Endocrine Abstracts

Objective: Testosterone levels are decreased in male obesity, the mechanism of which is incompletely understood. The aim of this study was to explore determinants affecting the feedback mechanism of the hypothalamic–pituitary–gonadal axis in male obesity and type 2 diabetes (DM2), such as aromatase expression and lipotoxicity.

Materials and methods: Circulating levels of testosterone were quantified (<1000 h with LC–MS/MS) in 37 middle-aged morbidly obese men (of which 23 had DM2) and 19 non-obese controls of similar age. LH and triglyceride levels were measured through standardized assays and aromatase expression was determined in subcutaneous adipose tissue biopsies using real-time PCR analysis.

Results: Mean testosterone levels were different among the groups, with 572, 372 and 207 ng/dl in non-obese, morbidly obese and morbidly obese men with DM2 respectively (P<0.01). Statistical differences in LH levels could not be established. Median triglyceride levels were higher in obese men vs non-obese men (P<0.05), with 96, 154 and 148 mg/dl in non-obese, morbidly obese and morbidly obese men with DM2 respectively. In non-obese men, age-adjusted Pearson’s analysis showed that testosterone levels correlated positively with LH (r=0.490, P=0.054) and inversely with aromatase expression (r=−0.635, P=0.036). In obese men, an inverse association was found between testosterone and triglyceride levels (r=−0.715, P=0.013). Although in obese men with DM2 correlations with testosterone could not be established, LH was inversely correlated with triglyceride concentrations (r=−0.535, P=0.010).

Conclusion: Although testosterone in normal men may depend on aromatase activity, these data show that testosterone concentrations in male obesity are inversely associated with triglyceride concentrations, which have been suggested as a marker of lipotoxicity.