 wk of age, the mice consumed a high-fat diet. In the aortic root, ARKO mice showed increased atherosclerotic lesion area (+80%, P < 0.05). Compared with placebo, testosterone reduced lesion area both in Orx wild-type (WT) mice (by 50%, P < 0.001) and ARKO mice (by 24%, P < 0.05). However, lesion area was larger in testosterone-supplemented ARKO compared with testosterone-supplemented WT mice (+57%, P < 0.05). In WT mice, testosterone reduced the presence of a necrotic core in the plaque (80% among placebo-treated vs. 12% among testosterone-treated mice; P < 0.05), whereas there was no significant effect in ARKO mice (P = 0.20). In conclusion, ARKO mice on apolipoprotein E-deficient background display accelerated atherosclerosis. Testosterone treatment reduced atherosclerosis in both WT and ARKO mice. However, the effect on lesion area and complexity was more pronounced in WT than in ARKO mice, and lesion area was larger in ARKO mice even after testosterone supplementation. These results are consistent with an AR-dependent as well as an AR-independent component of testosterone atheroprotection in male mice.

Novel approaches for the molecular classification of prostate cancer

Novel approaches for the molecular classification of prostate cancer

Testosterone exacerbates neuronal damage following cardiac arrest and cardiopulmonary resuscitation in mouse

Male animals exhibit greater neuronal damage following focal cerebral ischemic injury in many experimental injury models, however the mechanism of this is unknown. This study used cardiac arrest and cardiopulmonary resuscitation (CA/CPR) in male mice exposed to physiological vs. pharmacological doses of testosterone and tested the hypothesis that testosterone increases damage following global cerebral ischemia. Analysis of histological damage 72 h after resuscitation revealed a complex dose–response curve for testosterone, such that low and high doses of testosterone exacerbated ischemic neuronal damage, while intermediate doses had no effect on neuronal survival. In agreement with these histological observations of neuronal damage, both low and high doses of testosterone increased sensorimotor deficit following CA/CPR compared to vehicle treated animals. Finally, the androgen receptor antagonist flutamide inhibited the increase in neuronal damage and sensorimotor impairment observed in testosterone treated mice. Our data showed that low and supra-physiological levels of testosterone increase neuronal damage following global cerebral ischemia and that blockade of androgen receptors limits this injury. Therefore, this study indicated that testosterone may have a role in determining sex-linked differences in cerebrovascular disease as well as having important health implications in clinical conditions of elevated testosterone.

Population based evaluation of a multi-parametric steroid profiling on administered endogenous steroids in single low dose

Steroid profiling provides valuable information to detect doping with endogenous steroids. Apart from the traditionally monitored steroids, minor metabolites can play an important role to increase the specificity and efficiency of current detection methods. The applicability of several minor steroid metabolites was tested on administration studies with low doses of oral testosterone (T), T gel, dihydrotestosterone (DHT) gel and oral dehydroepiandrosterone (DHEA). The collected data for all monitored parameters were evaluated with the respective population based reference ranges. Besides the traditional markers T/E, T and DHT, minor metabolites 4-OH-Adion and 6α-OH-Adion were found as most sensitive metabolites to detect oral T administration. The most sensitive metabolites for the detection of DHEA were identified as 16α-OH-DHEA and 7β-OH-DHEA but longest detection up to three days (after oral administration of 50 mg) was obtained with non-specific 5β-steroids and its ratios. Steroids applied as a gel had longer effects on the metabolism but were generally not detectable with universal decision criteria. It can be concluded that population based reference ranges show limited overall performance in detecting misuse of small doses of natural androgens. Although some minor metabolites provide additional information for the oral testosterone and DHEA formulations, the topical administered steroids could not be detected for all volunteers using universal reference limits. Application of other population based threshold limits did not lead to longer detection times.

