In recent years there is increasing evidence of an interaction between metabolic syndrome and testicular function. Metabolic syndrome, in particular obesity, affects testicular function by reducing total testosterone and sex hormonebinding globulin levels, as well as having a detrimental effect on spermatogenesis. On the other hand, hypogonadism further increases insulin resistance, which is the main pathophysiological feature of metabolic syndrome. There are implications that testosterone replacement can improve not only testicular function, but also parameters of the metabolic syndrome. Although the exact pathophysiological mechanisms remain unclear, leptin, resistin and ghrelin appear to play crucial roles in the interaction between metabolic syndrome and testicular function. All of this evidence supports the notion that the metabolic syndrome is a complex clinical entity characterized by pathophysiological mechanisms that affect the endocrine system as a whole; for these reasons it has been proposed to rename it ‘metabolic–neuroendocrine syndrome’.
Keywords: Metabolic syndrome, reproduction, testis, leptin, resisitin, ghrelin