Testosterone In Obese Men Research Articles

An association between adropin hormone and total testosterone in obese men: a case-control study

BackgroundObesity is associated with low testosterone levels that could be caused by many mechanisms. Adropin, a peptide hormone, its levels are decreased in obesity and its receptors are expressed in the hypothalamus, the pituitary gland, and the testis. Adropin association to total testosterone in obese men is not detected yet. This study tries to find out possible associations between serum levels of adropin, adiponectin, total testosterone, and lipid profile in obese men.MethodsSerum levels of adropin, adiponectin, total testosterone, and lipid profile parameters were measured in 43 obese men and 40 age-matched normal-weight men.ResultsAdropin, adiponectin, and testosterone levels were significantly lower in obese men versus normal-weight men. In all participants, positive correlations between adropin, adiponectin, and total testosterone were detected. Adropin is considered a predictor risk factor for testosterone.ConclusionsThis study suggests a possible causal relationship between adropin and total testosterone which needs further investigation.Trial registrationClincialtrials.gov NCT03724825, registered October 30th, 2018.

Associations of body shape phenotypes with sex steroids and their binding proteins in the UK Biobank cohort

Associations of sex steroids and their binding proteins with body shape are unclear, because waist and hip circumference are correlated strongly with body size. We defined body shape using “a body shape index” (ABSI) and hip index (HI), which are independent of weight and height by design, and examined associations in multivariable generalised linear models for the UK Biobank cohort (179,902 men, 207,444 women). Total testosterone was associated inversely with ABSI, especially in men. Free testosterone was lowest for large-ABSI-large-HI (“wide”) and highest for small-ABSI-small-HI (“slim”) in men, but lowest for small-ABSI-large-HI (“pear”) and highest for large-ABSI-small-HI (“apple”) in women. Oestradiol was associated inversely with ABSI in obese pre-menopausal women but positively with HI in obese men and post-menopausal women not using hormone replacement therapy. Sex-hormone binding globulin (SHBG) was associated inversely with ABSI but positively with HI and was lowest for “apple” and highest for “pear” phenotype in both sexes. Albumin was associated inversely with HI in women, but matched the pattern of free testosterone in obese men (lowest for “wide”, highest for “slim” phenotype). In conclusion, sex steroids and their binding proteins are associated with body shape, including hip as well as waist size, independent of body size.

The role of leptin and low testosterone in obesity.

Obesity is a medical condition associated with metabolic disorders and low-grade systemic inflammation. Another characterizing feature of obesity is high circulating levels of leptin (a hormone predominantly made by adipose cells and enterocytes in the small intestine that helps to regulate energy balance), a phenomenon termed hyperleptinemia. Hyperleptinemia is associated with both low-grade systemic inflammation and metabolic dysfunction in obese human beings. Moreover, obesity is associated with low testosterone in men, which correlates with high body fat. The association between leptin and low testosterone could potentially be explained via the imbalanced leptin levels that results in higher estrogen levels, which further increases the aromatase activity. The increase in aromatase activity in turn reciprocally inhibits the testosterone levels and hypothalamic pituitary gonadal axis. Novel strategies are being used to treat obesity, including leptin and testosterone therapy. However, the efficacy and adverse effects of these strategies need further validation through preclinical and clinical studies. Additionally, further studies are needed to establish the molecular mechanism behind leptin-modulated changes to testosterone in obese men. This review summarizes the available literature on the role of leptin and low testosterone during obesity.

Lifestyle modification-induced increase in serum testosterone and SHBG decreases arterial stiffness in overweight and obese men

BackgroundArterial stiffness—a risk factor for cardiovascular diseases—is more frequently observed in obese men. Moreover, the male sex hormone testosterone has an anti-atherogenic effect. Serum testosterone levels are found to be lower in obese men than in age-matched normal-weight men. However, the effect of lifestyle modification on testosterone in obese men has not been elucidated. Here, we examined the effect of lifestyle modifications on serum testosterone levels and arterial stiffness in overweight and obese men. MethodsEleven overweight and obese men (mean age: 53 ± 3 years) completed a 12-week lifestyle modification program. Before and after the program, we measured the mean blood pressure (MBP), carotid-femoral pulse wave velocity (cfPWV; as an index of arterial stiffness), and the serum total testosterone levels in all participants. ResultsWe observed a significant weight loss after the 12-week lifestyle modification program. After the program, MBP and cfPWV significantly decreased and serum testosterone levels significantly increased. Moreover, we observed a negative relationship between the change in serum testosterone levels and that in cfPWV, although this relationship was affected by change in MBP. ConclusionsLifestyle modification increased the serum testosterone levels in overweight and obese men. The increase in serum testosterone levels was associated with a corresponding reduction in MBP and arterial stiffness. These results suggest that an increase in the testosterone levels may be an important mechanism underlying the beneficial effect of lifestyle modification on arterial stiffness. However, the association may not be direct, but may be mediated by a change in the MBP.

Comparing Effects of Low- and High-Volume Moderate-Intensity Exercise on Sexual Function and Testosterone in Obese Men

Comparing Effects of Low- and High-Volume Moderate-Intensity Exercise on Sexual Function and Testosterone in Obese Men

Comparing Effects of Low- and High-Volume Moderate-Intensity Exercise on Sexual Function and Testosterone in Obese Men

Obesity and inactivity are associated with erectile dysfunction and hypogonadism. To compare the effects of low volume (LV) and high volume (HV) of moderate-intensity exercise on sexual function, testosterone, lower urinary tract symptoms (LUTS), endothelial function, and quality of life (QoL) in obese men. Weight, waist circumference (WC), body composition, International Index of Erectile Function 5-item (IIEF-5), International Prostate Symptom Scale (IPSS) (for LUTS), and 36-item Short Form Survey version 2 Instrument (SF-36) (for QoL) scores, plasma testosterone, sex-hormone binding globulin, glucose, insulin and lipids, and endothelial function (by Reactive Hyperaemia Index [RHI] using finger plethysmography) were measured at baseline and 24 weeks. Ninety abdominally obese (body mass index > 27.5 kg/m(2), WC > 90 cm), sedentary (exercise ≈ 80 minutes/week) Asian men (mean age 43.6 years, range 30-60) were prescribed a diet to reduce daily intake by ≈ 400 kcal below calculated requirement and randomized to perform moderate-intensity exercise of LV (<150 minutes/week) or HV (200-300 minutes/week) (n = 45 each) for 24 weeks. Seventy-five men (83.3%) completed the study. Weekly exercise volume was significantly greater in the HV (236 ± 9 minutes) than the LV (105 ± 9 minutes) group. The HV group had significantly greater increases in IIEF-5 score (2.6 ± 0.5 points) and testosterone (2.06 ± 0.46 nmol/L) and reductions in weight (-5.9 ± 0.7 kg, -6.2%), WC (-4.9 ± 0.8 cm, -4.9%), and fat mass (-4.7 ± 1.0 kg, -14.5%) than the LV group (-2.9 ± 0.7 kg, -3.0%; -2.7 ± 0.7 cm, -2.5%; -1.1 ± 0.8 kg, -3.2%; 0.79 ± 0.46 nmol/L; and 1.8 ± 0.5 points). Improvements in IPSS and SF-36 scores, and RHI, were similar. Moderate-intensity HV aerobic exercise > 200 minutes/week produces greater improvements in sexual function, testosterone, weight, WC, and fat mass than smaller exercise volume.

Effects of testosterone therapy on sleep and breathing in obese men with severe obstructive sleep apnoea: a randomized placebo‐controlled trial

High doses of short-term testosterone have been shown to acutely worsen sleep-disordered breathing in men with obstructive sleep apnoea (OSA). The effects of lower, near-conventional doses of testosterone in obese men with OSA may differ over the longer term but have not been systematically studied. We assessed sleep and breathing effects of near-conventional testosterone treatment as an adjunct to weight loss in obese men with severe OSA. An 18-week randomized, double-blind, placebo-controlled, parallel group trial in 67 men. All subjects were placed on a hypocaloric diet and then received intramuscular injections of 1000 mg testosterone undecanoate or placebo at 0, 6 and 12 weeks. Sleep and breathing were measured by nocturnal polysomnography at 0, 7 and 18 weeks. Testosterone, compared to placebo, worsened the oxygen desaturation index (ODI) by 10·3 events/h (95%CI, 0·8-19·8 events/h; P = 0·03) and nocturnal hypoxaemia (sleep time with oxygen saturation <90%, SpO(2) T90%) by 6·1% (95%CI, 1·5-10·6; P = 0·01) at 7 weeks. Testosterone therapy did not alter ODI (4·5, -5·4 to 14·4 events/h; P = 0·36) or SpO(2) T90% at 18 weeks (2·9, -1·9-7·7%; P = 0·23) compared to placebo. The testosterone treatment effects on ODI and SpO(2) T90% were not influenced by baseline testosterone concentrations (testosterone by treatment interactions, all P > 0·35). Blood testosterone concentrations did not correlate with ODI or SpO(2) T90% (all P > 0·19). Testosterone therapy in obese men with severe OSA mildly worsens sleep-disordered breathing in a time-limited manner, irrespective of initial testosterone concentrations. This time-dependency was not related to testosterone concentrations. www.anzctr.org.au Identifier: ACTRN1260-6000404527.

