Type 1 and Type 2 Diabetic‐Erectile Dysfunction: Same Diagnosis (ICD‐9), Different Disease?

Abstract

ABSTRACT Introduction Although hyperglycemia is a common defining feature of both type 1 and type 2 diabetes, many unique characteristics distinguish these diseases, including insulin and lipid levels, obesity status, and inflammatory agent profiles. In the laboratory, the presence of erectile dysfunction (ED) has been established in animal models of both type 1 and type 2 diabetes. Aim The purpose of this study was to determine whether unique mechanisms underlie ED in type 1 vs. type 2 diabetic animal models. Main Outcome Measures Many mechanisms can underlie ED, including impaired dilatory signaling, heightened contractile sensitivity, and veno-occlusive disorder. Methods Using PubMed, the literature was mined to evaluate what is known about which mechanism underlie ED in type 1 vs. type 2 diabetic animal models. Results Impaired cavernosal vasodilation has been established in type 1 diabetic rodents. This dysfunction appears to be mediated by a severe defect in non-adrenergic–non-cholinergic nerve signaling, as well as impairment in penile endothelial function. In contrast, type 2 diabetic animals appear to have minimal impairment in parasympathetic-mediated dilatory function, but do have evidence of endothelial dysfunction. Type 2 diabetic models also exhibit a significant and striking increase in cavernosal contractile sensitivity, and a significant veno-occlusive disorder, neither of which is consistently reported in type 1 diabetic animals. Conclusions With the distinct mechanisms underlying the ED phenotype in animal models of type 1 and type 2 diabetes, tailoring therapeutic treatments for diabetic-ED to the specific mechanisms underlying this disease complication may be warranted. Further examination of mechanisms underlying ED in diabetic human patients may thus lead to significant changes in the way urologists diagnose, code, and treat diabetic-ED.