FIG 2 - uploaded by Werner F Blum
Content may be subject to copyright.
![Baseline serum OB levels in the 22 hypogonadal men compared to the normal range established with 393 normal men [mean (solid line) and 5th and 95th percentiles (stippled lines)].](profile/Werner-Blum/publication/13967473/figure/fig2/AS:601752709656605@1520480434843/Baseline-serum-OB-levels-in-the-22-hypogonadal-men-compared-to-the-normal-range.png)
Baseline serum OB levels in the 22 hypogonadal men compared to the normal range established with 393 normal men [mean (solid line) and 5th and 95th percentiles (stippled lines)].
Source publication
The ob gene product leptin (OB) is a feedback signal from the adipocyte to the hypothalamus and is involved in regulation of food intake and energy expenditure in rodents. A major determinant of serum OB levels is fat mass. Several studies suggest that men have lower OB levels than women even after adjustment for percent body fat. We, therefore, in...
Context in source publication
Context 1
... baseline, mean OB levels for all 22 hypogondal men were 12.39 2.93 g/L and significantly elevated (P 0.01) compared to the BMI-dependent normal range for men (1.20 0.20 sd score). For normal men with similar BMI, a mean OB level of 4.28 0.52 g/L (95th percentile, 12.19 1.48 g/L) was calculated (Fig. 2). In 7 of 22 hypogonadal men, OB levels exceeded the 95th percentile of the normal range. Between treatment groups no significant differences The type of hypogonadism refers to primary vs. secondary hypog- onadism. Significant differences between groups were detected for age, estradiol (E2), cholesterol, LDL-cholesterol, and triglycerides. a P 0.05. in OB levels were observed (TE, 13.70 5.62; TPEL, 11.30 2.87 g/L). With substitution of T, a highly significant decrease in serum OB levels occurred in both groups (P 0.01), which was more prolonged in the TE group (Fig. 1). Serum OB concentrations reached a nadir on day 126 with 4.61 1.02 g/L in the TE group and 4.34 0.91 g/L in the TPEL group, not different from their expected normal value. Par- allel to the earlier decreases in serum T and the A/E ratio in the TPEL group compared to the TE group, OB levels started to increase in the TPEL group earlier than in the TE group (Fig. 1). After cessation of substitution, OB levels completely returned to the elevated baseline levels. There were now significant differences in OB levels between men with pri- mary and secondary hypogonadism at any time ...
Similar publications
The present study aimed to determine the prevalence and etiology of erectile dysfunction in Saudi type 2 diabetic patients.
429 Saudi type 2 diabetic male patients aged more than 30 years were recruited. Total and bio-available serum testosterone, sex hormone binding globulin and free testosterone levels were measured by ELISA-IBL GMBH Germany.
47...
Introduction:
Obesity and inactivity are associated with erectile dysfunction and hypogonadism.
Aim:
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.
Main outcome measu...
Introduction
In men suffering from metabolic syndrome, accompanying insulin resistance may result in a lowering of sex hormone–binding globulin (SHBG) plasma levels and cause changes in their androgenic status.
Aim
The objective of the research was to assess selected androgens and SHBG plasma levels in males meeting diagnostic criteria for MS comp...
Although hypogonadism is a risk factor for bone loss and fractures, the different etiopathophysiology and hormonal profile of classical and obesity-induced hypogonadism may lead to differences in musculoskeletal profile. This is a cross-sectional study of hypogonadal men between 40 and 74 years old. Our outcomes include: areal bone mineral density...
Background: Some studies indicated that body mass index (BMI) is inversely proportional to serum testosterone concentrations in men. Purposes: This study aimed to analyze the effects of aging and obesity on total testosterone (TT), free testosterone (FT), bioavailable testosterone (BT), luteinizing hormone (LH), and sex hormone-binding globulin (SH...
Citations
... It is proposed that this may be due to oestradiol stimulating leptin synthesis and testosterone suppressing it (56). At the onset of puberty, leptin increases in girls and decreases in boys, potentially reflecting the increase in fat mass in girls (34), in addition to the potential role of testosterone in suppressing the leptin production (57). By the age of 15, there is an increase in IL-6, IL-8, IL-10 serum concentrations in obese and overweight girls compared to normal weight females even after adjustment for pubertal status, but no significant difference was observed in boys (58). ...
Worrying trends of increased cardiovascular disease (CVD) risk in children, adolescents and young people in the Modern Era have channelled research and public health strategies to tackle this growing epidemic. However, there are still controversies related to the dynamic of the impact of sex, age and puberty on this risk and on cardiovascular health outcomes later in life. In this comprehensive review of current literature, we examine the relationship between puberty, sex determinants and various traditional CVD-risk factors, as well as subclinical atherosclerosis in young people in general population. In addition, we evaluate the role of chronic inflammation, sex hormone therapy and health-risk behaviours on augmenting traditional CVD-risk factors and health outcomes, ultimately aiming to determine whether tailored management strategies for this age group are justified.
... Studies have found that sex differences in the regulation of leptin synthesis are mediated by steroid hormones (23). Particularly, T inhibits leptin secretion and leptin mRNA production in adipocytes, while E2 positively regulates obese gene expression and leptin secretion in female adipocytes (24). Tanaka et al. (25) showed that E2 increased serum leptin concentrations and leptin mRNA expression in adipose tissue of immature rats. ...
Objective
The present research aimed to study the relationship between body mass index (BMI), sex hormones, leptin, and irisin in children and adolescents with different body types.
Methods
In this study, a stratified cluster random sampling method was used to select students aged 8-15 years from two 9-year schools as the research subjects. Based on a case-control study, 183 overweight/obese students were selected. After using sex and age matching to create a matched sample of normal-weighted students, a total of 366 students, including 214 boys (58.5%) and 152 girls (41.5%) were included. We measured their height and weight and calculated their body mass index BMI. Afterward, their concentrations of leptin, irisin, oestradiol (E2), and testosterone (T) in the serum were detected.
Results
There were significant differences in T, E2, leptin, and irisin between normal-weighted boys and girls ( p < 0.05). There were statistically significant differences in T, E2, and irisin between overweight/obese boys and girls ( p < 0.05). Overweight/obese students had higher concentrations of irisin and leptin than normal-weight students (p < 0.05). The direct effect of BMI on irisin was not statistically significant in either normal or overweight/obese students, but their indirect effects via leptin were statistically significant (for normal-weight boys and girls, standardized indirect effect coefficient: 0.29 and 0.38, respectively; for overweight/obese boys and girls, standardized indirect effect coefficient: 0.36 and 0.34, respectively). There was a negative pathway of E2 → leptin → irisin in normal-weight boys (standardized indirect effect coefficient: −0.24) and a negative pathway of T → leptin → irisin in overweight/obese boys (standardized indirect effect coefficient: −0.27).
Conclusion
The indirect effects of BMI on irisin via leptin exist in children and adolescents of different body types. E2 was negatively correlated with leptin in normal-weight boys, whereas T was negatively correlated with leptin in overweight/obese boys.
... T therapy in obese hypogonadal men with type 2 diabetes has led to the reduction of high-density lipoprotein cholesterol and glycated hemoglobin A1c, and the normalization of serum T concentrations [193]. Jockenhovel et al. showed that T administration in hypogonadal men resulted in normalization of leptin levels [194]. Moreover, an observational cohort study showed that T therapy was linked with decreased risk of death in men with low T levels [195]. ...
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.
... Reproductive hormones greatly affect leptin production. Androgenic hormones inhibit leptin synthesis, while estrogens stimulate leptin synthesis [42]. In one study, it was thought that increased estrogen concentrations caused an increase in leptin concentration, which may have been caused by leptin stimulating gonadotrophin releasing hormone (GnRH) synthesis and thus increasing estrogen synthesis [43]. ...
Adipose tissue (AT) in the body plays a very important role in the regulation of energy metabolism. AT regulates energy metabolism by secreting adipokines. Some of the adipokines released are vaspin, resistin, adiponectin, visfatin and omentin, and leptin. In addition to regulating energy metabolism, leptin plays a role in the regulation of many physiological functions of the body such as regulation of blood pressure, inflammation, nutrition, appetite, insulin and glucose metabolism, lipid metabolism, coagulation, and apoptosis. Among all these physiological functions, the relationship between leptin, oxidative stress, and apoptosis has gained great importance recently due to its therapeutic effect in various types of cancer. For this reason, in this study, the release of leptin, its cellular effects and its effect on oxida-tive stress, and apoptosis are discussed in line with current information.
... [123][124][125][126] Behre et al 127 found that hypogonadal men have elevated leptin levels. Jockenhovel et al 128 reported that testosterone supplementation reduces leptin levels. Many studies have reported the inverse correlation between leptin and testosterone levels in men. ...
Nowadays influence of gender and obesity on pain perception have been received substantial pragmatic attention. This may have implications for pain management among individuals. This systematic review was aimed to analyse the impact of gender and obesity on pain perception. The electronic databases of the Cochrane Central Register of Controlled Trials (CENTRAL), PubMed, and EMBASE were searched using combinations of terms for gender, sex hormones, obese, body mass index, leptin, analgesic requirements, endogenous opioids, pain measurement, and pain perception/sensitivity/threshold. Studies without comparison as well as cross-sectional studies, case series, and case reports were excluded. In the context of summary of results of extensive literature search, we found that pain sensitivity against noxious stimuli is more experienced in obese as well as females whereas it is less experienced in lean as well as males. We also found that sex hormones have influence on leptin levels whereas leptin do not affect the level of sex hormones. This review reveals that from gender perspective sex hormones and from obesity perspective leptin play an important interlinked role in pain modulation. Gender and body mass index specific tailoring of pain treatments might become a conceivable outcome in the foreseeable future.
... Increase in leptin level has been observed in men with hypogonadism and decreased serum leptin observed after testosterone replacement (Jockenhovel et al. 1997;Kalinchenko et al. 2010). This effect might be the link between the frequent associations of low serum testosterone with visceral obesity. ...
... 113,114 Interestingly, this modulation seems to be reciprocal as leptin inhibits testosterone production due to the action both at the hypothalamus and testis, but also testosterone suppresses leptin secretion from adipocytes and decreases its circulating levels independently of changes in the adipose tissue size. 115,116 Although the pathways that lead to metabolism modulation in testicular cells by leptin remains to be fully elucidated, it is well recognized that both leptin and testosterone take part of a vicious cycle, which culminates in the potentiation of increased adiposity and decreased testosterone levels, with negative consequences for men with obesity reproductive function. ...
Obesity prevalence, particularly in children and young adults, is perilously increasing worldwide foreseeing serious negative health impacts in the future to come. Obesity is linked to impaired male gonadal function and is currently a major cause of hypogonadism. Besides signs and symptoms directly derived from decreased circulating testosterone levels, males with obesity also present poor fertility outcomes, further evidencing the parallelism between obesity and male reproductive function. In addition, males with androgen deficiency also exhibit increased fat accumulation and reduced muscle and mineral bone mass. Thus, compelling evidence highlights a vicious cycle where male hypogonadism can lead to increased adiposity, while obesity can be a cause for male hypogonadism. On the opposite direction, sustained weight loss can attain amelioration of male gonadal function. In this scenario, a thorough evaluation of gonadal function in men with obesity is crucial to dissect the causes from the consequences in order to target clinical interventions towards maximized improvement of reproductive health. This review will address the causes and consequences of the bidirectional relationship between obesity and hypogonadism, highlighting the implicit male reproductive repercussions.
... Weight loss leads to reductions in leptin levels, with an associated increase in bone resorption markers 30,31 . The sustained reduction in CTx in testosterone-treated men compared to men receiving placebo is consistent with previous studies reporting reduced leptin resistance following testosterone treatment 32,33 . The strengths of this double-blind placebo controlled RCT include the unique design combining testosterone treatment with a rigorous weight loss program and the focus on obese men with lowered testosterone levels. ...
To assess the effect of testosterone treatment on bone remodelling and density in dieting obese men, 100 obese men aged 53 years (interquartile range 47-60) with a total testosterone level <12 nmol/L receiving 10 weeks of a very low energy diet (VLED) followed by 46 weeks of weight maintenance were randomly assigned at baseline to 56 weeks of intramuscular testosterone undecanoate (n = 49, cases) or matching placebo (n = 51, controls). Pre-specified outcomes were between-group differences (mean adjusted difference, MAD) in serum c-telopeptide (CTx), N-terminal propeptide of type 1 procollagen (P1NP) and bone mineral density (BMD). At trial end, CTx was significantly reduced in men receiving testosterone compared to placebo, MAD -66 ng/L (95% CI -113, -18), p = 0.018, and this was apparent already after the 10 week VLED phase, MAD -63 ng/L (95% CI -108, -18), p = 0.018. P1NP was marginally increased after VLED, MAD +4.2 ug/L (95% CI -0.01, +8.4), p = 0.05 but lower at study end, MAD -5.6 ug/L (95% CI -10.1, -1.1), p = 0.03. No significant changes in sclerostin, lumbar spine BMD or femoral BMD were seen. We conclude that in obese men with low testosterone levels undergoing weight loss, bone remodelling markers are modulated in a way that may have favourable effects on bone mass.
