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There have been a lot of discussions concerning the relationship between testosterone serum levels in males and diabetes. Low testosterone is commonly associated with type 2 diabetes and metabolic syndrome. Testosterone therapy alters the body composition in a metabolically favorable manner. In this article we shed some light on the bidirectional relation between hypotestosteronemia and diabetes discussing also the possible mechanisms and the benefit of treatment.
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PMID:Low testosterone and diabetes. 2385 7

Testosterone deficiency (TD) is a common clinical condition that causes sexual and non-sexual symptoms. Low serum concentrations of testosterone also predict significant health outcomes, such as diabetes, metabolic syndrome, and increased mortality. Treatment with testosterone therapy (TTh) effectively improves symptoms, and also has a positive impact on body composition and bone density. Since there is no serum testosterone value that reliably identifies men who will respond to treatment from those who will not, healthcare providers must exercise clinical judgment in making the diagnosis of TD. Multiple formulations of TTh are available, each with advantages and disadvantages. Overall, TTh is relatively safe but the risks, such as erythrocytosis, makes long-term monitoring mandatory. The evidence does not support concerns regarding cardiovascular and prostate cancer risks.
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PMID:The evaluation and management of testosterone deficiency: the new frontier in urology and men's health. 2399 11

Testosterone is important in the physiology of various organs and tissues. The serum testosterone concentration gradually declines as one of the processes of aging. Thus, the concept of late-onset hypogonadism has gained increasing attention in the last few years. Reported symptoms of late-onset hypogonadism are easily recognized and include diminished sexual desire and erectile quality, particularly in nocturnal erections, changes in mood with concomitant decreases in intellectual activity and spatial orientation, fatigue, depression and anger, a decrease in lean body mass with associated decreases in muscle volume and strength, a decrease in body hair and skin alterations, and decreased bone mineral density resulting in osteoporosis. Among these various symptoms, sexual dysfunction has been the most common and necessary to treat in the field of urology. It is well known that a low serum testosterone level is associated with erectile dysfunction and hypoactive sexual libido and that testosterone replacement treatment can improve these symptoms in patients with hypogonadism. Recently, in addition to sexual dysfunction, a close relationship between metabolic syndrome, characterized by central obesity, insulin resistance, dyslipidemia, and hypertension, and late-onset hypogonadism has been highlighted by several epidemiologic studies. Several randomized control trials have shown that testosterone replacement treatment significantly decreases insulin resistance in addition to its advantage for obesity. Furthermore, metabolic syndrome is one of the major risk factors for cardiovascular disease, and a low serum testosterone level is closely related to the development of atherosclerosis. Presently, it is speculated that a low serum testosterone level may increase the risk for cardiovascular disease. Thus, testosterone is a key molecule in men's health, especially that of elderly men.
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PMID:The Relationship between Testosterone Deficiency and Men's Health. 2404 7

We define dyslipemia as the abnormally elevated presence of lipids in the blood. The main ones are hypercholesterolemia (cholesterol over 240 mg/dl), hypertrigliceridemia (triglicerides level over 200 mg/dl) and hipo-alphalipoproteinemia (High density lipoproteins,also called HDL Cholesterol, below 40 mg/dl). The presence of excessive lipids contributes to arteriosclerosis and they are an independent cardiovascular risk factor. It may be primary, if they have genetic origin and they are not associated with other diseases, but in most cases they are secondary to other pathological entities such as diabetes, hypothyroidism, obesity and metabolic syndrome (MS). In our current society, sedentary lifestyle and unadequatelly hypercaloric diets are making obesity and MS prevalences grow, and their relation to dyslipemias has become tighter. Obesity is related with all the criteria for MS. But obesity is not at all synonymous of MS. On the one hand neither fat distribution is the same in all individualas nor confers the same risk. Accordingly, we know that abdominal localization of fat is related to higher intensity of insulin resistance (IR) and MS. On the other hand, it seems that certain components of MS are determined by genetic factors, since there are morbid obese persons that are metabolically healthy and other patients develop insulin resistance without obesity. So that, it seems that the excess in visceral adiposity in the presence of certain genetic factors would be the most related cause of the appearance of peripheral insulin resistance and diabetes mellitus, hyperlipidemia (increase of very low density pipoproteins (VLDL), decrease of highdensity lipoproteins (HDL) arterial hypertension, and hypogonadotropic hypogonadism, composing what we call metabolic syndrome. In this scenario, we urologists are being first-hand witnesses.On the one hand, and in relation with cardiovascular risk factors, we know that all of them, and independently,not only can produce erectile dysfunction due to endothelial dysfunction, but also it generally appears years before the cardiovascular event. On the other hand, and in relation to the hypogonadotropic hypogonadism of patients with MS, we urologists may contributein greatly to the detection of patients with MS whose only symptom is erectile dysfunction or diminished libido, but specially we may play a key role in the improvement of these patients, since it is known that testosterone replacement therapy has a major potential to diminish or stop the progression of MS or its cardiovascular effects. Testosterone treatment not only improves the lipid profile, hypertension, insulin resistance, or reduces the abdominal circumference, but also it may help to get a better adherence to diet and exercise, so contributing to change unhealthy lifestyle habits whch are the origin of the problem.
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PMID:[Patient with testosterone deficit syndrome and dyslipemia]. 2404 36