The potent synthetic androgens, dimethandrolone (7α,11β-dimethyl-19-nortestosterone) and 11β-methyl-19-nortestosterone, do not require 5α-reduction to exert their maximal androgenic effects

Dimethandrolone (DMA: 7α,11β-dimethyl-19-nortestosterone) and 11β-methyl-19-nortestosterone (MNT) are potent androgens in development for hormonal therapy in men. As 5α-reduced androgens, such as 5α-dihydrotestosterone (DHT), may raise the risk of benign prostate hyperplasia, accelerate the development of prostate carcinoma, and increase male pattern baldness and acne, we investigated the role of 5α-reduction in the androgenic activity of DMA and MNT. The authentic 5α-reduced metabolites, 5α-dihydroDMA (5α-DHDMA) and 5α-dihydroMNT (5α-DHMNT), were prepared by chemical synthesis and compared in vitro and in vivo to the parent compounds . Both 5α-reduced androgens bound with high affinity to the rat androgen receptor (AR) and were potent inducers of transactivation of 3XHRE-LUC in CV-1 cells cotransfected with a human AR expression plasmid. To examine in vivo androgenic (stimulation of ventral prostate [VP] and seminal vesicle [SV] weights) and anabolic (stimulation of levator ani [LA] muscle weights) activity, 22-day-old castrate male rats were treated sc for 7 days with various doses of DMA, 5α-DHDMA, or testosterone (T) or MNT, 5α-DHMNT, or T and necropsied on day 8. 5α-DHDMA was at least threefold more potent than T in stimulating growth of the VP but only 30–40% as potent as DMA. 5α-DHMNT was four- to eightfold more potent than T, whereas MNT was approximately equipotent to T. To assess the possible role of 5α-reduction in VP and SV growth, castrate immature rats were treated with maximally effective doses of T, DHT, DMA, MNT, or the related 19-norandrogen, 7α-methyl-19-nortestosterone (MENT), or vehicle, with or without dutasteride (DUT), an inhibitor of 5α-reductases types 1 and 2. In rats treated with T + DUT, serum T was significantly higher ( P < 0.05) than in rats treated with T alone, and serum DHT was decreased ( P < 0.001) to levels observed in castrate vehicle-treated rats. DUT significantly reduced both VP and SV weights in T-treated rats, whereas there was no significant effect of DUT on weights of these accessory sex glands in rats treated with DMA, MNT, DHT, or MENT. These results indicate that inhibition of 5α-reductase activity in vivo does not affect the androgenic potency of DMA, MNT, or MENT.

The Effects of Injected Testosterone Dose and Age on the Conversion of Testosterone to Estradiol and Dihydrotestosterone in Young and Older Men

During testosterone (T) therapy, T is partly converted to 17beta-estradiol (E2) and 5alpha-dihydrotestosterone (DHT). Effects of age, testosterone dose, and body composition on total and free E2 and DHT levels are unknown. We evaluated age and dose-related differences in E2 and DHT levels in response to graded doses of testosterone enanthate in young and older men. Fifty-one young (aged 19-35 yr) and 52 older (aged 59-75 yr) men completed treatment with monthly injections of a GnRH agonist plus randomly assigned weekly doses of testosterone enanthate (25, 50, 125, 300, or 600 mg) for 5 months. During testosterone administration, total and free E2 levels increased dose-dependently (dose effect, P<0.001) in both young and older men. Total and free E2 levels and E2:T ratios during T administration were higher in older than young men, but age-related differences in free E2 and free E2:T ratios were not significant after adjusting for testosterone levels, percentage fat mass, and SHBG. DHT levels and DHT:T ratios were dose-related but did not differ between young and older men. Mechanistic modeling of free hormone data revealed that the conversions of T to E2 and DHT were both consistent with saturable Michaelis-Menten kinetics. The in vivo Km values were estimated to be 1.83 nm for aromatase and 3.35 nm for 5alpha-reductase, independent of age. The Vmax parameter for E2 was 40% higher in older men than younger men, but Vmax for DHT was not significantly different between age groups. During im testosterone administration, E2 and DHT levels exhibit saturable increases with dose. The rate of whole body aromatization is higher in older men, partly related to their higher percentage fat mass, SHBG, and testosterone levels.

