High-fat diet induces obesity in adult mice but fails to develop pre-penile and penile vascular dysfunction.

Abstract

Obesity can lead to cardiovascular disease, diabetes, and erectile dysfunction (ED) which decreases overall quality of life. Mechanisms responsible for obesity induced ED are unknown. Current mouse models of high fat diet (HFD) induced obesity yield conflicting results. Genetic variants among common “wild type” strains may explain contradictory data. Adult male C57BL/6N and 6J mice were fed a 45% HFD for 12 weeks. Weekly food intake, weight gain, and body fat percentage were measured. After 12 weeks, ex vivo vascular reactivity was measured in aortas, internal pudendal arteries, and penises. We assessed smooth muscle contractility, endothelial-dependent and -independent relaxation, and penile neurotransmitter mediated relaxation. C57BL/6N mice developed greater obesity and glucose sensitivity compared to C57BL/6J mice. Aortas from both strains fed a HFD had decreased contraction, yet contraction was unchanged in HFD pudendal arteries and penises. Interestingly, endothelial-dependent and -independent relaxation was unchanged in both systemic and penile vasculature. Likewise, HFD did not impair penile neurotransmitter mediated relaxation. Both strains fed 12 weeks of HFD developed obese phenotypes. However, HFD did not impair pre-penile or penile smooth muscle vasoreactivity as demonstrated in previous studies, suggesting this preclinical model does not accurately represent the clinical phenotype of obesity induced ED.