Comparative evaluation of insulin resistance and adipokine status in men with hypogonadism associated with obesity
TL;DR
Hypogonadism in men with obesity is associated with abdominal obesity, hyperinsulinemia, and insulin resistance, and the HOMA-IR and Caro indices may be recommended as screening tools for detecting metabolic disturbances in this patient population.
Abstract
Background
: Obesity is a significant risk factor for development of hypogonadism in men and is associated with pronounced metabolic disturbances, including insulin resistance.
Aim
: To assess the prevalence of hypogonadism across different body mass index categories in men and to investigate its association with key metabolic disturbances, including adipokine dysregulation.
Methods
: The study included 103 men divided into groups with hypogonadism ( n = 57) and without hypogonadism ( n = 46). Anthropometric parameters, carbohydrate and lipid metabolism markers, immunoreactive insulin, total testosterone levels, as well as insulin resistance indices (HOMA-IR, Matsuda, Caro) and adipokines (visfatin, resistin) were evaluated. Statistical analysis included non-parametric methods and correlation analysis.
Results
: Patients with hypogonadism demonstrated significantly higher body mass index, waist circumference, and insulin levels, as well as pronounced insulin resistance. The HOMA-IR and Caro indices showed greater sensitivity to decreased testosterone levels compared to the Matsuda index. Statistically significant negative correlations were found between testosterone levels and visfatin (r = −0.732; p <0.001) and resistin (r = −0.750; p <0.001). However, intergroup differences in adipokine levels did not reach statistical significance.
Conclusion
: Hypogonadism in men with obesity is associated with abdominal obesity, hyperinsulinemia, and insulin resistance. The HOMA-IR and Caro indices may be recommended as screening tools for detecting metabolic disturbances in this patient population. The identified correlations between testosterone levels and adipokines suggest a potential role of visfatin and resistin in the pathogenesis of androgen deficiency and warrant further investigation.