Role Of Testosterone Research Articles

TESTOSTERONE AND SEX HORMONE-BINDING GLOBULIN IN DYSGLYCEMIC WOMEN AT HIGH CARDIOVASCULAR RISK: A REPORT FROM THE OUTCOME REDUCTION WITH AN INITIAL GLARGINE INTERVENTION TRIAL

The role of testosterone and sex hormone-binding globulin (SHBG) in female cardiovascular disease and dysglycemia is debated. The present objective was to investigate the prognostic impact of total (TT) and free testosterone (FT) and SHBG in women at high cardiovascular risk and dysglycemia.

Do Androgens Modulate the Pathophysiological Pathways of Inflammation? Appraising the Contemporary Evidence.

The role of testosterone in the pathophysiology of inflammation is of critical clinical importance; however, no universal mechanism(s) has been advanced to explain the complex and interwoven pathways of androgens in the attenuation of the inflammatory processes. PubMed and EMBASE searches were performed, including the following key words: “testosterone”, “androgens”, “inflammatory cytokines”, “inflammatory biomarkers” with focus on clinical studies as well as basic scientific studies in human and animal models. Significant benefits of testosterone therapy in ameliorating or attenuating the symptoms of several chronic inflammatory diseases were reported. Because anti–tumor necrosis factor therapy is the mainstay for the treatment of moderate-to-severe inflammatory bowel disease; including Crohn’s disease and ulcerative colitis, and because testosterone therapy in hypogonadal men with chronic inflammatory conditions reduce tumor necrosis factor-alpha (TNF-α), IL-1β, and IL-6, we suggest that testosterone therapy attenuates the inflammatory process and reduces the burden of disease by mechanisms inhibiting inflammatory cytokine expression and function. Mechanistically, androgens regulate the expression and function of inflammatory cytokines, including TNF-α, IL-1β, IL-6, and CRP (C-reactive protein). Here, we suggest that testosterone regulates multiple and overlapping cellular and molecular pathways involving a host of immune cells and biochemical factors that converge to contribute to attenuation of the inflammatory process.

Effect of Testosterone Use on Bone Mineral Density in HIV-Infected Men.

HIV-infected men have increased rates of osteoporosis and fracture compared to HIV-uninfected men. Testosterone use among HIV-infected men is common. In HIV-uninfected men, testosterone increases bone mineral density (BMD), but its effects have not been evaluated in HIV-infected men. In a substudy of Multicenter AIDS Cohort Study (MACS), the Bone Strength Substudy (BOSS) enrolled 202 HIV-infected and 201 HIV-uninfected men aged between 50 and 69 years. Study participants underwent dual-energy X-ray absorptiometry (DXA) at the lumbar spine (LS), total hip (TH), and femoral neck (FN) and detailed assessment of osteoporosis risk factors. We used multivariable linear regression to determine associations and 95% confidence intervals (CIs) between self-reported testosterone use and T-scores at the LS, TH, and FN after adjustment for demographics, behavioral covariates, comorbidities, and other traditional osteoporosis risk factors. HIV-infected men reported more frequent testosterone use (22% vs. 4%; p < .001) and had lower median BMD T-score at TH than HIV-uninfected men (0.0 vs. 0.3; p = .045) but similar T-scores at LS and FN. In the overall study population, testosterone use was associated with significantly greater BMD T-score at LS (0.68; 95% CI: 0.22-1.13). In HIV-infected men with virologic suppression, testosterone was significantly associated with higher BMD T-score at LS (0.95; 95% CI: 0.36-1.54) and TH (0.45; 95% CI: 0.04-0.86). Current testosterone use is common in HIV-infected men and was associated with higher BMD, compared to those not taking testosterone. Testosterone's role in reducing fracture risk in HIV-infected men should be investigated.

Aromatase Derived Estradiol Within the Thalamus Modulates Pain Induced by Varicella Zoster Virus.

