Testosterone is the main male hormone controlling sexual and reproductive functions. Testosterone deficiency is associated with male hypogonadism, a syndromic condition that encompasses the well-recognised sexual and reproductive failure. Male hypogonadism has been, in fact, recently associated to an increased cardiovascular and metabolic risk (metabolic syndrome), most probably because testosterone deficiency is a stigmata of visceral adiposity. A stepwise reduction in testosterone has been described in human and animal models of increased abdominal adiposity. The biological significance of obesity-induced testosterone deficiency is still a matter of debate, because it can have a detrimental effect, further increasing visceral fat accumulation, or a protective role, by limiting reproductive potential, or it can represent only a marker of a decreased wellness. Nonetheless, meta-analysis of intervention trials on hypogonadism in metabolic syndrome indicate that testosterone supplementation can increase insulin sensitivity and decrease visceral adiposity. Although it is generally assumed that a decreased androgen signalling will restrain prostate overgrowth, having therefore a therapeutic potential for benign prostate hyperplasia (BPH), recent data indicate that both metabolic syndrome and obesity-induced hypogonadism might have a causative role on BPH-associated lower urinary tract symptoms (LUTS). In an animal model of high fat diet-induced metabolic syndrome and hypogonadism, we found that the prostate, as well as the liver, was affected by fibrosis, hypoxia and inflammation. Similar changes, although of a more limited extent, was observed in the bladder. Testosterone supplementation was able to revert hypoxia and fibrosis and to decrease prostate and bladder inflammation. It is therefore conceivable that testosterone supplementation in pathological conditions, such as metabolic syndrome, might have favourable effects not only in increasing insulin sensitivity and decreasing visceral adiposity, but also in ameliorating prostate function and LUTS.
Declaration of interest: The author declares that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector
05 - 09 May 2012
European Society of Endocrinology