To investigate the ralationship between body fat distribution, sex hormones, and hyperinsulinemia in male obesity, we examined 52 obese men (body mass index [BMI], 35.0 ± 6.1, mean ± SD) and 20 normal-weight controls. Their waist to hip circumference ratio (WHR), which was used as an index of fat distribution, was 0.985 ± 0.052 and 0.913 ± 0.061 (P < .005), respectively. Compared with controls, obese men presented significantly lower levels of total (357 ± 132 v 498 ± 142 ng/dL; P < .005) and free testosterone (14.2 ± 2.9 v 17.1 ± 2.6 pg/mL; P < .05) and sex hormone-binding globulin (SHBG; 41.7 ± 31.9 v 66.2 ± 18.6 nmol/L; P < .001) without any significant difference on the other sex steroid or on gonadotropin concentrations. Fasting and glucose-stimulated insulin and C-peptide levels were significantly higher in obese than in controls, and in obese with the WHR value greater than 0.97 (corresponding to the distribution median) than in those with WHR lower or equal to 0.97. BMI was negatively correlated with testosterone (P < .005), free testosterone (P < .01), and SHBG (P < .001) and positively with fasting (P < .001) and glucose-stimulated (P < .005) C-peptide concentrations, whereas no relationship was found between these variables and WHR values. On the contrary, WHR was significantly correlated with fasting and post-glucose insulin levels (P < .05), but not with those of sex steroids. The correlation coefficients did not change significantly after correction for BMI, age, and WHR values. Moreover, we found a significant negative correlation between insulin concentrations and SHBG or testosterone levels, regardless of the effect of BMI, WHR, and age. These results, therefore, suggest that in obese men, at variance with what was observed in obese women, sex steroid abnormalities mainly depend on the degree of obesity, whereas the degree of hyperinsulinemia seems to be more correlated with the type of body fat distribution. Moreover, they suggest the possibility that hyperinsulinemia may be involved in the regulation of sex hormone metabolism in obese men, by mechanisms that probably differ from those involved in the development of hyperandrogenism in obese women.