Herpes zoster or shingles is the result of varicella zoster virus (VZV) infection and often results in chronic pain that lasts for months after visible symptoms subside. Testosterone often attenuates pain in males. Previous work demonstrates ovarian estrogen effects γ-aminobutyric acid (GABA) signaling in the thalamus, reducing pain but the role of testosterone within the thalamus is currently unknown. Because aromatase affects pain and is present in the thalamus we tested a hypothesis that testosterone converted to estrogen in the thalamus attenuates herpes zoster induced pain. To address this hypothesis, male Sprague-Dawley rats received whisker pad injection of either MeWo cells or MeWo cells containing VZV. To reduce aromatase derived estrogen in these animals we injected aromatase inhibitor letrozole systemically or infused it into the thalamus. To test if estrogen was working through the estrogen receptor (ER) agonist, 4, 4′, 4″-(4-Propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol (PPT) was infused concomitant with letrozole. Motivational and affective pain was measured after letrozole and/or PPT treatment. Vesicular GABA transporter (VGAT) is important in pain signaling. Because estrogen effects VGAT expression we measured its transcript and protein levels after letrozole treatment. Virus injection and letrozole significantly increased the pain response but thalamic infusion of PPT reduced zoster pain. Letrozole increased the number of thalamic neurons staining for phosphorylated ERK (pERK) but decreased VGAT expression. The results suggest in male rats aromatase derived estradiol interacts with the ER to increase VGAT expression and increase neuronal inhibition in the thalamus to attenuate VZV induced pain.

Sexual dimorphism in immunity across animals: a meta-analysis.

In animals, sex differences in immunity are proposed to shape variation in infection prevalence and intensity among individuals in a population, with females typically expected to exhibit superior immunity due to life-history trade-offs. We performed a systematic meta-analysis to investigate the magnitude and direction of sex differences in immunity and to identify factors that shape sex-biased immunocompetence. In addition to considering taxonomic and methodological effects as moderators, we assessed age-related effects, which are predicted to occur if sex differences in immunity are due to sex-specific resource allocation trade-offs with reproduction. In a meta-analysis of 584 effects from 124 studies, we found that females exhibit a significantly stronger immune response than do males, but the effect size is relatively small, and became non-significant after controlling for phylogeny. Female-biased immunity was more pronounced in adult than immature animals. More recently published studies did not report significantly smaller effect sizes. Among taxonomic and methodological subsets of the data, some of the largest effect sizes were in insects, further supporting previous suggestions that testosterone is not the only potential driver of sex differences in immunity. Our findings challenge the notion of pervasive biases towards female-biased immunity and the role of testosterone in driving these differences.

On the Role of Testosterone in Anxiety-Like Behavior Across Life in Experimental Rodents.

Testosterone affects brain functions and might explain some of the observed behavioral sex differences. Animal models may help in elucidating the possible involvement of sex hormones in these sex differences. The effects of testosterone have been intensively investigated, especially in anxiety models. Numerous experiments have brought inconsistent results with either anxiolytic or anxiogenic effects. Besides methodological variations, contradictory findings might be explained by the divergent metabolism of testosterone and its recognition by neurons during prenatal and postnatal development. Gonadectomy and subsequent supplementation have been used to study the role of sex hormones. However, the variable duration of hypogonadism might affect the outcomes and the effect of long-term androgen deficiency is understudied. Testosterone can be metabolized to dihydrotestosterone strengthening the androgen signaling, but also to estradiol converting the androgen to estrogen activity. Moreover, some metabolites of testosterone can modulate γ-aminobutyric acid and serotonergic neurotransmission. Here we review the currently available experimental data in experimental rodents on the effects of testosterone on anxiety during development. Based on the experimental results, females are generally less anxious than males from puberty to middle-age. The anxiety-like behavior of females and males is likely influenced by early organizational effects, but might be modified by activational effects of testosterone and its metabolites. The effects of sex hormones leading to anxiogenesis or anxiolysis depend on factors affecting hormonal status including age. The biological and several technical issues make the study of effects of testosterone on anxiety very complex and should be taken into account when interpreting experimental results.

The CATCH checklist to investigate adult-onset hypogonadism.