Section 6: Nonpharmacologic Management and Health Care Maintenance in Patients With Chronic Heart Failure

Section 6: Nonpharmacologic Management and Health Care Maintenance in Patients With Chronic Heart Failure

Kinetics of removal of intravenous testosterone pulses in normal men

Testosterone is secreted into the bloodstream episodically, putatively distributing into total, bioavailable (bio) nonsex hormone-binding globulin (nonSHBG-bound), and free testosterone moieties. The kinetics of total, bio, and free testosterone pulses are unknown. Design Adrenal and gonadal steroidogenesis was blocked pharmacologically, glucocorticoid was replaced, and testosterone was infused in pulses in four distinct doses in 14 healthy men under two different paradigms (a total of 220 testosterone pulses). Testosterone kinetics were assessed by deconvolution analysis of total, free, bioavailable, SHBG-bound, and albumin-bound testosterone concentration-time profiles. Independently of testosterone dose or paradigm, rapid-phase half-lives (min) of total, free, bioavailable, SHBG-bound, and albumin-bound testosterone were comparable at 1.4+/-0.22 min (grand mean+/-S.E.M. of geometric means). Slow-phase testosterone half-lives were highest for SHBG-bound testosterone (32 min) and total testosterone (27 min) with the former exceeding that of free testosterone (18 min), bioavailable testosterone (14 min), and albumin-bound testosterone (18 min; P<0.001). Collective outcomes indicate that i) the rapid phase of testosterone disappearance from point sampling in the circulation is not explained by testosterone dose; ii) SHBG-bound testosterone and total testosterone kinetics are prolonged; and iii) the half-lives of bioavailable, albumin-bound, and free testosterone are short. A frequent-sampling strategy comprising an experimental hormone clamp, estimation of hormone concentrations as bound and free moieties, mimicry of physiological pulses, and deconvolution analysis may have utility in estimating the in vivo kinetics of other hormones, substrates, and metabolites.

Should women receive androgen replacement therapy, and if so, how?

The available clinical evidence supports efficacy of testosterone therapy for the treatment of postmenopausal women with hypoactive sexual desire disorder (HSDD) who have undergone a comprehensive clinical evaluation. Although few preparations designed to deliver an appropriate dose of testosterone for women are available, use of testosterone by women for the management of HSDD is widespread. Issues that continue to simulate debate in this therapeutic area include whether HSDD is a condition that merits pharmacotherapy, how effective is such treatment and whether testosterone therapy is safe. Hence the question, should women receive androgen replacement therapy, and if so, how?

The influence of testosterone in the expression of androgen receptors in rat ovary

