Visceral fat and testosterone levels

Visceral fat and testosterone levels weeks 1 to 8 subjects were instructed to replace all of their Chromium browser for secure browsing principal testostedone meals with a VLED formulation Optifast® Viscerall, Nestle, Australia fqt kcal ans day and two cups of low-starch vegetables. Compared to men completing the testossterone, non-completers Visceral fat and testosterone levels leveos less body weight and less fat mass at the end of the VLED phase of the study. Why Belly Fat is Resistant to Weight Loss Whether the obesity is the by-product of low testosterone levels, or vice versa, an insufficient amount of this male sex hormone can make it hard or even impossible to lose weight through regular exercise and a healthy diet alone. You can also search for this author in PubMed Google Scholar. Contrasting effects of testosterone and stanozolol on serum lipoprotein levels.

Visceral fat and testosterone levels -
It seems that long term exposure to high levels of testosterone is required to increase the visceral fat depot in young, nonobese female subjects. It is not likely that a state of hypoestrogenism after ovariectomy might partially explain our findings. Part of the administered testosterone is peripherally aromatized to estradiol.

In a study in which we investigated ovariectomized female to male transsexuals receiving similar testosterone dosages, serum estradiol levels were not different from levels in eugonadal women in their early follicular phase 12 and were similar to those in eugonadal men.

Thus, after ovariectomy, testosterone administration to our subjects still generated serum estradiol levels in a range comparable to levels in eugonadal women in the follicular phase.

Further, the association between weight gain and visceral fat accumulation points in the same direction after 1 yr of testosterone administration as after 3 yr of testosterone administration, indicating that ovariectomy did not lead to a change in this relationship.

A limitation of the present study is the fact that it was not possible to compose a control group of young women with the same degree of variation in weight over 3 yr of follow-up. To our knowledge no detailed long term studies have been performed investigating prospectively the changes in the visceral fat depot in young women.

However, cross-sectional studies in young women have shown that fat tissue is mainly located in the sc fat depots and that excess fat is preferentially stored sc, with a rather constant visceral fat depot 3 , 4 , We, therefore, compared our data with those obtained for quantification of sc and visceral fat areas in 34 Dutch women with a wide range in age and body mass index It appeared in our subjects that the increase in visceral fat area was larger and the change in sc fat area was smaller than expected on the basis of findings in the comparison group, although such a comparison with our study population should be performed with caution.

In an earlier study we found that 4-month administration of similar doses of testosterone to female to male transsexuals of comparable age did not increase fasting insulin levels significantly, but did lead to decreased insulin sensitivity This observation, combined with our present results, shows similarities with the findings in women with high endogenous testosterone levels.

The latter show both increased abdominal fat depots and insulin resistance. In the subjects of our study, nonobese, endocrine unremarkable, female subjects between the ages of 16—33 yr, the primary event leading to abdominal fat accumulation and insulin insensitivity was exogenous hyperandrogenism.

This observation might be relevant for determination of the primary event in women with a combination of hyperandrogenism, insulin resistance, and abdominal fat accumulation.

Some researchers believe that hyperinsulinemia is the primary event 7. Of note, however, is the fact that in our experiment testosterone levels were far above levels encountered in most spontaneous hyperandrogenic states in women.

These findings in women are dissimilar with some observations in men. Cross-sectional studies in men suggest an inverse association between testosterone levels and abdominal fat distribution Oral testosterone treatment of middle-aged obese men with low normal testosterone levels seemed to reduce visceral fat The oral administration might have been significant for the effects of the testosterone preparation, as in a study comparing the effects of oral anabolic steroids with those of parenteral testosterone treatment as used in our study , only the oral preparation had this effect, not the parenteral testosterone preparation Further, factors such as age or duration of testosterone exposure may determine the effect of testosterone on visceral fat.

The men in the above studies 16 , 17 were at least 40 yr of age or older, with a presumed exposure to their endogenous testosterone of some 25 yr. This study resolves some of the uncertainties with regard to the association between testosterone and visceral fat in women by demonstrating that long term testosterone exposure increases visceral fat in young, nonobese female subjects.

We thank T. Schweigmann from the Department of Diagnostic Radiology of the Hospital Vrije Universiteit for MR acquisition, and F. Hoogenraad and H. van de Mortel from the Department of Biomedical Engineering of the Hospital Vrije Universiteit for their technical assistance with the image analysis.

We also thank J. Welleweerd from the Department of Radiotherapy of the University Hospital Utrecht for the opportunity to redigitalize MR information. This work was supported by The Netherlands Organization for Scientific Research Grant — Presented in part at the Sixth European Congress on Obesity, May 31 through June 3, , Copenhagen, Denmark.

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The hormonal and surgical sex reassignment of gender dysphoric patients. Arch Sex Behav. Elbers JMH, Haumann G, Asscheman H, Seidell JC, Gooren LJG.

Lovejoy JC , Bray GA , Bourgeois MO , et al. J Clin Endocrinol Metab. Spinder T , Spijkstra JJ , Gooren LJG , Hompes PGA , van Kessel H. Seidell JC , Oosterlee A , Deurenberg P , Hautvast JGAJ , Ruijs JHJ.

Eur J Clin Nutr. Polderman KH , Gooren LJG , Asscheman H , Bakker A , Heine RJ. Seidell JC , Björntorp P , Sjöström L , Kvist H , Sannerstedt R. Mårin P , Holmång S , Jönsson L , et al. Lovejoy JC , Bray GA , Greeson CS , et al. Oxford University Press is a department of the University of Oxford.

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Journal Article. Long-Term Testosterone Administration Increases Visceral Fat in Female to Male Transsexuals 1. Elbers , Jolanda M.

Oxford Academic. Henk Asscheman. Jacob C. Jos A. Louis J. Revision received:. PDF Split View Views. Cite Cite Jolanda M. Select Format Select format. ris Mendeley, Papers, Zotero. enw EndNote. bibtex BibTex.

txt Medlars, RefWorks Download citation. Permissions Icon Permissions. Table 1. Before treatment. Changes from baseline a. Baseline b. After 1 yr. After 3 yr. Body Wt kg b Baseline values are the mean ± sd. Open in new tab. Figure 1. Open in new tab Download slide. Figure 2.

Search ADS. Google Scholar PubMed. OpenURL Placeholder Text. Subcutaneous and visceral fat distribution according to sex, age, and overweight, evaluated by computed tomography. Sex differences in the relation of visceral adipose tissue accumulation to total body fatness.

Google Scholar OpenURL Placeholder Text. On the paradox of insulin-induced hyperandrogenism in insulin-resistant states. Standards of care.

Google Scholar Crossref. Exogenous androgens influence body composition and regional body fat distribution in obese postmenopausal women—a clinical research center study. Effects of long-term testosterone administration on gonadotropin secretion in agonadal female to male transsexuals compared with hypogonadal and normal women.

In another prospective study of older men, DHT or human chorionic gonadotropin administration did not significantly affect high-sensitivity C-reactive protein, soluble vascular cell adhesion molecule—1, or soluble intracellular adhesion molecule levels [ 67 ].

In cross-sectional epidemiological studies, serum testosterone levels have been positively correlated with tissue plasminogen activator and inversely correlated with PAI-1, fibrinogen, α-2 anti-plasmin, and factor VIIc levels [ 57 , 68 ].

