title: Type 1 and Type 2 diabetic-erectile dysfunction: same diagnosis (ICD-9), different disease?
abstract: BACKGROUND
  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.
  
  
  OBJECTIVE
  The purpose of this study was to determine whether unique mechanisms underlie ED in type 1 vs. type 2 diabetic animal models.
  
  
  METHODS
  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.
authors.affiliation: University of Washington, Department of Urology, Seattle, WA 98109, USA. kanchanc@u.washington.edu
authors.forename: Kanchan
authors.initials: K
authors.lastname: Chitaley
mesh_terms: D000818:Animals; D001682:Biological Availability; D003922:Diabetes Mellitus, Type 1 / Q000150:complications*; D003924:Diabetes Mellitus, Type 2 / Q000150:complications*; D003937:Diagnosis, Differential; D004195:Disease Models, Animal; D004558:Electric Stimulation; D004576:Electromyography; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology; D007172:Erectile Dysfunction / Q000175:diagnosis* / Q000209:etiology*; D006801:Humans; D038801:International Classification of Diseases; D008297:Male; D009119:Muscle Contraction / Q000502:physiology; D009130:Muscle, Smooth / Q000201:enzymology; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism; D010413:Penis / Q000098:blood supply; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism; D014661:Vasoconstriction; D014680:Veins
chemical_list: D011942:Receptors, Adrenergic, alpha; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase