Role of insulin and testosterone in prostatic growth: who is doing what?

Previous studies have demonstrated increased incidence of benign prostatic hyperplasia in insulin-resistant individuals. In addition to androgens, prostatic growth is sensitive to the peptide growth factors including insulin. Experimental studies employing intervention of selective β-cell toxin streptozotocin and castration suggest that depletion of either insulin or testosterone results in the severe prostatic atrophy (>80%). Exogenous testosterone and diet-induced experimental hyperinsulinemia induces prostatic enlargement in rats. Further, hyperinsulinemia sensitizes prostate towards the growth promoting effect of testosterone, and testosterone augments prostatic growth even in the hypoinsulinemic rats. However, in castrated rats diet-induced hyperinsulinemia fails to promote prostatic growth. Based on these evidences it is hypothesized that in the presence of testosterone insulin plays an important role in the prostatic growth. The epidemiological reports witnessing increased incidences of prostatic enlargement in men with metabolic syndrome, which are known to have increased level of insulin, provides a validating clue to the hypothesis. Further, the hypothesis suggests that targeting insulin signaling pathway could be a new objective for the treatment of prostatic enlargement.