Energy restriction ameliorates metabolic syndrome-induced cavernous tissue structural modifications in aged rats.

High-fat (HF) diet regular intake along life highly contributes to vascular dysfunction and to an increment in prevalence of metabolic syndrome (MetS) and erectile dysfunction (ED), a surrogate symptom of occult vascular disease, in the elderly. However, little is known about the effects of energy restriction (ER) alone/or after an HF-feeding period. We show here that in male Sprague-Dawley rats, 16 months of HF-diet consumption led to an increase in body adiposity, blood pressure, lipidemia, C-reactive protein, and insulin resistance and to hypoadiponectinemia, conditions that cluster in MetS. In addition, this treatment strongly favored collagen deposition in cavernous tissue and myocardium. Conversely, for the same time period, the ingestion of 75 % of ad libitum energy intake by controls (ER) extensively counteracted these outcomes. The impact of 6-month ER after 10-month HF period was also analyzed, and despite the decrease in body weight, adiposity, blood pressure, lipidemia, and C-reactive protein and improvement of insulin sensitivity, no differences were observed either in adiponectin blood levels or in retroperitoneal fat pad mass. Moreover, this treatment led to a reduction in cavernous tissue collagen deposition, but not in the myocardium, and evidenced differential mobilization of adipose tissue accretions. The data show the ability of HF diet to cause MetS and produce unwanted effects on myocardium and corpora vascular structure. They also indicate that these consequences are preventable upon ER diet starting early, but not later, in life.