Event Abstract Back to Event The influence of testosterone in the expression of androgen receptors in rat ovary Ioannis Kyriakidis1*, Theodora Papamitsou2, Maria Dermentzopoulou-Theodoridou2, Ioannis Makaronidis1, Kyriaki Papadopoulou2, Fotios Tsanakalis1 and Paraskevi Papaioannidou1 1 Aristotle University of Thessaloniki, Department of Pharmacology, Greece 2 Aristotle University of Thessaloniki, Laboratory of Histology-Embryology and Anthropology, Greece Aim of our study was to investigate the localization of androgen receptors (ARs) in rat ovary, to examine the induction of ARs in the ovaries of female Wistar rats when administered with high dosages of testosterone, to measure any effects on weight and to record any toxic effects on the ovarian structure or function. For the purpose of this study female adult Wistar rats (6 weeks old, weighing from 150 to 200 gr, fed ad libitum) were used and separated in three groups. The first group received intramuscularly 25 mg of testosterone at the third day after menses and the second group received 12.5 mg of testosterone at also the same period. The third group was the control group. Ten days after the testosterone administration, euthanasia via ether was performed to the rats, while tissue samples from the ovaries were obtained, fixed and prepared for immunohistochemical study of ARs with polymerization. Ovaries in testosterone treated rats did not differ significantly with controls as regards their weight, while the first group -and moderately the second group- showed macroscopically hyperemia and hypertrophy. The expression of AR in the ovaries of rats who took high dose of testosterone was positive in various places of stromatic ovary cells and in some granule cells of secondary ovarian follicle with antrum. In the second group, AR staining was positive with increased expression in ovary’s germinal cells, in stromal cells and also in ovarian follicle’s granule cells and in radiata corona’s cells of the oocytes. In conclusion, AR expression was less positive in ovary’s follicle cells of the rats who took high doses of testosterone than in those who took lower doses. Keywords: Testosterone, Ovary, rat, androgen receptor Conference: 8th Southeast European Congress on Xenobiotic Metabolism and Toxicity - XEMET 2010, Thessaloniki, Greece, 1 Oct - 5 Oct, 2010. Presentation Type: Poster Topic: Xenobiotics and reproduction Citation: Kyriakidis I, Papamitsou T, Dermentzopoulou-Theodoridou M, Makaronidis I, Papadopoulou K, Tsanakalis F and Papaioannidou P (2010). The influence of testosterone in the expression of androgen receptors in rat ovary. Front. Pharmacol. Conference Abstract: 8th Southeast European Congress on Xenobiotic Metabolism and Toxicity - XEMET 2010. doi: 10.3389/conf.fphar.2010.60.00154 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 05 Mar 2011; Published Online: 04 Nov 2010. * Correspondence: Dr. Ioannis Kyriakidis, Aristotle University of Thessaloniki, Department of Pharmacology, Thessaloniki, Greece, kyriakidis@auth.gr Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Ioannis Kyriakidis Theodora Papamitsou Maria Dermentzopoulou-Theodoridou Ioannis Makaronidis Kyriaki Papadopoulou Fotios Tsanakalis Paraskevi Papaioannidou Google Ioannis Kyriakidis Theodora Papamitsou Maria Dermentzopoulou-Theodoridou Ioannis Makaronidis Kyriaki Papadopoulou Fotios Tsanakalis Paraskevi Papaioannidou Google Scholar Ioannis Kyriakidis Theodora Papamitsou Maria Dermentzopoulou-Theodoridou Ioannis Makaronidis Kyriaki Papadopoulou Fotios Tsanakalis Paraskevi Papaioannidou PubMed Ioannis Kyriakidis Theodora Papamitsou Maria Dermentzopoulou-Theodoridou Ioannis Makaronidis Kyriaki Papadopoulou Fotios Tsanakalis Paraskevi Papaioannidou Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Testosteron und das metabolische Syndrom

Abdominal obesity as a key cardiovascular risk factor as well as metabolic syndrome and type 2 diabetes mellitus are associated with low testosterone levels. In line with these facts, investigations of patients undergoing androgen ablation therapy for prostate cancer have shown a negative effect of this treatment approach on insulin sensitivity and body fat mass. The effects of physiological doses of testosterone seem to have less impact on the parameters of lipid metabolism. However, supraphysiological levels of testosterone can lower HDL levels. At present data on glycemic control in patients with type 2 diabetes are not yet uniform, but negative effects on glycemic control in type 2 diabetics have not been reported. In fact two studies were able to demonstrate a positive effect of testosterone on glycemic control in patients with type 2 diabetes. It is currently not yet possible to conclusively evaluate the significance of testosterone treatment in patients with metabolic syndrome and type 2 diabetes mellitus. Only larger, randomized prospective trials will show whether testosterone therapy is helpful in metabolic syndrome or type 2 diabetes. However, administration of testosterone in hypogonadal men with metabolic syndrome appears to be a promising treatment option to improve metabolic control.