Measurement of Serum Testosterone in Nondiabetic Young Obese Men: Comparison of Direct Immunoassay to Liquid Chromatography-Tandem Mass Spectrometry.

Hypoandrogenemia, a frequent finding in men with obesity, is defined by low concentrations of serum testosterone. Although immunoassay (IA) is the most used method for the determination of this steroid in clinical practice, liquid chromatography-mass spectrometry (LC-MS/MS) is considered a more reliable method. In this study, we aimed to compare IA versus LC-MS/MS measurement for the diagnosis of hypoandrogenemia in a cohort of 273 nondiabetic young obese men.

Adiposity is Associated with Decreased Serum 17-Hydroxyprogesterone Levels in Non-Diabetic Obese Men Aged 18-49: A Cross-Sectional Study.

Obesity is associated with decreased circulating testosterone levels, the main male sex hormone. However, there are a number of different male sex hormones whose dynamics remain poorly understood regarding this pathology. In this regard, 17 hydroxyprogesterone (17-OH progesterone), as an important precursor of testosterone synthetized in testes and adrenal glands, could play an essential role in testosterone deficiency in male obesity.

Prevalence of and risk factors for erectile dysfunction in young nondiabetic obese men: results from a regional study.

Erectile dysfunction (ED), a condition closely related to cardiovascular morbidity and mortality, is frequently associated with obesity. In this study, we aimed to determine the prevalence of ED and evaluate the associated risk factors in a cohort of 254 young (18-49 years) nondiabetic obese (body mass index [BMI] ≥ 30 kg m) men from primary care. Erectile function (International Index of Erectile Function [IIEF-5] questionnaire), quality of life (Aging Males' Symptoms [AMS scale]), and body composition analysis (Tanita MC-180MA) were determined.

Cross-Sectional, Primary Care-Based Study of the Prevalence of Hypoandrogenemia in Nondiabetic Young Men with Obesity.

Objective: Obesity-associated hypoandrogenemia is increasing in parallel to the obesity epidemic. The prevalence of hypoandrogenemia in nondiabetic young men with obesity is not known. This study aimed to evaluate the prevalence of hypoandrogenemia and associated risk factors in this population.

Effects of SHBG rs1799941 Polymorphism on Free Testosterone Levels and Hypogonadism Risk in Young Non-Diabetic Obese Males.

Introduction: Obesity has been associated with increased risk of presenting hypogonadism. Free testosterone (FT) is the fraction of testosterone that carries out the biological function of testosterone, and is determined from total testosterone (TT) and sex-hormone binding globulin (SHBG) levels. We aimed to study the SHBG polymorphism rs1799941 in a cohort of young non-diabetic obese males to unravel the possible implication of this polymorphism in obesity-related hypogonadism.

Impact of selenium co-administration on methylmercury exposed eleutheroembryos and adult zebrafish (Danio rerio): Changes in bioaccumulation and gene expression.

Mercury still represents one of the most hazardous threats for the aquatic ecosystem due to its high toxicity, and the fact that it can be easily incorporated into the food chain by accumulation in fish as MeHg. On the other hand, selenium is a micronutrient that is part of different antioxidant enzymes that regulate the cellular redox state, and whose complex interaction with Hg has been extensively studied from a toxicological point of view. In order to evaluate the protective effect of Se(IV) co-administration against MeHg accumulation and toxicity, we have selected an in-vivo model at two developmental stages: zebrafish eleutheroembryos and adult fish.

A quantitative proteomic approach for unveiling novel mechanisms associated with MeHg-induced toxicity: effects on the methylation cycle.

Methylmercury (MeHg) is still a major threat for human health and the environment due to its extremely high toxicity that mainly affects the nervous system. Despite the great efforts made during the last few decades, the specific molecular mechanisms involved in MeHg-induced toxicity are still not completely unveiled. In this work we explored such mechanisms using neuroblastoma cells (Neuro-2a) and SILAC as a quantitative proteomic approach.

Extracellular vesicles produced by the Gram-positive bacterium Bacillus subtilis are disrupted by the lipopeptide surfactin.

Previously, extracellular vesicle production in Gram-positive bacteria was dismissed due to the absence of an outer membrane, where Gram-negative vesicles originate, and the difficulty in envisioning how such a process could occur through the cell wall. However, recent work has shown that Gram-positive bacteria produce extracellular vesicles and that the vesicles are biologically active. In this study, we show that Bacillus subtilis produces extracellular vesicles similar in size and morphology to other bacteria, characterized vesicles using a variety of techniques, provide evidence that these vesicles are actively produced by cells, show differences in vesicle production between strains, and identified a mechanism for such differences based on vesicle disruption.

Analytical and bioanalytical approaches to unravel the selenium-mercury antagonism: a review.

Mercury is a well-known risk to ecosystems and human health. Considering that no effective treatment is available to counteract mercury toxicity, the effectiveness of different trace elements, agents and nutrients with antioxidant properties to protect or reverse mercury toxicity is crucial. In this article we present the main analytical and bioanalytical strategies that have been used to study the potential of selenium as a protective agent against mercury-induced toxicity.

Identification of mitochondrial dysfunction in Hutchinson-Gilford progeria syndrome through use of stable isotope labeling with amino acids in cell culture.

Unlabelled: Hutchinson-Gilford progeria syndrome (HGPS) is a rare segmental premature aging disorder that recapitulates some biological and physical aspects of physiological aging. The disease is caused by a sporadic dominant mutation in the LMNA gene that leads to the expression of progerin, a mutant form of lamin A that lacks 50 amino acids and retains a toxic farnesyl modification in its carboxy-terminus. However, the mechanisms underlying cellular damage and senescence and accelerated aging in HGPS are incompletely understood.