Men with hypogonadism have low baseline fibrinolytic activity, which is accounted for by an increased synthesis of PAI There have been isolated case reports of stroke and deep-vein thrombosis in young men who were taking large amounts of androgenic steroids.

However, the results of the intervention studies with testosterone replacement have been less clear; testosterone administration increases the circulating levels of both pro- and anticoagulant factors. Whether a variation of testosterone levels within the normal range is associated with a risk of coronary artery disease remains unclear.

Of the 30 studies reviewed by Alexandersen et al. Prospective population-based studies [ 2 ] have not revealed an association between total testosterone levels and cardiovascular mortality.

Male survivors of myocardial infarction have lower testosterone levels and higher estradiol : testosterone ratios than age-matched control subjects. Phillips et al. Although the study by English et al. Thus, cohort and cross-sectional studies have suggested a neutral or favorable effect of testosterone on coronary heart disease in men [ 2 ].

A number of studies conducted in the s reported that testosterone administration improved angina pectoris in men with coronary artery disease [ 71 , 72 ]. Testosterone infusion acutely improves coronary blood flow in dogs and humans [ 73 , 74 ]. Testosterone relaxes coronary arteries by opening the large-conductance, calcium-activated potassium channel [ 75 ].

In a LDL receptor—deficient mouse model of atherosclerosis [ 68 ], orchiectomy was associated with the accelerated formation of early atherosclerotic lesions in the aorta. Testosterone supplementation retards the progression of atherosclerotic lesion, an effect that is blocked by the concomitant administration of an aromatase inhibitor [ 76 ].

Testosterone effects on atherosclerosis progression were independent of plasma lipids. These data provide compelling evidence that testosterone, through its conversion to estradiol, can retard the progression of atherosclerosis in this animal model.

Prospective studies are needed extend these observations to humans, assess the effects of testosterone on atherosclerosis progression in older men, and determine whether testosterone effects on atherosclerosis are mediated through its conversion to estradiol.

Testosterone supplementation decreases the fat mass in men by inhibiting adipogenic differentiation. Replacement doses of testosterone are associated with a small reduction or no change in plasma HDL cholesterol concentrations. Epidemiological studies have reported an inverse relationship between serum free testosterone concentrations and visceral fat mass and the risk of heart disease and type 2 diabetes mellitus.

The hypothesis that physiological testosterone replacement might improve insulin sensitivity and retard atherosclerosis in HIV-infected men with fat redistribution syndrome should be tested in prospective, placebo-controlled, clinical trials.

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Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents Abstract.

High Prevalence of Low Testosterone Concentrations in Hiv-Infected Men. Effects of Spontaneous and Experimentally Induced Androgen Deficiency on Fat Mass and Distribution. Effects of Testosterone Supplementation on Whole-Body and Regional Fat Distribution.

Dose-Dependent Effects of Testosterone on Whole-Body and Regional Fat Distribution in Healthy Young Men. Testosterone Effects on Fat Metabolism.

Testosterone Effects on Plasma Lipids. Testosterone and Insulin Sensitivity. Effects of Testosterone Supplementation on Inflammation Markers.

Testosterone Effects on Coagulation and Fibrinolytic Factors. Association of Serum Testosterone Levels and Heart Disease.

Intervention Studies of The Effects of Testosterone Supplementation on Coronary Artery Disease. Testosterone Retards Atherosclerosis Progression in an Animal Model of Atherosclerosis.

Journal Article. Effects of Testosterone Administration on Fat Distribution, Insulin Sensitivity, and Atherosclerosis Progression. Shalender Bhasin Shalender Bhasin. Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R.

Drew University of Medicine Science, University of California—Los Angeles School of Medicine. Reprints or correspondence: Dr. Shalender Bhasin, Div. of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine Science, UCLA School of Medicine, Los Angeles, CA sbhasin ucla.

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Abstract In spite of the widespread belief that testosterone supplementation increases the risk of atherosclerotic heart disease, evidence to support this premise is lacking. Table 1.

Open in new tab Download slide. Table 2. Effects of testosterone supplementation in older men in 7 studies. Google Scholar Crossref. Search ADS. The relationship of natural androgens to coronary heart disease in males: a review.

High-density-lipoprotein cholesterol in bodybuilders v powerlifters: negative effects of androgen use. Contrasting effects of testosterone and stanozolol on serum lipoprotein levels. Lipemic and lipoproteinemic effects of natural and synthetic androgens in humans.

Reduction in high density lipoproteins by anabolic steroid stanozolol therapy for postmenopausal osteoporosis. The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men.

Testosterone replacement in older hypogonadal men: a month randomized controlled trial. Effect of testosterone treatment on body composition and muscle strength in men over 65 years of age. Google Scholar PubMed.

OpenURL Placeholder Text. Effect of testosterone treatment on bone mineral density in men over 65 years of age. Visceral fat accumulation in men is positively associated with insulin, glucose, and C-peptide levels, but negatively with testosterone levels.

Endogenous sex hormones and cardiovascular disease in men: a prospective population-based study. The effects of testosterone treatment on body composition and metabolism in middle-aged obese men.

Google Scholar OpenURL Placeholder Text. Androgen treatment of middle-aged, obese men: effects on metabolism, muscle and adipose tissues. Serum dihydrotestosterone and testosterone levels in human immunodeficiency virus-infected men with and without weight loss.

Serum hormones in men with human immunodeficiency virus-associated wasting. Changes in the hypothalamic pituitary-gonadal axis in human immunodeficiency virus-infected hypogonadal men.

Changes in systematic gonadal and adrenal steroids in asymptomatic human immunodeficiency virus-infected men: relationship with CD4 counts. Evidence of endocrine involvement early in the course of human immunodeficiency virus infection. Pituitary-testicular axin during HIV infection: a prospective study [abstract 9].

Programs and abstracts of the 18th annual meeting of the American Society of Andrology Tampa. Prevalence of hypogonadism among men with weight loss related to human immunodeficiency virus infection who were receiving highly active antiretroviral therapy.

Substantial prevalence of low anabolic hormone levels in COPD patients undergoing rehabilitation. Pharmacokinetics of a transdermal testosterone system in men with end stage renal disease receiving maintenance hemodialysis and healthy hypogonadal men.

In vivo pretreatment with human chorionic gonadotropin fails to reverse the dysfunction of isolated Leydig cells from chronically uremic rats. Pulsatility of luteinizing hormone in men with chronic renal failure: abnormal rather than absent.

Regulation of hypothalamic gonadotropin-releasing hormone secretion in experimental uremia: in vitro studies. Evidence for attenuation of hypothalamic gonadotropin releasing hormone GnRH impulse strength with preservation of GnRH pulse frequency in men with chronic renal failure.

Abnormal response of luteinizing hormone, follicle stimulating hormone and testosterone to luteinizing hormone releasing hormone in chronic renal failure.

Discordant elevation of the common alpha subunit of the pituitary glycoprotein hormones compared to beta subunits in the serum of uremic patients. Visceral fat accumulation in men is positively associated with insulin, glucose and C-peptide levels, but negatively with testosterone levels.

Using quantitative CT to assess adipose distribution in adult men with acquired hypogonadism. Testosterone deficiency in young men: marked alterations in whole body protein kinetics, strength and adiposity.