... Key exclusion criteria [13] included classic hypogonadism due to pituitary or testicular disease, contraindications to testosterone treatment, use of weight-altering medications including insulin, previous VLED failure, and bariatric surgery. Participants were randomized to receive either 1000 mg of testosterone undecanoate (the standard ampoule strength in Australia) or visually identical placebo by deep intramuscular buttock injection at weeks 0, 6 (manufacturer-recommended loading dose), 16,26,36, and 46 to ensure therapeutic trough levels of 10 to 15 nmol/L [13]. In addition, all subjects received a VLED providing 640 kcal per day for 10 weeks, followed by a 46-week weight maintenance phase based on the Australian Commonwealth Scientific and Industrial Research Organization Total Wellbeing Diet [13]. ...
... Whether such testosterone-associated alterations in leptin levels, evident over and above those achieved by caloric restriction alone, are mechanistically involved in the regulation of body fat mass by testosterone requires further study. However, as suggested previously [26], low testosterone levels may contribute to leptin resistance in obese men. Therefore, it is tempting to speculate that testosterone treatment may restore HPT axis responsiveness to leptin, which may in turn promote further reduction in fat mass. ...
Context
In obese men with lowered testosterone levels, testosterone treatment augments diet-associated loss of body fat.
Objective
We hypothesized that testosterone treatment modulates circulating concentrations of hormonal mediators of fat mass and energy homeostasis in obese men undergoing a weight loss program.
Design
Prespecified secondary analysis of a randomized, double-blind, placebo-controlled trial.
Setting
Tertiary referral center.
Participants
Obese men (body mass index ≥30 kg/m²) with a repeated total testosterone level ≤12 nmol/L.
Intervention
One hundred participants mean age 53 years (interquartile range 47 to 60 years) receiving 10 weeks of a very low–energy diet followed by 46 weeks of weight maintenance were randomly assigned at baseline to 56 weeks of intramuscular testosterone undecanoate (cases, n = 49) or matching placebo (controls, n = 51). Eighty-two men completed the study.
Main outcomes
Between-group differences in leptin, adiponectin, ghrelin, glucagon like peptide-1, gastric inhibitory polypeptide, peptide YY, pancreatic polypeptide, and amylin levels.
Results
At study end, compared with controls, cases had greater reductions in leptin [mean adjusted difference (MAD), −3.6 ng/mL (95% CI, −5.3 to −1.9); P < 0.001]. The change in leptin levels between cases and controls was dependent on baseline fat mass, as the between-group difference progressively increased with increasing fat mass [MAD, −0.26 ng/mL (95% CI, −0.31 to −0.26); P = 0.001 per 1 kg of baseline fat mass]. Weight loss–associated changes in other hormones persisted during the weight maintenance phase but were not modified by testosterone treatment.
Conclusions
Testosterone treatment led to reductions in leptin beyond those achieved by diet-associated weight loss. Testosterone treatment may reduce leptin resistance in obese men.
... The following several studies would give an explanation for the gender-based differences of circulating leptin levels. Jockenhövel et al. [30] found that testosterone substitution could normalize the elevated serum leptin levels in hypogonadal men. Administration of human adipocytes with androgens clearly suppressed leptin secretion and mRNA expression in in vitro study [31]. ...
The aim of the study is to investigate the changes of serum leptin and kisspeptin levels in children and adolescents with different pubertal stages and nutritional states. A total of 647 Chinese children and adolescents were recruited, and serum estradiol, testosterone, pituitary gonadotropins, leptin, and kisspeptin levels were measured. The results showed that serum leptin levels of boys in T2 stage were the highest among the five stages, while they showed a gradual increase from T1 to T5 stage in girls and reached the highest in T5 stage ( P<0.05 ). Conversely, serum kisspeptin levels of boys were higher in T4 and T5 stages than those in T1 stage, while its levels of girls were the highest in T2 stage, 21.4% higher than those in T1 stage ( P<0.05 ). Both leptin and kisspeptin levels were positively correlated with BMI, WC, and weight in all boys and girls (all P<0.05 ). In conclusion, kisspeptin levels were firstly found to be notably changed in pubertal stages and nutritional status in Chinese children and adolescents with a significant sexual dimorphism. Obese/overweight girls had higher kisspeptin levels, and there was a positive correlation between kisspeptin and FSH and LH and obesity-related parameters in all boys and girls.