Adult-onset hypogonadism is a syndrome often underdiagnosed, undertreated, or incompletely explored. There are various reasons for this: firstly, undefined age range of men in whom testosterone levels should be investigated and then no definitive serum cutoff point for the diagnosis of hypogonadism; and finally, variable and non-specific signs and symptoms; men and physicians do not pay adequate attention to sexual health. All these factors make the diagnostic criteria for hypogonadism controversial. The evaluation of the clinical features and causes of this syndrome, its link with age, the role of testosterone and other hormone levels, and the presence of any comorbidities are all useful factors in the investigation of this population. The purpose of this manuscript, after an accurate analysis of current literature, is to facilitate the diagnosis of hypogonadism in men through the use of the CATCH acronym and a checklist to offer a practical diagnostic tool for daily clinical practice. A narrative review of the relevant literature regarding the diagnosis of late-onset hypogonadism or adult-onset hypogonadism was performed. PubMed database was used to retrieve articles published on this topic. A useful new acronym CATCH (Clinical features [symptoms] and Causes, Age, Testosterone level, Comorbidities, and Hormones) and a practical checklist to facilitate the evaluation of hypogonadism in aging men were used. The evaluation of the clinical features and causes of hypogonadism, the link with age, the role of Testosterone and other hormones, and the evaluation of comorbidities are important in investigating adult-onset hypogonadism. The CATCH checklist could be helpful for clinicians for an early diagnosis of both hypogonadism and associated comorbidities. We suggest the use of this acronym to advocate the investigation of declining testosterone in aging men.

Investigating the effect of testosterone by itself and in combination with letrozole on 1,25-dihydroxy vitamin D and FGF23 in male rats.

Testosterone deficiency might be associated with vitamin D levels in hypogonadal men, but it is not clear whether testosterone can affect vitamin D and fibroblast growth factor-23 (FGF23), either directly or indirectly via aromatization to estradiol. We aimed to investigate the role of testosterone on vitamin D metabolism and serum FGF23 in male rats. A total of 48 male rats were divided into 4 equal groups: sham; O, orchiectomy; O + T, orchiectomized rats treated with testosterone; and O + T+L, orchiectomized rats treated with combination of testosterone and letrozole. We compare the vitamin D metabolism biochemical parameters in these four groups, before and after the study. We detected a significant reduction in 25-hydroxyvitamin D (25(OH)D), vitamin D binding protein (DBP), FGF23, and 1,25-dihydroxyvitamin D (1,25(OH)2D) serum level in O group compared to sham group (p = 0.004, p = 0.009, p < 0.001 and p < 0.001, respectively), and a significant increase in serum phosphorus, parathyroid hormone (PTH), and alkaline phosphatase (ALP) levels in orchiectomized rats in comparison to sham group (p < 0.001, p = 0.022, and p = 0.006, respectively). However, these changes were corrected by testosterone replacement in O + T and O + T+L groups. In addition, we found that DBP and 1,25(OH)2D serum levels were significantly higher in O + T group in comparison to O + T+L group (p = 0.030 and p = 0.026, respectively). Testosterone plays a significant role on regulating 25(OH)D, DBP, FGF23, phosphate (Phos), PTH, and 1,25(OH)2D serum levels in male rats. Also, testosterone has a potent effect on 1,25(OH)2D and DBP by its conversion to estradiol.

Оценка тестостеронемии у мужчин, подвергнутых оперативному лечению стриктур мочеиспускательного канала

Testosterone plays an important role in the functioning of various organs and systems of the male body. Its diagnostic and prognostic values are studied both in urological diseases and in the patients undergoing non-urologic surgery. To investigate changes in testosterone level in patients with urethral strictures (US) depending on its baseline level, the cause of US, the age of patients and the number of surgeries. The study comprised 30 patients aged 19-63 years with traumatic (76.7%) and inflammatory (23.3%) US. Primary and recurrent US were diagnosed in 25 (83.3%) and 5 (16.7%) patients, respectively. Nineteen (63.3%) patients underwent excision and primary anastomosis, while replacement urethroplasty was performed in 11 (36.7%) patients. In addition to the standard diagnostic work-up, all patients were tested for total serum testosterone 24 hours prior to surgery and at 1, 3, 7, 14 days after the operation. 33.3% of men with US had a testosterone deficiency in the absence of any testicular or endocrine injuries and diseases. Surgery was associated with a drop in testosteronemia in 83.3% of patients. The degree of postoperative testosterone level decline and its changes were significantly influenced by the age of patients and the number of operations. Men who had baseline testosterone deficiency and underwent repeat surgeries remained in a hypogonadal state throughout the postoperative period. Investigating the clinical value of testosterone in men with US and the risks of their surgical treatment associated with testosterone deficiency will provide insight into the role of testosterone in the treatment of this condition and the decision-making regarding pharmacological correction of testosterone deficiency in patients undergoing surgery for US.

Testosterone and All-Cause Mortality in Older Men: The Role of Metabolic Syndrome.