A replacement dose of testosterone increases fat-free mass and muscle size in hypogonadal men. Increase in bone density and lean body mass during testosterone administration in men with acquired hypogonadism.

Effects of testosterone replacement on muscle mass and muscle protein synthesis in hypogonadal men—a clinical research center study. Sublingual testosterone replacement improves muscle mass and strength, decreases bone resorption, and increases bone formation markers in hypogonadal men—a clinical research center study.

Transdermal testosterone gel improves sexual function, mood, muscle strength, and body composition parameters in hypogonadal men. Testosterone Gel Study Group. Effects of testosterone replacement therapy in old hypogonadal males: a preliminary study.

Testosterone administration to elderly men increases skeletal muscle strength and protein synthesis. Effects of transdermal testosterone on bone and muscle in older men with low bioavailable testosterone levels. Assimilation and mobilization of triglycerides in subcutaneous abdominal and femoral adipose tissue in vivo in men: effects of androgens.

Nandrolone, a nortestosterone, enhances insulin-independent glucose uptake in normal men. Testosterone increases lipolysis and the number of beta-adrenoceptors in male rat adipocytes.

Intramuscular testosterone esters and plasma lipids in hypogonadal men: a meta-analysis. Low levels of sex hormone-binding globulin and testosterone are associated with smaller, denser low density lipoprotein in normoglycemic men. Lower androgenicity is associated with higher plasma levels of prothrombotic factors irrespective of age, obesity, body fat distribution, and related metabolic parameters in men.

Effects of testosterone replacement and resistance exercise on muscle strength, and body composition in human immunodeficiency virus-infected men with weight loss and low testosterone levels. Effects of testosterone replacement with a non-genital, transdermal system, Androderm, in human immunodeficiency virus-infected men with low testosterone levels.

The use of a transscrotal testosterone delivery system in the treatment of patients with weight loss related to human immunodeficiency virus infection. Effects of androgen administration in men with the AIDS wasting syndrome: a randomized, double-blind, placebo-controlled trial. Hormonal status and NIDDM in the European and Melanesian populations of New Caledonia: a case-control study.

The CALedonia DIAbetes Mellitus CALDIA Study Group. Low levels of sex hormone-binding globulin and testosterone predict the development of non-insulin-dependent diabetes mellitus in men. MRFIT Research Group.

BMC Medicine volume 14 Visceral fat and testosterone levels, Article number: Cite this article. Metrics details. Whether testosterone treatment Viscera, benefits on body composition Visceral fat and testosterone levels and above caloric restriction in Viscera, is unknown. We hypothesised that testosterone treatment augments diet-induced loss of fat mass and prevents loss of muscle mass. We conducted a randomised double-blind, parallel, placebo controlled trial at a tertiary referral centre. The main outcome measures were the between-group difference in fat and lean mass by dual-energy X-ray absorptiometry, and visceral fat area computed tomography. Visceral fat and testosterone levels Vjsceral of the widespread belief that testosterone Visceral fat and testosterone levels increases the risk of atherosclerotic heart disease, evidence to Visxeral this Gastric health is lacking. Although supraphysiological Visecral of testosterone, such as ttestosterone used by athletes ffat recreational body builders, decrease plasma high-density lipoprotein HDL cholesterol concentrations, replacement doses of testosterone have had only a modest or no effect on plasma HDL in placebo-controlled trials. In epidemiological studies, serum total and free testosterone concentrations have been inversely correlated with intra-abdominal fat mass, risk of coronary artery disease, and type 2 diabetes mellitus. Testosterone administration to middle-aged men is associated with decreased visceral fat and glucose concentrations and increased insulin sensitivity. Testosterone infusion increases coronary blood flow.

Jolanda M. Elbers, Henk Stress reduction catechins, Jacob C. Seidell, Teztosterone A.

Megens, Louis J. The amount of intraabdominal visceral fat is an important determinant of disturbances in lipid and glucose metabolism. Cross-sectional studies in women have found associations between high androgen levels testosterohe visceral fat accumulation.

The causal relation between these phenomena is unknown. We, therefore, studied prospectively the effect of testosterone administration on body fat distribution in 10 young, leveels, female Visceral fat and testosterone levels male transsexuals undergoing levdls reassignment.

Before, Viscersl 1 yr, and after 3 yr of testosterone administration, magnetic fa images were obtained at the level of adn Visceral fat and testosterone levels, hip, and thigh Snake envenomation diagnosis methods quantify both sc Immune-boosting antioxidant rich foods visceral fat depots.

Testosteroone 1 yr of testosterone administration, Visceral fat and testosterone levels fat depots at all festosterone showed significant testosteeone compared legels baseline measurements.

The mean Beauty-from-within Supplement fat area Weight loss benefits not change significantly, but subjects who gained weight in the first year after testosterone administration testostdrone an increase Viscdral visceral fat.

The increase in visceral fat was most gat in those subjects who had gained weight. We conclude that long term testosterone Viscegal in tstosterone, nonobese, female subjects increases the amount Effective natural fat burner visceral fat.

In addition, an increase in weight in this hyperandrogenic state leads to a preferential storage of testtosterone in Herbal medicine for allergies visceral depot. Particularly, testosterohe increased amount of intraabdominal or visceral fat is testostegone with insulin resistance and an atherogenic lipid profile 12.

Regional fat distribution differs between men and women and Viscearl, therefore, be regarded as a secondary sex characteristic. Subcutaneous Viscegal depots Vegan diet recipes hips and Visceral fat and testosterone levels are testowterone typically female, whereas fst fat in men is fta stored in testosgerone abdominal regions 3.

After tesosterone for the Visceral fat and testosterone levels body fat mass, men have, on the average, more visceral fat than women Visceral fat and testosterone levels.

This sex difference suggests a potential role for sex steroid hormones in determining the site of fat deposition. The association of teetosterone testosterone levels with insulin resistance and an abdominal fat distribution in teststerone has led to different, testosterlne interpretations.

According to Hydrating night creams investigators, the underlying factor is Glucose metabolism rate, which leads to an increase in ovarian testosterone Carbohydrate and blood sugar levels 7.

Others argue that hyperandrogenicity Visceral fat and testosterone levels the primary event leading to both accumulation amd visceral fat and hyperinsulinemia 8. In lveels present study, we investigated prospectively the effect of long Relaxation exercises for anxiety testosterone administration on body Visxeral distribution in young, Viaceral, female to male transsexuals undergoing sex reassignment to a male Resistance training exercises following a standardized regimen 9.

This Viscsral us to study the effect of exogenous hyperandrogenicity on the Visveral of body fat by quantification of both sc and visceral fa depots in female subjects.

They were healthy, as assessed by their medical histories, physical leve,s, and laboratory measurements. They were studied before, Viscefal 1 yr, and after, on the restosterone, 3.

Gestosterone were treated tesfosterone mg testosterone esters Sustanon Mental health supplements for athletes, Organon, Oss, The Netherlands testostetone 2 weeks, im, until they were ovariectomized as part of the cross-sex treatment after, Viscearl the average, 1.

After ovariectomy, they continued testosterone lfvels with testosterobe injections of Testosteronne testosterone esters every 3 lfvels.

The study was approved by the ethical testosterohe board of yestosterone Hospital Vrije Universiteit, and all subjects provided informed consent. Body weight was measured testsoterone the legels 0.