Circulating free testosterone in obese men after bariatric surgery increases in parallel with insulin sensitivity.

Male hypogonadism has been linked to obesity and diabetes. We aimed to study the association of changes in insulin sensitivity and testosterone levels in severe obese patients submitted to bariatric surgery. Prospective intervention study with twenty consecutive patients who underwent bariatric surgery studied before and after significant weight loss. Serum testosterone, SHBG, fasting glucose, and insulin were measured among others. Free testosterone was calculated with the Vermeulen formula and insulin sensitivity with the homeostatic model assessment (HOMA). At baseline, thirteen patients had low total testosterone levels, whereas eight of these patients also had free testosterone levels below the reference range obtained from the control group. After bariatric surgery total testosterone, SHBG, and free testosterone significantly increased and achieved normal values in all evaluated patients. Insulin sensitivity improved in all of them. Multivariate linear regression showed that changes in fasting glucose (β=-1.868, p=0.001), insulin (β=-3.782, p=0.001), weight (β=-0.622, p=0.002), and SHBG (β=-0.635, p=0.022) were associated with changes in free testosterone (adjusted R2=0.936, F=26.613, p=0.001). When insulin resistance calculated by HOMA was in the model instead of insulin and glucose, it also was associated (β=-3.488, p=0.008) with free testosterone (adjusted R2=0.821, F=11.111, p=0.005). Circulating tes tos terone in obese men increases after bariatric surgery in parallel with an improvement in insulin sensitivity.

High Prevalence of Prolonged QT Interval in Obese Hypogonadal Males

Obese subjects show several electrocardiographic alterations, including prolonged QT interval, a marker for fatal cardiac arrhythmias. Prolonged QT interval has recently been linked to low testosterone levels, a frequent occurrence in male obese patients but no study has yet assessed whether hypoandrogenism contributes to QT interval prolongation in this population. Aim of this study was to evaluate whether prolonged QT interval is linked to hypogonadism in male obese subjects. QT interval corrected for heart rate (QTc) was measured from standard electrocardiogram recordings in 136 obese men (BMI 30 >kg/m(2), range 30.1-75.4 kg/m(2)). Obese men were classified as eugonadal or hypogonadal according to serum total testosterone levels (i.e., greater or less than 9.9 nmol/l). Our study showed that QTc measurements corrected by either Bazett (419 ± 3.2 vs. 408 ± 3.4 ms, P < 0.05), Fridericia (406.3 ± 3.39 vs. 396.4 ± 3.03 ms, P < 0.05) or Hodges (407.0 ± 3.12 vs. 397.3 ± 2.84 ms, P < 0.05) were longer in hypogonadal compared with eugonadal obese men; further, prolonged QTc interval (i.e., >440 ms) was more frequent among hypogonadal compared with eugonadal obese men (23% vs. 10%, P < 0.05). The degree of weight excess, diabetes, sleep apnoea and potassium levels were not associated with prolonged QTc. In conclusion, obese hypogonadal men show a greater prevalence of prolonged QT interval compared with their eugonadal counterparts. It appears therefore that low levels of testosterone in obese men may contribute to the arrhythmogenic profile of these patients, a heretofore unknown link which warrants further clinical attention.

