THE EFFECT OF A HIGH FRUCTOSE DIET ON ERECTILE FUNCTION IN BILATERAL CAVERNOUS NERVE INJURY RAT MODEL

Metabolic syndrome (MetS) is a cluster of many risk factors, such as insulin resistance, elevated blood glucose levels, and hypertension. In addition, excessive consumption of fructose is likely to increase the risk of developing MetS. Previous data suggest a causal association between MetS and erectile dysfunction (ED). ED, a common complication of radical prostatectomy (RP) for treating prostate cancer, is caused by cavernous nerve damage. MetS can increase the risk of prostate cancer and may also exacerbate the severity of the disease. Furthermore, patients with MetS who have RP are likewise more likely to develop ED. MetS induces insulin resistance, related to nerve injury and decreased neuron regeneration. The current study aimed to assess the effect of MetS on ED in a rat model with bilateral cavernous nerve injury (BCNI).

Male Wistar Albino rats (n = 32) were divided into four groups: 1) Sham-operated control rats, 2) BCNI rats, 3) fructose-treated (10 % in drinking water, 1 month)-rats, and 4) fructose-treated and BCNI rats. In vivo erectile responses and in vitro relaxant responses were measured. Western blot and immunohistochemistry analyses were used to determine the expression and localization of endothelial nitric oxide synthase (eNOS), neuronal NOS (nNOS), transforming growth factor-beta (TGFbeta1), hypoxia-inducible factor-1 alpha (HIF-1alpha). The ratio of smooth muscle to collagen was calculated using Masson trichrome.

Rats with MetS displayed a reduced erectile response, worsened by BCNI. The rats with BCNI and MetS had reduced relaxant responses to acetylcholine and electrical field stimulation (EFS), as well as contractile responses to phenylephrine, EFS, and KCl in corpus cavernosum strips. MetS further decreased eNOS and nNOS protein levels in BCNI rats. MetS also increased TGFbeta1 and HIF-1alpha protein expression, partially reducing smooth muscle mass, with BCNI amplifying this effect.

High fructose consumption and cavernous nerve damage from BCNI increased MetS, resulting in ED via reducing endothelial and neurogenic relaxation. The interaction of inflammatory mediators is likely to lead to MetS and ED. Additional research is needed to properly elucidate the underlying mechanism of MetS and CNI-induced ED.

There is no conflict of interest.