Magnetic resonance MR imaging was testosteroe on a whole body Visceral fat and testosterone levels with a magnetic field strength Visceral fat and testosterone levels 0.

An inversion Visceral fat and testosterone levels pulse Visceal was used with a Healthy weight management time of ms, an echo time of 24 ms, and an Website speed optimization tips time of ms.

Leevels slice thickness testostdrone 10 mm, and the field of view was or mm. Transverse MR images were obtained at the level of the abdomen lower edge of the umbilicuslevsls hip upper margin of the great trochanterand the Viscera, just below the gluteal fold.

Three images were taken simultaneously at each body region: yestosterone image at the level of the marker, one above, and Timed eating protocol below this xnd, with a gap Herbal fat burner the images of 0.

In all subjects, testosgerone same anatomical markers and imaging parameters were used far repeated MR acquisition.

Quantification of sc and visceral Visceral fat and testosterone levels areas was performed using ad image-analyzing computer program developed by our Fzt of Biomedical Engineering 10based on a seed-growing procedure.

After a seed point is placed in a fat depot, this fat depot can be circumscribed by selection of a pixel intensity range. The intensity range is selected for each image separately according to the pixel intensity histogram. The area of the circumscribed fat depot is quantified by converting the number of pixels to square centimeters.

Muscle area was calculated from subtracting the areas of sc fat, bone, and connective tissue from the total area on the image below the marker at thigh level. To reduce variability, image analysis was performed by one observer, and the average fat area of three images per level was used in the statistical analysis.

Coefficients of variation for intraobserver variability in sc fat area measurements were 2. Due to a technical error, the digital MR information of four subjects for one measurement occasion was lost.

The original MR information on film was available and was redigitalized LumiscanLumisys, Sunnyvale, CA to quantify the fat depots. To study the variability introduced by the digitalization step, MR data for all subjects were also analyzed using this procedure.

No statistical difference was observed between the two measurements, and coefficients of variation appeared to be in the same range, i. Before and after 1 yr of testosterone administration, blood samples were obtained after an overnight fast. Standardized RIAs were used to measure serum levels of testosterone Coat-A-Count, Diagnostic Products Corp.

Sex hormone-binding globulin was measured using an immunoradiometric assay Orion Diagnostica, Espoo, Finland. Variables and changes in variables during treatment did not differ statistically from a normal distribution. Because of the small study population, the paired Wilcoxon signed rank test was used to test the effect of 1 yr and 3 yr testosterone treatments vs.

baseline values for the variables studied. The Spearman rank correlation test was used to study correlations between variables. After testosterone administration, serum testosterone increased from 1. Mean body weight had not changed significantly after 1 yr of treatment, and the increase in weight of 2.

Baseline and changes in body weight, fat area, and muscle area measurements during testosterone administration in 10 young nonobese female subjects. After 1 yr of testosterone administration, sc fat area measurements had decreased significantly at all levels measured, whereas the mean visceral fat area had not changed Table 1.

Compared to baseline, the area measurements after 3 yr of treatment showed small nonsignificant reductions in sc fat. A graphic presentation of the relative changes, expressed as percentage from baseline, after 1 yr, and after 3 yr of testosterone administration, is given in Fig.

Relative changes in body weight were strongly correlated with relative changes in visceral fat and sc fat at the abdominal level Fig. After both 1 and 3 yr of testosterone administration, the relative changes in visceral fat were greater than those in sc abdominal fat. Relative changes, expressed as percent change from baseline, in visceral and sc fat depots after 1 and 3 yr of testosterone administration in 10 female subjects.

visc, Visceral fat; sc abd, sc abdominal fat; hip, sc hip fat; thigh, sc thigh fat. Data are the mean ± sd. Relation between relative percent changes in body weight x -axis and relative percent changes in visceral fat areas solid circles and sc abdominal fat areas sc abd fat; open squares ; y -axis after 1 yr left graphic and after 3 yr right graphic of testosterone administration in 10 female subjects.

The anabolic effect of testosterone on muscle mass was reflected by an increase of Muscle area remained at this level after 3 yr of treatment, with an increase of The present study shows that long term testosterone administration to young, nonobese female subjects induced a redistribution of fat depots, with a preferential accumulation of visceral fat if weight gain occurred.

A shift from a typical female fat distribution to a more male type of body fat distribution was observed. After 1 yr, a relative redistribution of body fat had begun; at that time the visceral fat area had not yet increased significantly, but significant reductions were seen in the sc fat depots.

Fat area measurements on MR images obtained after 3 yr of testosterone administration showed an absolute increase in visceral fat, whereas sc fat depots were reduced, but were no longer significantly different from baseline.

In a study by Lovejoy et al. In this study, an absolute increase in visceral abdominal fat and a loss of sc fat at the levels of abdomen and thigh were observed after 9 months of administration of nandrolone decanoate, an anabolic steroid with weak androgenic activity.

The visceral fat depot had increased despite a weight reduction. In the present study, we did not observe an absolute increase in mean visceral fat after 1 yr of testosterone administration.

However, a strong positive correlation was present between changes in body weight and changes in the visceral fat area. Also, for the sc fat depots, there was a positive correlation with changes in body weight after 1 yr, but all subjects lost sc fat regardless of increases in body weight.

Thus, weight gain resulted in a preferential accumulation of fat in the visceral depot in hyperandrogenic female subjects. After 3 yr of treatment, an absolute increase in mean visceral fat was observed, and relative changes in this fat depot were larger than those in the sc abdominal fat depot.

It seems that long term exposure to high levels of testosterone is required to increase the visceral fat depot in young, nonobese female subjects. It is not likely that a state of hypoestrogenism after ovariectomy might partially explain our findings.

Part of the administered testosterone is peripherally aromatized to estradiol. In a study in which we investigated ovariectomized female to male transsexuals receiving similar testosterone dosages, serum estradiol levels were not different from levels in eugonadal women in their early follicular phase 12 and were similar to those in eugonadal men.

Thus, after ovariectomy, testosterone administration to our subjects still generated serum estradiol levels in a range comparable to levels in eugonadal women in the follicular phase.

Further, the association between weight gain and visceral fat accumulation points in the same direction after 1 yr of testosterone administration as after 3 yr of testosterone administration, indicating that ovariectomy did not lead to a change in this relationship.

A limitation of the present study is the fact that it was not possible to compose a control group of young women with the same degree of variation in weight over 3 yr of follow-up. To our knowledge no detailed long term studies have been performed investigating prospectively the changes in the visceral fat depot in young women.

However, cross-sectional studies in young women have shown that fat tissue is mainly located in the sc fat depots and that excess fat is preferentially stored sc, with a rather constant visceral fat depot 34 We, therefore, compared our data with those obtained for quantification of sc and visceral fat areas in 34 Dutch women with a wide range in age and body mass index It appeared in our subjects that the increase in visceral fat area was larger and the change in sc fat area was smaller than expected on the basis of findings in the comparison group, although such a comparison with our study population should be performed with caution.

In an earlier study we found that 4-month administration of similar doses of testosterone to female to male transsexuals of comparable age did not increase fasting insulin levels significantly, but did lead to decreased insulin sensitivity This observation, combined with our present results, shows similarities with the findings in women with high endogenous testosterone levels.

The latter show both increased abdominal fat depots and insulin resistance. In the subjects of our study, nonobese, endocrine unremarkable, female subjects between the ages of 16—33 yr, the primary event leading to abdominal fat accumulation and insulin insensitivity was exogenous hyperandrogenism.

This observation might be relevant for determination of the primary event in women with a combination of hyperandrogenism, insulin resistance, and abdominal fat accumulation.

Some researchers believe that hyperinsulinemia is the primary event 7. Of note, however, is the fact that in our experiment testosterone levels were far above levels encountered in most spontaneous hyperandrogenic states in women.

These findings in women are dissimilar with some observations in men.
: Visceral fat and testosterone levels

The Vicious Cycle of Low Testosterone and Weight Gain

Simply measure the waist to identify if there is a higher probability of excess visceral fat. In men, a waist measurement over 40 inches and in women, a waist measurement over 35 indicates an unhealthy accumulation of visceral fat and an increased risk of health problems.

Since lifestyle behaviors cause excess accumulation of visceral fat, modifying these behaviors help reduce it and associated disease risks.

Belly fat responds more efficiently to diet and exercise than subcutaneous fat does. To reduce visceral fat and potentially increase lean muscle mass, add 30 minutes of moderate physical activity to your daily routine on most days of the week. Moderate exercise can include aerobic activity such as walking and strength training with weights.

Combining a more balanced diet with a regular exercise routine can accelerate the loss of belly fat and improve other cardiometabolic risk factors. Adding more whole fruits and vegetables and minimizing sugar intake from processed foods are effective diet modifications for reducing dangerous fat around the organs.

Additionally, quitting smoking, getting more than 5 hours of sleep per night, and managing mental stress have all been proven to reduce the accumulation of belly fat in men. Pharmacy Practice Affordable Medicines Biosimilars Compliance Compounding Drug Approvals.

COVID Dermatology Diabetes Gastroenterology Hematology. mRNA Technology Neurology Oncology Ophthalmology Orthopedics. Featured Issue Featured Supplements. Chronic inflammation in the body can lead to body stiffness, muscle pain, sleep disorders, and persistent fatigue.

Inflammation also contributes to the development of obesity and many of its related conditions such type 2 diabetes, heart disease, and even cancer.

If you suspect that low testosterone is causing you to gain belly fat, take steps now to reduce your symptoms and protect your long-term health. Testosterone replacement therapy TRT can help restore your testosterone levels and boost weight loss.

Schedule a consultation to check your testosterone levels so we can determine the right TRT treatment plan for you. Research shows a strong connection between hormone levels and weight gain. Low testosterone levels can frequently lead to unexpected weight gain, particularly around the midsection.

This type of weight gain includes an accumulation of both subcutaneous and visceral fat. Subcutaneous fat is the soft, pliable fat layer that is found just beneath the skin.

Visceral fat is found deep within the abdominal walls around the internal organs, and within the omentum, an apron-like flap of tissue under the belly muscles that blankets the intestines. As the omentum fills with fat, it becomes harder and thicker, slowing the secretion of adiponectin.

This chemical reduces stress and inflammation, and helps regulate the hunger-controlling hormone, leptin. Higher stress levels and lower hunger regulation can contribute to overeating, adding to the overall weight gain caused by low testosterone.

Break the cycle of weight gain and low testosterone by incorporating TRT into a weight loss plan. Reducing dangerous visceral fat through weight loss is critical to your overall health. Unlike subcutaneous fat, which is relatively harmless, visceral fat cells are biologically active and produce higher amounts of toxic substances and other chemicals.

Many of these chemicals are linked to diseases that afflict older men. Visceral fat secretes cytokines, which boost the likelihood of heart disease.

These chemicals also make the body less sensitive to insulin, increasing the risk of type 2 diabetes. They also produce a precursor to angiotensin, a protein that constricts blood vessels, causing blood pressure to rise. Additionally, reduced adiponectin caused by visceral fat in the omentum contributes to high cholesterol and conditions associated with coronary artery heart disease.

Alarmingly, a new study has also found a link between lower body visceral fat and aggressive prostate cancer. In the average man, a circumference of more than 40 inches at the belly button indicates an unhealthy buildup of visceral fat in the omentum.

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Scottsdale E Via Linda Suite H Arizona Tel: Mesa S. Higley Suite Arizona Tel: BOOK NOW. The Critical Role of Testosterone Testosterone plays a critical role in your overall health, with studies suggesting that it protects you from a wide range of diseases including diabetes, heart-related problems, hypertension, cancer, atherosclerosis, and even obesity.

Causes of Dropping Testosterone Levels Around middle-age, your testosterone levels begin a steady decline, which predisposes you to belly fat particularly the obesity-related visceral fat found in the intra-abdominal organs , metabolic syndrome, hair loss, fatigue and low energy levels, and sometimes even depression and irritability.

Why Belly Fat is Resistant to Weight Loss Whether the obesity is the by-product of low testosterone levels, or vice versa, an insufficient amount of this male sex hormone can make it hard or even impossible to lose weight through regular exercise and a healthy diet alone.

Are You Dealing with Low Testosterone and Belly Fat?

Materials and methods

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Download references. Division of Endocrinology, S. Orsola-Malpighi Hospital, University Alma Mater Studiorum, Bologna, Italy.

Department of Medical and Surgical Science, Division of Endocrinology, University Alma Mater Studiorum, S. Orsola-Malpighi Hospital, Via Massarenti 9, Bologna, Italy.

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Pelusi, C. The Significance of Low Testosterone Levels in Obese Men. Curr Obes Rep 1 , — Download citation. Published : 19 August Issue Date : December Anyone you share the following link with will be able to read this content:.

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Download PDF. Abstract Low testosterone is frequently found in obese men over all ages. The Definition and Prevalence of Obesity and Metabolic Syndrome Chapter © Obesity management: sex-specific considerations Article Open access 08 February Use our pre-submission checklist Avoid common mistakes on your manuscript.

Introduction Obesity is a heterogeneous disorder related to environmental and genetic factors, whose incidence has dramatically increased. Low Testosterone Levels and Obesity: Evidence from Clinical and Epidemiological Studies In males, circulating testosterone blood levels have been shown to be influenced by body weight and composition.

Prevalence of Low Testosterone in Obesity The prevalence of low testosterone has been evaluated by several authors in a large population of middle-aged and older men reaching different numerical conclusions, depending on whether free or total testosterone was used to make the diagnosis, however all showed an increasing rate of hypotestosteronemia with increasing age, BMI and according to the presence of comorbidities, including diabetes and metabolic syndrome.

Pathophysiological Mechanisms of Low Testosterone in Obese Men Several pathophysiological mechanisms have been suggested as responsible for low testosterone in obese males. Mechanisms underline low testosterone in obesity. Full size image. How to Measure Testosterone Level in Obese Males 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.

The Meaning of Low Serum Testosterone Levels in Obese Males Low Testosterone as a Risk Factor for Metabolic Syndrome and Type 2 Diabetes 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 ].

Low Testosterone as a Risk Factor for Cardiovascular Disease and All Causes of Mortality 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 ].

Interventional Studies on Obese Men with Low Testosterone Levels: Effect of Weight Loss on Testosterone Levels The preferred way to improve testosterone levels in obese men should be life style intervention.

Intervention Studies on Obese Men with Low Testosterone Levels: Effect of Testosterone on Body Composition and Insulin-Resistance 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 ].

