Acknowledgements MNTF was Visceral fat and testosterone levels by faat postgraduate scholarship and MG by a Career Development Fellowship both from the National Health and Medical Research Council Australia. R package version 1. Google Scholar Crossref.

Visceral fat and testosterone levels -

This may contribute in worsening metabolic abnormalities which in men with OSA exceed those expected on the basis of the degree of obesity and pattern of fat distribution. There is an increased turnover and production of glucocorticoids in obesity.

This increased glucocorticoid flux has been suggested to reflect an abnormal control of the hypothalamic pituitary adrenal axis in obese patients, which may determine an inhibition of the hypothalamic-pituitary gonadal axis.

This topic has been extensively reviewed in a recent review for more details, see Pasquali et al. In general, the biochemical diagnosis of androgen deficiency characterized by subphysiological serum levels of total testosterone remains a controversial issue due to the variety and relative diagnostic accuracy of assays usually available in most laboratories.

Total testosterone concentrations are measured by semi- automated radioimmunoassays, immunometric assays, or liquid chromatography tandem mass spectrometry. The widely used methods electro chemiluminescent immunoassay and liquid chromatography tandem mass spectrometry have been compared, showing no significant differences in values usually found in the male physiological range [ 56 ].

However, there is general agreement that total testosterone might not reflect the true androgen status. Total testosterone levels are influenced by SHBG whose levels can be altered by different conditions or diseases, such as aging, obesity, diabetes, hyper- and hypothyroidism, and acromegaly, as well as by certain medications [ 57 ].

In the presence of obesity SHBG may be variably reduced as a consequence of the coexistent insulin-resistant state [ 25 ], therefore the measurement of total testosterone may not be diagnostic in obese men, in whom clinicians should evaluate eventually the bioavailable or free testosterone fraction.

Since the measurement of free testosterone by radioimmunoassay has been criticized due to the lack of accuracy and linearity, free testosterone values, calculated from total testosterone, SHBG and albumin using the equilibrium —binding theory or empirical equations, should be preferably used [ 58 ].

However, normal ranges for free and bioavailable testosterone levels in healthy young men are still undefined and in addition they may vary among laboratories and assays used [ 57 , 59 ]. In addition, there is evidence that testosterone blood values may depend on some genetic background.

In fact, a recent meta-analysis of genome wide association studies revealed novel genetic variations within the SHBG gene and on the X chromosome which significantly affect circulating testosterone concentrations in men.

The clinical usefulness of these genetic variations remains to be elucidated since they may impact testosterone bioavailability and action at target tissue levels.

Interestingly, these data open a new prospective in the identification of men with low testosterone levels in whom genetic of SHBG as well as its circulating blood levels should be taken into account. Several longitudinal population studies analyzing the association between testosterone and the metabolic syndrome revealed that low baseline testosterone concentrations in middle-aged and older men are a strong predictor for the incidence of the metabolic syndrome and future development of type 2 diabetes [ 61 — 66 ].

Furthermore, the MMAS [ 61 ] and a Finish study conducted by Laaksonen and colleagues [ 64 ] demonstrated that the relationship between testosterone and future development of metabolic syndrome and diabetes was relatively independent of adiposity.

Similar findings were also reported by the Third National Health and Nutrition Survey NHANES III where adult men were analyzed [ 68 ]. This study showed that men in the lowest tertile of either free or bioavailable testosterone, but not total testosterone, are approximately four times more likely to develop diabetes compared with those in the third tertile after adjustment for adiposity, age, race and ethnicity.

To further reinforce this perspective, Muller and colleagues [ 69 ] showed that higher testosterone and SHBG levels in aging males were independently associated with a higher insulin sensitivity and a reduced risk of the metabolic syndrome, regardless of insulin levels and parameters of body composition, which suggests that normal androgen status may be protective against the development of the metabolic syndrome.

On the other hand, Laaksonen et al. The authors showed that men with the metabolic syndrome were 2. In addition, those developing the metabolic syndrome during the follow up had a three fold higher risk of becoming hypogonadic, while in those men who had the metabolic syndrome at both baseline and during the follow up had and continued to have a metabolic syndrome during the study, the relative risk was 5.

Several studies analyzing the impact of low testosterone levels on cardiovascular diseases, revealed that decreasing testosterone levels were associated with an increased incidence of atherosclerosis [ 70 ], stroke , or transient ischemic attacks [ 71 ] and with higher mortality rate, largely due to cardiovascular disease, particularly in aged men [ 67 , 72 , 73 ].