It is now known that BNP and NT-proBNP levels are decreasing with increased BMI, regardless of other metabolic syndrome (MS) constituents. Additionally, testosterone deficiency may intensify frequency of ventricular rhythm disorders in obese individuals by inhibition of the parasympathetic system. Determination of heart rhythm turbulence (HRT) is a useful, noninvasive method used for evaluation of equilibrium of the vegetative system. The aim of the study was to evaluate effect of testosterone therapy on HRT and NT-proBNP levels in MS patients. Eighty males were qualified for the study. They were divided into 3 groups: I (n=30), males with testosterone deficiency syndrome and metabolic syndrome (MS+TDS+); II (n=25), males with MS+TDS-; III (n=25), healthy males. The patients with MS+TDS+ received Omnadrem 250 in the form of intramuscular injections for 9 weeks. Laboratory tests and 24-h Holter ECG were taken twice before the therapy and directly after completion of the therapy. Males with MS+TDS+ more often presented irregular HRT parameters and were characterised by lower NT-proBNP levels compared to the healthy individuals. Testosterone replacement therapy caused improvement of HRT and had no significant effect on the NT-proBNP level. Testosterone replacement therapy and body weight reduction may significantly decrease negative consequences of MS and TDS.
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PMID:Testosterone therapy improves the heart rate turbulence without effect on NT-proBNP level in men with metabolic syndrome. 2406 90

Klinefelter syndrome (KS) (47, XXY) is the most abundant sex-chromosome disorder, and is a common cause of infertility and hypogonadism in men. Most men with KS go through life without knowing the diagnosis, as only 25% are diagnosed and only a few of these before puberty. Apart from hypogonadism and azoospermia, most men with KS suffer from some degree of learning disability and may have various kinds of psychiatric problems. The effects of long-term hypogonadism may be diffi cult to discern from the gene dose effect of the extra X-chromosome. Whatever the cause, alterations in body composition, with more fat and less muscle mass and diminished bone mineral mass, as well as increased risk of metabolic consequences, such as type 2 diabetes and the metabolic syndrome are all common in KS. These findings should be a concern as they are not simply laboratory findings; epidemiological studies in KS populations show an increased risk of both hospitalization and death from various diseases. Testosterone treatment should be offered to KS patients from early puberty, to secure a proper masculine development, nonetheless the evidence is weak or nonexisting, since no randomized controlled trials have ever been published. Here, we will review the current knowledge of hypogonadism in KS and the rationale for testosterone treatment and try to give our best recommendations for surveillance of this rather common, but often ignored, syndrome.
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PMID:The role of hypogonadism in Klinefelter syndrome. 2440 86

Testosterone levels are lower in men with metabolic syndrome and type 2 diabetes mellitus (T2DM) and also predict the onset of these adverse metabolic states. Body composition (body mass index, waist circumference) is an important mediator of this relationship. Sex hormone binding globulin is also inversely associated with insulin resistance and T2DM but the data regarding estrogen are inconsistent. Clinical models of androgen deficiency including Klinefelter's syndrome and androgen deprivation therapy in the treatment of advanced prostate cancer confirm the association between androgens and glucose status. Experimental manipulation of the insulin/glucose milieu and suppression of endogenous testicular function suggests the relationship between androgens and insulin sensitivity is bidirectional. Androgen therapy in men without diabetes is not able to differentiate the effect on insulin resistance from that on fat mass, in particular visceral adiposity. Similarly, several small clinical studies have examined the efficacy of exogenous testosterone in men with T2DM, however, the role of androgens, independent of body composition, in modifying insulin resistance is uncertain.
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PMID:Sex steroids and glucose metabolism. 2445 40