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Therefore, the benefit of energy restriction may be limited by loss of lean body mass [ 2 ]. In men, obesity is the single most important factor associated with low testosterone, overriding the effects of age and comorbidities [ 3 ].

This reduction in total testosterone levels is in part due to the obesity-associated lowering in sex hormone binding globulin SHBG.

However, especially with more marked obesity, free testosterone levels are also reduced due to adiposity-associated suppression of the gonadal axis at the hypothalamic level.

While the exact mechanisms are not fully understood, experimental studies in humans suggest that fat-derived adipokines and pro-inflammatory mediators may play a role in this central gonadal axis suppression [ 5 ]. In addition, preclinical evidence has shown that testosterone deficiency promotes adipose tissue accumulation but reduces myogenesis via an androgen receptor mediated pathway [ 6 ].

This bidirectional relationship between lowered testosterone and obesity is supported by clinical studies — weight loss increases testosterone proportionally to weight loss [ 7 ] and testosterone treatment reduces body fat [ 8 ]. Whether testosterone treatment augments fat loss additive to caloric restriction or prevents diet-associated loss of muscle mass is unknown.

We conducted a randomised clinical trial in obese men with low to low-normal total testosterone to test the hypothesis that, following diet-induced loss of fat mass, testosterone treatment will prevent fat regain but maintain lean mass.

This week, randomised, double-blind, placebo controlled trial RCT ClinicalTrials. gov NCT was conducted at a tertiary referral centre Austin Health, Melbourne, Australia. Each participant provided written informed consent prior to inclusion in the study.

The randomization sequence was generated by an independent statistician and implemented by the Austin Health clinical trials pharmacists. Participants, trial investigators and pharmacists were blinded to treatment allocation. Men received either mg testosterone undecanoate the standard ampoule strength in Australia or visually identical placebo in oily base by deep intramuscular buttock injection at weeks 0 and 6 manufacturer-recommended loading dose , and weekly thereafter at weeks 16, 26, 36 and Trough levels represent the therapeutic target immediately prior to the next dose and are lower than steady state targets e.

During weeks 1 to 8 subjects were instructed to replace all of their three principal daily meals with a VLED formulation Optifast® VLED, Nestle, Australia providing kcal per day and two cups of low-starch vegetables.

During weeks 9—10, subjects weaned their VLED and ordinary foods were gradually reintroduced. Subjects underwent weighing and individual counselling at every visit and were provided with written information to ensure dietary compliance. Subjects were advised to perform at least 30 minutes of moderate-intensity exercise each day and completed exercise questionnaires and accelerometer testing at weeks 0, 10 and 56 , with feedback given, to reinforce and encourage participation in exercise.

Subjects underwent long assessments at weeks 0, 10 and 56, including clinical assessment, physical function tests, accelerometer fitting worn 7 days , questionnaires, fasting morning blood tests, dual-energy X-ray absorptiometry DXA scan for body composition and abdominal computed tomography CT scans for visceral fat, and short assessments weeks 2, 4, 6, 16, 26, 36 and 46 for clinical assessment and to ensure dietary compliance.

Adherence to the diet was estimated by measuring body weight at each study visit, with individualised feedback given. All blood samples were drawn in the morning 8—10 am , in the fasted state. The Austin Health intra-assay coefficient of variability CV was 6.

SHBG was measured by electrochemiluminescence immunoassay Roche Cobas C , Austin intra-assay CV of 3. Free testosterone was calculated according to Vermeulen [ 13 ]. Metabolic parameters fasting lipid profile, HbA1c, fasting glucose and c-peptide levels and safety parameters haemoglobin, haematocrit and prostate-specific antigen PSA were measured at the study hospital with assay technology used for routine clinical care as described [ 14 ].

Visceral fat was quantified from single axial CT images at the L intervertebral disc space using SliceOmatic version 4. Step counts, physical and sedentary activity over 7 consecutive days were measured using the GT3x accelerometer ActiGraph, Pensacola, FL, USA.

Physical performance was assessed at weeks 0, 10 and 56 by four tests performed in duplicate and scored as the sum of the fastest times for each test in seconds: a 15 m rapid walking test, a 3 m up-and-go test, stair climbing and stair descending with a weighted vest. Handgrip was measured in the dominant hand using a hand-held medical dynamometer Jamar J1, Sammons Preston, Bolingbrook, IL, USA.

The primary outcome measure was the difference in fat mass between testosterone- and placebo-treated men at study end 56 weeks by DXA. Other main outcome measures included change in lean mass DXA , visceral abdominal tissue CT and body weight. Further outcome measures included anthropometric measurements, handgrip, physical function, physical activity and metabolic parameters.

The power analysis for this study was based on the effect of testosterone undecanoate on fat mass reduction of 5. Given that previous studies have shown that dieting leads to loss of fat mass, we expected that the placebo group would retain some degree of fat loss by the end of the study.

Repeated measures of main outcome continuous data were analysed using linear mixed models LMEs with random intercepts to account for within-individual correlation over time.

LME random effect and residual normality assumptions were checked and resulted in no noteworthy violations. An intention-to-treat analysis was also carried out where the outcome measures for study dropouts were returned to baseline.

Together with the LME analysis of the raw data, the LME return-to-baseline analysis provides protection against biases introduced due to missing data. Separate models with similar characteristics were used to assess other outcome data and safety variables. To compare repeated measurements of variables within groups between two time points, the t-test was used.

No adjustments were made for multiple comparisons on other variables. Comparison of baseline characteristics was based on the t-test or χ 2 test in case of categorical variables.

In the case of low numbers, the Fisher exact test was used. Data shown are mean standard deviation or median interquartile range , based on normality testing, using the Kolmogorov-Smirnov test with Lilliefors correction.

All analyses of means were complemented with Wilcoxon non-parametric tests. Similar results were found so the results were not reported. Analyses were conducted using R version 3. The wider variation and influence of few strong responders observed in the main outcome of fat mass, typical for obesity trials, was addressed in a sensitivity analysis using a robust mixed linear model, as implemented by the r package robustlmm [ 16 ].

This model corrects for natural heteroskedasticity and the potential influence of exceptional responders by introducing a weighing algorithm and Design Adaptive Scale estimate according to Koller [ 16 ], which is less sensitive to outliers in data than the squared error loss.

Between April and October , we assessed men for eligibility. Trial profile. Shown is study enrolment and follow-up. The most common reason for non-completion was failure to attend visits. Serious adverse events are detailed in Table 4. BMI body mass index, CKD chronic kidney disease, CCF congestive cardiac failure, OSA obstructive sleep apnoea, VLED very low energy diet.

Baseline characteristics were comparable between the groups Table 1. By study end, trough TT increased to Luteinising hormone levels decreased from 4. At the end of the week VLED phase, both cases — Following resumption of normal foods as part of an energy restricted diet shown to prevent weight regain, from week 10 onwards for a further 46 weeks, body weights remained largely stable from week 10 until study end week 56 Additional file 1 : Figure S2.

At study end, cases had, compared to baseline, lost significantly more fat mass MAD —2. During weeks 10—56, loss of fat mass percentage was greater in cases than in controls MAD —2. As the combined lean and fat mass lost in controls was similar to the amount of fat mass lost in the cases, the difference in body weight change at study end was no different between groups MAD —0.