Previous studies have shown controversial results about the role of testosterone in all-cause mortality in elderly men. We hypothesized that metabolic syndrome (MetS) could partly explain this discrepancy. We therefore examined the association of all-cause mortality with total and bioavailable testosterone, taking into account the MetS. We used data from the Three-City Cohort (3C) study with 12-year follow-up. The 3C study included 3650 men aged >65 years in three French cities. Hormone was measured in a random subsample of 444 men, and MetS was determined as stated by the International Diabetes Federation criteria. We used inverse-probability–weighted Cox regression to estimate hazard ratios (HRs) and 95% confidence intervals (95% CIs). Of 444 men included in the analysis, 106 (23.9%) had MetS at baseline, and 166 died over the follow-up. There was a significant interaction between testosterone level and MetS for all-cause mortality (P = 0.002 and P = 0.008 for total and bioavailable testosterone, respectively). Among men with MetS, a decrease in one standard deviation of testosterone was associated with higher mortality risk [HR 1.78 (95% CI 1.13 to 2.78) and HR 1.83 (95% CI 1.17 to 2.86) for total and bioavailable testosterone, respectively]. By contrast, there was no association of testosterone with mortality risk among men without MetS. Our results suggest that MetS modifies the association between testosterone and mortality in older men. If confirmed, these findings could contribute to improve risk stratification and better manage the health of older men.

Decision-making, financial risk aversion, and behavioral biases: The role of testosterone and stress

We examine the relation between testosterone, cortisol, and financial decisions in a sample of naïve investors. We find that testosterone level is positively related to excess risk-taking, whereas cortisol level is negatively related to excess risk-taking (correlation coefficient [r]: 0.75 and −0.21, respectively). Additionally, we find support for the dual-hormone hypothesis in a financial context. Specifically, the testosterone-to-cortisol ratio is significantly related to loss aversion. Individuals with a higher ratio are 3.4 times more likely to sell losing stocks (standard error [SE]: 1.63). Furthermore, we find a positive feedback loop between financial success, testosterone, and cortisol. Specifically, financial success is significantly related to higher post-trial testosterone and cortisol by a factor of 0.53 (SE: 0.14). Finally, we find that in a competitive environment, testosterone level increases significantly, leading to greater risk-taking than in noncompetitive environment. Overall, this study underscores the importance of the endocrine system on financial decision-making. The results of this study are relevant to a broad audience, including investors looking to optimize financial performance, industry human resources, market regulators, and researchers.

Immune Response to Native Lipoproteins Induces Visceral Obesity and Aortic Wall Injury in Rats: The Role of Testosterone.

The underlying mechanism of atherosclerosis and visceral obesity remains unknown.The purpose of this study was to test the hypothesis that atherosclerosis and visceral obesity are caused by an immune response to native plasma lipoproteins, and the atherogenic and adipogenic effects of the antibodies to native lipoproteins stem from the androgen deficiency that is created. Wistar rats were immunized with native human (nh) low-density (LDL) or high-density lipoproteins (HDL). Visceral fat, aortic wall structure, and testosterone levels were studied. Immunization with nhLDL or nhHDL induced in rats increased visceral abdominal fat and perivascular adipose tissue volume, the appearance of epicardial fat, and atherosclerosis-like changes in the aortic wall: accumulation of leucocytes, destruction of the intima, and disruption of the media structure. Immunized rats produced antibodies to native plasma lipoproteins, while there was no difference between immunized and adjuvant-injected rats with regard to the level of antibodies to oxidized LDL. The immune response to nhHDL caused testosterone disturbances, but it is not associated with visceral obesity and atherosclerosis. The immune response to native lipoproteins is atherogenic and adipogenic and testosterone is not involved in the atherogenic and adipogenic effects of antibodies to lipoproteins.

The role of testosterone in the regulation of P-glycoprotein functioning

The functional activity of P-glycoprotein (Pgp) was studied in Chinchilla rabbits after orchiectomy and administration of testosterone undecanoate after surgery. The functional activity of Pgp was determined by the pharmacokinetics of fexofenadine, its marker substrate. In addition, the localization of the transport protein was assessed in the liver, kidney, and jejunum by the immunohistochemistry. It was found that a decrease in the serum testosterone concentration after orchiectomy leads to an increase in Pgp activity on the 14th and 21st days after the surgery, which is accompanied by an increase in the staining intensity of Pgp-positive epithelium membranes of the proximal and distal renal tubules. It was found that the administration of testosterone at a dose of 6 mg/kg body weight in the period after the surgery neutralizes these changes.