The Klinefelter syndrome (KS), with an incidence of 1 to 2 per 1000 male neonates, is one of the most frequent congenital chromosome disorders. The 47,XXY karyotype causes infertility, testosterone deficiency and a spectrum of further symptoms and comorbidities. In recent years, significant progress has been made in the elucidation of the pathophysiology and the treatment of the KS. It became clear that, to a large extent, the clinical picture is determined by gene dosage effects of the supernumerary X-chromosome. The origin of the extra X-chromosome from either the father or the mother influences behavioural features of patients with KS. The CAGn polymorphism of the androgen receptor, located on the X-chromosome, has a distinct impact on the KS phenotype. KS predisposes to the metabolic syndrome and its cardiovascular sequelae, contributing to the increased mortality of patients with KS. Neuroimaging studies have correlated anomalies in brain structures with psychosocial problems. The unexpected possibility to produce pregnancies and live birth with either ejaculated sperm--about 8% of KS men have a few sperm in semen--or with sperm extracted from individual tubules obtained by testicular biopsy can be considered a breakthrough. Testosterone substitution requires further optimisation in terms of when to initiate therapy and which preparations and dosages to use. Recently developed animal models help to further elucidation the genetic and pathophysiological basis and may lead to new therapeutic approaches to KS.
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PMID:New approaches to the Klinefelter syndrome. 2479 90

Testosterone deficiency (TD) afflicts approximately 30% of men ages 40-79 years, with an increase in prevalence strongly associated with aging and common medical conditions including obesity, diabetes, and hypertension. There appears to be a strong relationship between TD and metabolic syndrome, though the relationship is not certain to be causal. Several studies have suggested that repletion of testosterone in deficient men with these comorbidities may indeed reverse or delay their progression. While testosterone repletion has been largely thought of in a sexual realm, we discuss its potential role in general men's health concerns: metabolic, body composition, and its association with decreased all-cause mortality. Recent guidelines and studies have suggested variable prevalence statistics and expanded uses of testosterone repletion in certain populations with both biochemical and clinical signs of testosterone deficiency. Yet, this is not done without risk. A recent randomized placebo-controlled trial of testosterone repletion in elderly frail men with limited mobility has suggested potential negative cardiovascular risks in this older, sicker group of men. Two more recent retrospective studies of variable clinical design and interpretation suggest testosterone poses an increased cardiovascular risk in older men than 65 years and younger men with heart disease. This review examines these and other studies, with practical recommendations for the diagnosis of testosterone deficiency and repletion in middle aged and older men, including an analysis of treatment modalities and areas of concern and uncertainty.
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PMID:Testosterone deficiency: myth, facts, and controversy. 2497 31

Epidemiological studies have found that men with low or low normal endogenous testosterone are at an increased risk of mortality than those with higher levels. Cardiovascular disease accounts for the greater proportion of deaths in those with low testosterone. Cancer and respiratory deaths in some of the studies are also significantly more prevalent. Disease-specific studies have identified that there are higher mortality rates in men with cardiovascular, respiratory and renal diseases, type 2 diabetes and cancer with low testosterone. Obesity, metabolic syndrome, type 2 diabetes, cardiovascular disease and inflammatory disorders are all associated with an increased prevalence of testosterone deficiency. Two major questions that arise from these findings are (1) is testosterone deficiency directly involved in the pathogenesis of these conditions and/or a contributory factor impairing the body's natural defences or is it merely a biomarker of ill health and the severity of underlying disease process? (2) Does testosterone replacement therapy retard disease progression and ultimately enhance the clinical prognosis and survival? This review will discuss the current state of knowledge and discuss whether or not there are any answers to either of these questions. There is convincing evidence that low testosterone is a biomarker for disease severity and mortality. Testosterone deficiency is associated with adverse effects on certain cardiovascular risk factors that when combined could potentially promote atherosclerosis. The issue of whether or not testosterone replacement therapy improves outcomes is controversial. Two retrospective studies in men with diagnosed hypogonadism with or without type 2 diabetes have reported significantly improved survival.
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PMID:Testosterone and mortality. 2504 Nov 42


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