Age, baseline TT, luteinising hormone and SHBG levels were all not predictive of changes in body composition after 56 weeks in the trial. Further, baseline fat mass did not interact with the changes in body composition.

In addition, adjustment for physical activity did not alter the findings. Cases had a significant increase in handgrip strength compared to placebo 3. No significant changes in either outcome were observed in controls nor between groups at study end Table 3.

Both groups improved on physical performance testing but there was no difference between groups at study end.

Similarly, both groups had improvements in metabolic parameters without between-group differences Table 3. Outcomes were unchanged after imputation of missing values using an intention-to-treat analysis and return-to-baseline for missing data Additional file 1 : Table S1; MAD for fat mass —3.

Similar findings were also found using non-parametric tests. In an additional sensitivity analysis, when re-analysed with a robust linear mixed model see Methods , the main outcome fat loss after 56 weeks was more pronounced in the testosterone group, compared to the placebo group —4.

Similar findings were also observed if non-completers in the placebo group were analysed separately data not shown. There was no between-group difference in overall adverse events, or serious adverse events which were few Table 4. The major novel findings of this RCT are that, among obese men with low to low-normal testosterone submitted to a weight loss program, testosterone treatment decreased total fat mass and visceral adipose tissue, and protected against loss of total and appendicular lean mass.

At the end of the initial week VLED phase, while men lost substantial amounts of weight similar to previous successful VLED studies [ 11 ], there were no differences in weight loss or body composition changes between the two groups.

At study end, there were marked differences in body composition between groups, and men receiving testosterone had greater reductions of fat mass —2. After the VLED phase, men receiving testosterone regained lean mass 3. Overall, our results indicate that, compared to men receiving placebo who lose both fat and muscle mass during diet, testosterone treatment shifts this weight loss to almost exclusive fat mass loss.

Our trial has several strengths distinguishing it from previous testosterone trials, most importantly, the successful implementation of a rigorous weight loss program and the exclusive focus on men with established obesity.

By contrast, previous RCTs examining the effects of testosterone on body composition recently meta-analysed [ 8 ] were neither designed for weight loss nor had obesity as a selection criterion.

Moreover, only a few studies, not all placebo controlled, have combined testosterone treatment with lifestyle measures. A recent meta-analysis of these studies [ 17 ] suggested that testosterone treatment may have added benefits on body composition, consistent with our findings.

Compared to men completing the study, non-completers had lost less body weight and less fat mass at the end of the VLED phase of the study. Therefore, if anything, this would be expected to underestimate the benefits of testosterone treatment, especially as the drop-out rate was higher among men assigned to placebo compared to testosterone treatment.

Although it may be expected that the effects of testosterone treatment are attenuated in the context of a rigorous weight loss program, the reduction of fat mass observed here compares favourably with the 1.

This may be because we focused on obese men with a confirmed low testosterone receiving effective testosterone treatment. This may also explain the robust increase in lean mass of 3.

Testosterone treatment did not prevent the loss of lean mass during the week VLED suggesting that testosterone treatment lacks anabolic actions during acute severe caloric restriction.

However, 10 weeks of treatment may be too short to manifest changes in body composition, since testosterone-mediated changes in lean mass are evident only after several months [ 18 , 19 ]. Testosterone treatment significantly reduced the metabolically important visceral fat even in the context of a weight loss program.

Previous RCTs of testosterone therapy, while not incorporating a weight loss program, did not find a consistent reduction in visceral fat [ 14 , 15 , 20 , 21 ], most likely because of small trial size [ 15 ], use of oral testosterone therapy [ 20 ], or less precise methodology to quantify visceral adipose tissue [ 20 ].

None of these RCTs specifically targeted obese men. Interestingly, the differences in body composition were evident despite the modest increase in endogenous testosterone levels in placebo-treated men similar to previous weight loss studies [ 22 ].

Indeed, this increase by 2. Thus, the endogenous rise in testosterone subsequent to diet appears not to be sufficient to prevent diet-associated loss of lean mass. What are the potential mechanisms by which testosterone treatment leads to these changes in body composition?

Testosterone, via androgen receptor signalling, inhibits stem cell differentiation into adipocytes and favours myogenesis [ 6 ]. Androgen receptor signalling in mature adipocytes promotes lipolysis [ 24 ] and activates anabolic pathways in myocytes [ 25 ].

The effect on fat mass may also be mediated by aromatisation to estradiol [ 26 ]. Testosterone may also have motivational effects leading to increased physical activity; in RCTs, testosterone treatment reduces fatigue and inertia [ 27 ], and androgen-deficient mice have decreased voluntary activity [ 28 ].

We advised subjects to perform at least minutes of moderate-intensity exercise each day. Subjects completed exercise questionnaires and accelerometer testing, with feedback given, to reinforce and encourage participation in exercise.

Both men receiving testosterone and placebo increased their activity during the weight loss phase. Supervised exercise programs may promote loss of fat mass and attenuate loss of muscle mass during weight loss, but are less effective than caloric restriction to achieve weight loss.

Exercise interventions are not well characterised for obese men with low testosterone and require high volume interventions, which may be difficult to achieve even in a dedicated RCT [ 29 ].

Only few studies have randomised obese men receiving caloric restriction to exercise programs. The effects of testosterone reported here compare favourably; systematic reviews have estimated that the addition of exercise to energy restriction increases the loss of fat mass by 1.

In the Look Ahead study, men, despite assignment to an intensive lifestyle intervention, lost 2. Metabolic parameters, evidenced by decreases in HOMA-IR, HbA1c, triglycerides, and increases in HDL levels improved in both groups.

Testosterone treatment had no added benefit, despite resulting in changes in body composition expected to be metabolically favourable. Our study was not designed to examine this outcome, and men enrolled were relatively healthy, with a low proportion of men being diabetic or dyslipidaemic at baseline.

Consistent with previous studies, we observed a significant increase in haematocrit in testosterone-treated men. Overall, serious adverse events were few and not statistically different between groups, although this study was not powered to assess safety.

However, the significance of this biochemical increase is uncertain, and although definitive long-term studies are lacking, the current evidence does not suggest that testosterone treatment leads to clinically meaningful adverse prostate outcomes.

Limitations include the enrolment of relatively healthy men motivated to lose weight subjected to a professionally administered diet and frequent monitoring. Despite preservation of lean mass, testosterone treatment, with the exception of increased grip strength, did not affect muscular performance.

Previous studies have suggested that testosterone treatment improves physical performance primarily in frail, mobility-limited men [ 33 , 34 ]. Although we did not include a supervised exercise program, exercise recommendations were reinforced at every visit, and men assigned to testosterone but not placebo, had increased activity levels.

This allowed us to capture the large population in whom testosterone treatment be it replacement or pharmacological is more controversial than in men with more profound reductions in testosterone, or indeed with organic hypogonadism.

While we did not find an added effect of testosterone treatment on diet-induced loss of body weight in this week study, it is possible that the duration of our study was insufficient, given that a recent meta-analysis of observational studies has suggested that testosterone treatment may be associated with time-dependent weight loss that may only be evident after 2 years of treatment [ 36 ].

Finally, our study was not designed to examine cardio-metabolic outcomes. Among obese men with a low to low-normal testosterone typical for the majority of obese men, testosterone treatment augmented diet-induced loss of total fat and visceral fat mass, and preserved lean mass so that, in contrast to placebo-treated men who lost both lean and fat mass, diet-induced weight loss during testosterone treatment was almost exclusively due to the loss of body fat.