PRACTICES OF USING TESTOSTERONE REPLACEMENT THERAPY IN MALE PATIENTS WITH ANDROGEN DEFICIENCY AND TYPE 2 DIABETES MELLITUS

Androgen deficiency in the aging male has become a topic of increasing interest both healthy men and with various endocrinology diseases, including type 2 diabetes mellitus. The low level of testosterone in obese men is reason of insulin resistance which leads to the type 2 diabetes mellitus. Many reports have shown that testosterone replacement therapy leads to improvement of parameters of a metabolic syndrome. Investigation and treatment androgen deficiency allow not only prevent diabetes type 2, but also have a good control of diabetes. In our work we have shown that testosterone gel is an effective preparation for androgen replacement therapy in patients with type 2 diabetes mellitus, allowing not only to restore normal level of testosterone but also to control of weight, lipids, insulin resistance and bone mineral density.

Letrozole once a week normalizes serum testosterone in obesity-related male hypogonadism

Isolated hypogonadotropic hypogonadism (IHH) is frequently observed in severely obese men, probably as a result of increased estradiol (E(2)) production and E(2)-mediated negative feedback on pituitary LH secretion. Aromatase inhibitors can reverse this process. This study evaluates whether letrozole once a week can normalize serum testosterone in severely obese men and maintain its long term effect. Open, uncontrolled 6-month pilot study in 12 severely obese men (body mass index>35.0 kg/m(2)) with obesity-related IHH and free testosterone levels <225 pmol/l, treated with 2.5 mg letrozole once a week for 6 months. Six weeks of treatment reduced total E(2) from 123+/-11 to 58+/-7 pmol/l (P<0.001, mean+/-s.e.m.), and increased serum LH from 4.4+/-0.6 to 11.1+/-1.5 U/l (P<0.001). Total testosterone rose from 5.9+/-0.5 to 19.6+/-1.4 nmol/l (P<0.001), and free testosterone from 163+/-13 to 604+/-50 pmol/l (P<0.001). Total testosterone rose to within the normal range in all subjects, whereas free testosterone rose to supraphysiological levels in 7 out of 12 men. The testosterone and E(2) levels were stable throughout the week and during the 6-month treatment period. Letrozole 2.5 mg once a week produced a sustained normalization of serum total testosterone in obese men with IHH. However, free testosterone frequently rose to supraphysiological levels. Therefore, a starting dose <2.5 mg once a week is recommended.

The effects of weight loss treatments on upper and lower body fat.

The intra-abdominal visceral deposition of adipose tissue, which characterises upper body obesity, is a major contributor to the development of hypertension, glucose intolerance and hyperlipidaemia. Conversely, individuals with lower body obesity may have comparable amounts of adipose tissue but remain relatively free from the metabolic consequences of obesity. This raises an obvious question-are there particular weight reducing treatments which specifically target intra-abdominal fat? In theory, surgical removal of upper body fat should be effective. In reality, neither liposuction nor apronectomy ('tummy tuck') have any beneficial metabolic effects, they simply remove subcutaneous adipose tissue which is often rapidly replaced. Vertical banded gastroplasty and gastric bypass operations may be dramatically effective in improving blood pressure, insulin sensitivity and glucose tolerance. However, these benefits result from a parallel reduction in visceral and total body fat. Studies of body fat distribution in postmenopausal women confirm that the marked decrease in adiposity, following a programme of very low calorie diet and exercise, reflects a comparable reduction in visceral and thigh fat. The reduction in waist circumference after a low fat/exercise programme suggests a similar situation in men. Exercise has an important role in treatment but, once again, the fat loss is generalised. Nevertheless, the improved metabolic parameters seen in exercising obese subjects, independent of weight loss, suggest other beneficial actions. Growth hormone (GH) has a marked lipolytic action. GH replacement treatment for GH deficient adults with pronounced abdominal fat deposition, has been shown to reduce intra-abdominal fat by 47% compared to 27% decrease in abdominal subcutaneous fat. Similar beneficial actions on abdominal fat have been reported following treatment with testosterone in obese men. The potential hazards of such treatments make them unsuitable therapy for obesity. Dexfenfluramine is effective in reducing total body fat but the results from a six month randomised controlled trial indicates that it does not specifically influence changes in waist circumference associated with weight loss. In conclusion, any treatment which reduces total body fat will, by its nature, reduce intra-abdominal visceral fat. There are presently no specific treatments which can be recommended for intra-abdominal fat but increasing knowledge of the biochemical aberrations associated with visceral adiposity may lead to more specific therapies for the future.