Decision-Making, Financial Risk Aversion and Behavioral Biases: The Role of Testosterone and Stress

We examine the relation between testosterone, cortisol, and financial decisions in a sample of naive investors. We find that testosterone level is positively related to excess risk-taking, whereas cortisol level is negatively related to excess risk-taking (correlation coefficient [r]: 0.75 and -0.21, respectively). Additionally, we find support for the dual-hormone hypothesis in a financial context. Specifically, the testosterone-to-cortisol ratio is significantly related to loss aversion. Individuals with a higher ratio are 3.4 times more likely to sell losing stocks (standard error [SE]: 1.63). Furthermore, we find a positive feedback loop between financial success, testosterone, and cortisol. Specifically, financial success is significantly related to higher post-trial testosterone and cortisol by a factor of 0.53 (SE: 0.14). Finally, we find that in a competitive environment, testosterone level increases significantly, leading to greater risk-taking than in noncompetitive environment. Overall, this study underscores the importance of the endocrine system on financial decision-making. Broader implications of this study include, but are not limited to, investors looking to optimize financial performance, industry human resources, market regulators, and academia.

Association of admission testosterone level with ST-segment resolution in male patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention

BackgroundLow level of testosterone may be associated with cardiovascular diseases in men, as some evidence suggests a protective role for testosterone in cardiovascular system. Little is known about the possible role of serum testosterone in response to reperfusion therapy in ST-elevation myocardial infarction (STEMI) and its relationship with ST-segment recovery. The present study was conducted to evaluate the association of serum testosterone levels with ST-segment resolution following primary percutaneous coronary intervention (PPCI) in male patients with acute STEMI.MethodsForty-eight men (mean age 54.55 ± 12.20) with STEMI undergoing PPCI were enrolled prospectively. Single-lead ST segment resolution in the lead with maximum baseline ST-elevation was measured and patients were divided into two groups according to the degree of ST-segment resolution: complete (> or =50%) or incomplete (<50%). The basic and demographic data of all patients, their left ventricular ejection fraction (LVEF) and laboratory findings including serum levels of free testosterone and cardiac enzymes were recorded along with angiographic finding and baseline TIMI (Thrombolysis in Myocardial Infarction) flow and also in-hospital complications and then these variables were compared between two groups.ResultsA complete ST-resolution (≥50%) was observed in 72.9% of the patients. The serum levels of free testosterone (P = 0.04), peak cardiac troponin (P = 0.03) were significantly higher and hs-CRP (P = 0.02) were lower in patients with complete ST-resolution compared to those with incomplete ST-resolution. In-hospital complications were observed in 31.2% of patients. The patients with a lower baseline TIMI flow (P = 0.03) and those who developed complications (P = 0.04) had lower levels of free testosterone. A significant positive correlation was observed between the left ventricular function and serum levels of free testosterone (P = 0.01 and r = +0.362).ConclusionThis study suggests that in men with STEMI undergoing PPCI, higher serum levels of testosterone are associated with a better reperfusion response, fewer complications and a better left ventricular function.

The role of the serum testosterone levels as a predictor of prostate cancer in patients with atypical small acinar proliferation at the first prostate biopsy.

The current literature does not support the usefulness of clinical markers on predicting which patients with atypical small acinar proliferation (ASAP) are more likely to progress to prostate cancer (PCa). Androgens have long been considered to be the potential risk factors for PCa. However, the role of testosterone is controversial. The present study aims to analyze the relationship between serum testosterone (TS) levels and the diagnosis of PCa after a first prostate biopsy in patients affected by ASAP. This retrospective study included 143 patients diagnosed with ASAP in an initial transrectal ultrasound-guided prostate biopsy for suspicious PCa according to the European Association of Urology guidelines. Their TS levels, age, PSA, prostate volume, digital rectal examination, and prostate biopsy Gleason score (GS) were collected retrospectively for statistical analysis. All patients included in the study had a second biopsy and were suitable for further analysis. Re-biopsy was carried out 3–6 months after the first diagnosis of ASAP. Low and normal TS groups were composed of 29 (20.3%) and 114 (79.7%) patients, respectively. The diagnosis of the second biopsy was ASAP in 25.2% and PCa in 36.4% of patients. The comparison between patients with PCa and those with negative or an ASAP result in the second biopsy reported that men with cancer had significantly higher levels of TS (P < 0.001). However, there was no statistically significant association between GS postbiopsy and TS (P = 0.324). Our experience demonstrated that eugonadal patients may be a clinical risk factor for the diagnosis of PCa on re-biopsy after ASAP diagnosis than hypogonadal.