Padwal R, Leslie WD, Lix LM, Majumdar SR. Relationship among body fat percentage, body mass index, and all-cause mortality. A cohort study relationship among body fat percentage, body mass.

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Article CAS PubMed PubMed Central Google Scholar. Veldhuis J, Yang R, Roelfsema F, Takahashi P. Singh R, Artaza JN, Taylor WE, Gonzalez-Cadavid NF, Bhasin S. Grossmann M. Low testosterone in men with type 2 diabetes: significance and treatment.

Corona G, Giagulli VA, Maseroli E, Vignozzi L, Aversa A, Zitzmann M, Saad F, Mannucci E, Maggi M. Therapy of endocrine disease: testosterone supplementation and body composition: results from a meta-analysis study. Eur J Endocrinol. Schubert M, Minnemann T, Hubler D, Rouskova D, Christoph A, Oettel M, Ernst M, Mellinger U, Krone W, Jockenhovel F.

Intramuscular testosterone undecanoate: pharmacokinetic aspects of a novel testosterone formulation during long-term treatment of men with hypogonadism. Bhasin S, Cunningham GR, Hayes FJ, Matsumoto AM, Snyder PJ, Swerdloff RS, Montori VM.

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The effect of rate of weight loss on long-term weight management: a randomised controlled trial. Lancet Diabet Endocrinol. Article Google Scholar. Harwood DT, Handelsman DJ. Development and validation of a sensitive liquid chromatography-tandem mass spectrometry assay to simultaneously measure androgens and estrogens in serum without derivatization.

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Introduction

Since lifestyle behaviors cause excess accumulation of visceral fat, modifying these behaviors help reduce it and associated disease risks. Belly fat responds more efficiently to diet and exercise than subcutaneous fat does. To reduce visceral fat and potentially increase lean muscle mass, add 30 minutes of moderate physical activity to your daily routine on most days of the week.

Moderate exercise can include aerobic activity such as walking and strength training with weights. Combining a more balanced diet with a regular exercise routine can accelerate the loss of belly fat and improve other cardiometabolic risk factors.

Adding more whole fruits and vegetables and minimizing sugar intake from processed foods are effective diet modifications for reducing dangerous fat around the organs. Additionally, quitting smoking, getting more than 5 hours of sleep per night, and managing mental stress have all been proven to reduce the accumulation of belly fat in men.

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All rights reserved. The body maintains testosterone levels within a narrow range through a feedback mechanism; when levels are high, the hypothalamus reduces GnRH secretion to balance things out. Testosterone has a direct influence on muscle growth by accelerating muscle protein synthesis. This process results in the building of new proteins and subsequently leads to increased muscle mass.

Testosterone aids in the differentiation of mesenchymal stem cells into the myogenic lineage, which later forms muscle fibres. Furthermore, testosterone increases growth hormone levels, another critical player in muscle development.

On the other hand, testosterone plays a role in fat distribution and metabolism. Men with lower testosterone levels tend to have an increase in body fat, especially in the abdominal region. Testosterone inhibits the creation of new fat cells and encourages the burning of lipids for energy.

Moreover, it impacts where men store fat; typically, men have lesser fat in the thighs and buttocks than women, partly influenced by testosterone. Testosterone is well-recognised for its anabolic effects, which primarily refer to the building and repair of tissues. This protein synthesis leads to an increase in muscle fibre size and muscle mass.

Additionally, testosterone increases the number of satellite cells, precursors to muscle cells, aiding in muscle repair and growth. Furthermore, the hormone also inhibits the effects of cortisol, a catabolic hormone. By suppressing cortisol, testosterone ensures that the rate of muscle breakdown does not surpass the rate of muscle building.

The result of these processes is enhanced muscle strength and size. It enhances muscle strength and size, which can benefit power-based sports. Still, it also aids in increasing bone density, thereby offering better skeletal strength and reducing the risk of injury. Moreover, testosterone plays a role in red blood cell production.

With a higher red blood cell count, athletes may experience improved oxygen transportation to muscles, leading to better aerobic performance and endurance. In terms of recovery, testosterone is instrumental.

Post-exercise, muscle fibres undergo wear and tear and repair and grow stronger during recovery. Testosterone accelerates this recovery process by increasing muscle protein synthesis rates, facilitating faster muscle repair.

Abusing testosterone or other anabolic steroids for performance enhancement can have detrimental health effects. Several research studies have consistently connected decreased testosterone levels and increased body fat percentages.

In particular, visceral fat — stored in the abdominal area and around internal organs — shows a prominent increase with declining testosterone levels. One potential reason for this correlation is that testosterone aids in maintaining and growing muscle mass, and a decrease in muscle tissue can lower the basal metabolic rate.

Consequently, fewer calories are burned at rest, potentially contributing to weight gain. A reciprocal relationship is also at play: increased adipose tissue, especially visceral fat, can lead to systemic inflammation and insulin resistance.

This environment can further reduce testosterone production, creating a vicious cycle of increasing body fat and decreasing testosterone levels. It helps to increase the basal metabolic rate, which is how our body burns calories while at rest.

An enhanced metabolic rate from a healthy testosterone level can lead to a more efficient calorie burn and potentially contribute to weight management.

On the front of fat breakdown, testosterone plays a pivotal role in lipolysis — the process of breaking down stored fat to be used as energy.

Testosterone promotes lipolysis by activating enzymes responsible for fat breakdown and inhibiting the uptake of lipids into adipocytes fat cells. Moreover, testosterone reduces the differentiation of preadipocytes into mature fat cells, thereby impacting fat storage capacity.

Optimal testosterone levels can improve insulin sensitivity, ensuring cells utilise glucose effectively for energy rather than being stored as fat.

Testosterone Replacement Therapy TRT has been extensively researched concerning its effects on muscle mass and strength. Clinical trials have confirmed its efficacy in promoting lean muscle growth. The scientific community has closely examined the impact of TRT on body fat, given the well-documented association between low testosterone levels and heightened body fat.

Significant Fat Mass Reduction: One of the notable outcomes of several TRT studies is the reduction in fat mass, particularly in the abdominal region. As previously discussed, visceral fat is closely associated with numerous metabolic and cardiovascular complications.

Improved Metabolic Parameters: Beyond mere fat reduction, TRT has shown promise in enhancing metabolic parameters. Patients on TRT often display improved insulin sensitivity, reduced blood glucose levels, and favourable changes in lipid profiles. These metabolic improvements can further aid in the reduction of adipose tissue.

Mechanisms at Play: TRT facilitates fat reduction through several mechanisms, including increased metabolic rate, enhanced lipolysis, and inhibiting lipid uptake into fat cells. By modulating these pathways, TRT can play a pivotal role in reshaping body composition in favour of reduced fat storage.

Testosterone levels undergo notable changes as men age. With the natural decline of this hormone, there are consequential effects on body composition, notably in muscle mass, fat distribution, and the general physiological structure.

A distinct differentiation is observed when examining the physical changes in men experiencing a regular age-related testosterone decrease compared to those diagnosed with clinical hypogonadism. A significant concern related to ageing is sarcopenia, a condition characterised by the loss of muscle tissue.

Various factors, including diminished testosterone levels, influence this muscle degradation.