An inverse relationship between carotid artery intima-media thickness, an independent marker of future adverse events for cardiovascular disease, and testosterone levels has been reported in different populations including relative young or aged men [ 74 ], men with diabetes [ 75 ] and finally overweight-obese men with glucose intolerance [ 76 ].

This relationship was independent of age, BMI and other metabolic abnormalities [ 77 ]. An additional prospective study of men aged found a marked progression of the degree of carotid intima media thickness over a four-years follow-up in subjects characterized by the lowest testosterone values at baseline [ 78 ].

In a prospective population-based study, total and bioavailable testosterone deficiency in aged men was associated with increased risk of death over the following 20 years, independently of other risk factors and pre-existing health condition [ 79 ].

This association was also independent of the presence of metabolic syndrome, diabetes, and prevalent cardiovascular diseases. In case-specific analyses, low testosterone predicted increased risk of cardiovascular disease mortality but was not significantly related to cancer death. These data confirmed those of the European Prospective Investigation Into Cancer in Norfolk EPIC-Norfolk case-control study that revealed an inverse relationship between endogenous testosterone concentration at baseline and mortality for all causes [ 70 ].

The preferred way to improve testosterone levels in obese men should be life style intervention. In fact, although the data regarding the effect of weight loss on sex steroids in men have been conflicting, the majority of them have shown that this hormonal abnormality can be reversed by significant weight reduction.

However, weight reduction has been associated either with an increase [ 34 , 86 ] or no influence on SHBG blood concentrations [ 83 ], which indirectly suggests that the increased androgen levels obtained after weight loss may not be only the consequence of changes in hormone transport binding.

On the other hand, Niskanen and colleagues have also demonstrated that rapid weight loss with a very low calorie diet followed by successful weight maintenance for 12 months in abdominally obese men with the metabolic syndrome lead to a substantial increase in total and free testosterone as well as SHBG levels [ 87 ].

These findings are also supported by animal studies in which it was reported that a high calorie diet caused a decrease in serum testosterone levels together with significant weight gain [ 88 ], whereas hypocaloric dieting aimed at reversing excess body weight was able to improve serum testosterone levels to normal levels [ 89 ].

By contrast, it should be taken into consideration that negative studies on the impact of weight loss on both total and free testosterone levels have been published [ 90 , 91 ], which reinforce the need of large long term randomized control studies.

Testosterone replacement therapy administered to established hypogonadic patients has been proven to achieve beneficial effects on body composition by reducing the amount of visceral fat content and by increasing lean body mass, and improving most of the metabolic comorbidities such as insulin sensitivity and dyslipidemia [ 92 ].

On the other hand, studies conducted in men with prostate cancer, where androgen deprivation therapy was used, showed an increased accumulation of abdominal fat mass and an impairment of insulin sensitivity [ 93 ]. The rationale of testosterone effects have been explained by in vitro studies in culture cells where androgens proved to promote myogenic differentiation of multipotent mesenchymal stem cells and to inhibit their differentiation into the adipogenic lineage [ 94 , 95 ].

Exogenous testosterone administration as a treatment for obesity has been examined in two double-blind studies and a few case reports. Two decades ago, Marin and colleagues treated 23 and 17 middle-aged obese men without diabetes with moderate doses of transdermal preparations of testosterone for 8 and 9 months respectively.

Testosterone treatment reduced both visceral fat amount, evaluated by CT scan, and insulin resistance, measured by euglycemic glucose clamp [ 96 , 97 ]. Since then, several other studies have been performed mainly in aged men with late onset hypogonadism with low-normal testosterone levels.

Besides using different testosterone doses and treatment duration, these studies informally confirmed the effect of testosterone in reducing body fat mass and increasing lean body mass, whereas conflicting results on changes in visceral fat mass, insulin levels and insulin-resistance have been reported.

These discrepancies indicate that more accurate and selective population-based long-term studies are needed to clarify the potential benefit of testosterone treatment in obese men with low testosterone levels. In summary, several related mechanisms have been suggested to explain low testosterone in men with obesity.

Whether low sex steroid levels precede or are the consequence of obesity is still unknown; however, it is clear that both conditions are unsafe since low testosterone and obesity per se are associated with an increased risk of developing the metabolic syndrome and cardiovascular disease and with higher mortality rates.