Novel risk factors for coronary artery disease – role of testosterone and high-sensitivity CRP in Sri Lankan males

Coronary artery disease (CAD) is multi-factorial in origin and develops as a result of both genetic and environmental factors. Traditional risk factors (generally smoking, hypertension, raised lipids, and diabetes mellitus) do not explain all of the risk for coronary disease events. There remain several other factors that contribute to the overall risk. Various new or emerging risk factors have been studied to improve global risk assessment for CAD. Inflammation indicated by markers as Creactive protein and low androgen (testosterone) status in males are among the emerging risk factors. In the local setting, the association of testosterone with CAD has not been explored, although this relationship has been well-studied in the Western population. Therefore we investigated, whether serum levels of total testosterone (TT) and high sensitivity C-reactive protein (hs-CRP) differ in men with CAD from those without CAD and to evaluate the relationship of serum TT and hs-CRP with the severity of CAD. Three hundred and nine males (103 patients with ST-elevation myocardial infarction (STEMI), 103 patients with angiographically-proven CAD, 103 controls without having a history of CAD) were studied. Serum TT, hs-CRP, lipids, cardiac troponin I (cTnI) and plasma glucose were estimated. Three angiogram-based severity scores were used in the severity assessment of angiographically-proven CAD. In STEMI patients, clinical risk scores and modified Selvester ECG QRS score were used in assessing the severity of myocardial infarction. We showed that low levels of total testosterone, high levels of hs-CRP, abnormal lipid profile and raised plasma glucose contribute to an atherogenic milieu. Low levels of total testosterone and high level of hs-CRP can be perceived as risk factors of coronary artery disease.

Testosterone role during seasons changes in the dogs testes

This study was conducted to evaluate the effect of seasons on serum testosterone level, testis histology examination and testosterone receptors by using cytoimmunochemistry techniques. Samples of blood and both testes were collected from 24 local dogs aged between 2-3 years and weighted 18-22 kg. This study carried out at 2015, divided into four seasons. No differences in testosterone level were observed between seasons. However, histological examinations were characterized by significant (P&lt;0.01) changes during seasons in tubular diameters, germinal thickness and tubular area. Cytoimmunochemistry investigation showed differences between seasons also, there was a distributions of testosterone hormone receptors in the Leydig cells, Sertoli cells and in germinal epithelium during spring and autumn, at the same time the winter season showed distribution of testosterone hormone receptors in Leydig and Sertoli cells only. The summer season characterize by diffuse of receptors in Leydig cells only. In conclusion there was a significant effect of season on testis of dog in Iraq, the summer season was the lowest in reproductive activity while the spring and autumn season was the highest of reproductive activity of dog in Iraq.

Testicular growth and development in puberty.

To describe pubertal testicular growth in humans, changes in testicular cell populations that result in testicular growth, and the role of testosterone and gonadotrophins follicle-stimulating hormone (FSH) and luteinizing hormone (LH) in testicular growth. When human data were not available, studies in nonhuman primates and/or rodents were used as surrogates. Testicular growth in puberty follows a sigmoidal growth curve, with a large variation in timing of testicular growth and adult testicular volume. Testicular growth early in puberty is due to increase in Sertoli cell number and length of seminiferous tubules, whereas the largest and fastest growth results from the increase in the diameter of the seminiferous tubules first due to spermatogonial proliferation and then due to the expansion of meiotic and haploid germ cells. FSH stimulates Sertoli cell and spermatogonial proliferation, whereas LH/testosterone is mandatory to complete spermatogenesis. However, FSH and LH/testosterone work in synergy and are both needed for normal spermatogenesis. Testicular growth during puberty is rapid, and mostly due to germ cell expansion and growth in seminiferous tubule diameter triggered by androgens. Pre-treatment with FSH before the induction of puberty may improve the treatment of hypogonadotropic hypogonadism, but remains to be proven.

Critical role of testosterone in both sexes

Critical role of testosterone in both sexes