There is still no consensus on how to treat obese men with low testosterone with life style intervention in addition or not to androgen supplementation. Short term replacement therapy with exogenous testosterone may be considered initially, although it cannot replace long term lifestyle measures including physical activity.

Doses and treatment periods should be different from established hypogonadic patients in whom well-known dosage regimes and lifelong therapy are needed.

Moreover, data regarding the chronic use of androgen supplementation in middle aged obese men in term of efficacy and safety are still missing.

Pathophysiological studies in obese subjects are needed to clarify the endocrine function of adipose tissue, that seems to have a dominant role in altering, either directly or indirectly, the hypothalamic pituitary gonadal activity, and therefore helping to find a more appropriate treatment for this condition.

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Weight loss and sex steroid metabolism in massively obese man. Stanik S, Dornfeld LP, Maxwell MH, Viosca SP, Korenman SG. Visceral fat releases free fatty acids FFA and other fat metabolites directly into the hepatic-portal system.

These then quickly accumulate in the liver and other organs causing it to store inappropriate amounts of fat and making it less sensitive to insulin. Consequently, an imbalance of your sex hormones can lead to greater deposition of visceral fat.

This, in turn, results in poorer insulin sensitivity. Given their different reproductive physiology, the exact relationship between hormonal imbalances, visceral fat and insulin sensitivity differs considerably between men and women.

Several studies suggest that, in men, low testosterone levels are associated with an increased amount of visceral fat. More specifically, rather than low absolute levels of testosterone, visceral fat deposition in men likely arises from low levels of testosterone relative to estrogen.

Check your Testosterone Level and Estrogen Production Traits for more information. In contrast to men, higher levels of testosterone and other androgens seem to be associated with greater amounts of visceral fat in women.

Again, it is likely to be a high level of testosterone relative to estrogens, rather than absolute levels of testosterone, that causes visceral fat deposition in women. In scientific terms, we sometimes describe this imbalance of having high levels of androgens and testosterone relative to estrogens as having a greater degree of androgenicity.

On this note, studies suggest that post-menopausal women are more likely to experience accumulation of visceral fat. As you may recall from the Estrogen Production blog , circulating levels of estrogen estradiol drop off dramatically during the menopause as the ovaries stop producing estrogen.

Given that testosterone and androgen production remains fairly stable during the same period, the ratio of testosterone to estrogen increases. This then leads to greater visceral fat deposition. Unfortunately, too much visceral fat can also upset further upset your balance of sex hormones.

In turn, this may lead to more visceral fat accumulation and further worsening of insulin sensitivity. One reason for this vicious cycle is that visceral fat acts as a metabolically active, endocrine organ — it secretes various hormones and other molecules that can alter the metabolism of sex hormones.

For example, in men, estrogen production largely takes place in peripheral tissues — including visceral fat. Visceral fat contains an enzyme called aromatase , which converts testosterone into estrogen. Men who carry more visceral fat are therefore likely to have greater aromatase activity, and consequently convert more testosterone into estrogen.

A qualified doctor having attained full GMC registration in , Haran also holds a first-class degree in Experimental Psychology MA Cantab from the University of Cambridge and an MSc in the philosophy of cognitive science from the University of Edinburgh.

Haran is a keen runner and has successfully completed a subhour marathon during his time at FitnessGenes. Create a FitnessGenes account to unlock your lifestyle-based reports for free, each with personalized insights and actions. No credit card details required. Login Get Started For Free.

What is visceral fat? In reality, we have three main different types of fat tissue also called adipose tissue , with excessive amounts of one type in particular, visceral fat, being linked to negative health outcomes: Subcutaneous fat This is the type of fat stored just beneath our skin.

Visceral fat Visceral fat sometimes called intra-abdominal fat is the type of fat tissue stored deep in your abdominal cavity, where it surrounds internal organs such as the liver, intestines and pancreas. Bone marrow fat We also store fat in our bone marrow.

KEY POINTS Our body has different types of fat tissue. Subcutaneous fat is just under our skin. Visceral fat visceral adipose tissue is deep in our abdomen and surrounds our internal organs. Visceral fat is worse for our health than subcutaneous fat.

Dr Haran Sivapalan A qualified doctor having attained full GMC registration in , Haran also holds a first-class degree in Experimental Psychology MA Cantab from the University of Cambridge and an MSc in the philosophy of cognitive science from the University of Edinburgh.

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