PS 21. Mechanisms of diabetes associated erectile dysfunction
Plenary Session

PS 21. Mechanisms of diabetes associated erectile dysfunction

Hunter Wessells

Department of Urology, University of Washington, Washington, USA

We used animal experimental approaches and human subjects to identify novel strategies for intervention and prevention against diabetes associated erectile dysfunction. Expression array analysis from streptozotocin (STZ) induced diabetic rats and citrate buffer controls identified genes differentially expressed in diabetic ED. One gene product, the copper binding protein ceruloplasmin, is overexpressed in diabetes. Targeted deletion of this gene, or chelation of copper directly, mitigated the deleterious effects of STZ diabetes in mice.

Longitudinal studies of 571 men with T1D enrolled in the Epidemiology of Diabetes Intervention and Complication study revealed that intensive glycemic control reduced the risk of subsequent ED (OR 0.62 95% CI 0.41-95, P=0.027) and that five-year mean systolic blood pressure exceeding 120 mmHg was associated with a significantly increased risk of ED (HR 1.5-3.3). Testosterone levels failed to reveal hypogonadism as a significant influence on ED. Finally, a pilot genome wide association search of the cohort identified two SNPs located on chromosome 3 in one genomic loci that were associated with ED with p < 1x 10- 7. Both of these SNPs were < 1Mb from the ALCAM (activated leukocyte cell adhesion molecule) gene.

Analyses performed in conjunction with the Urological Diseases in America project revealed that men with diabetes have a significantly higher probability of requiring second and third line therapy for the treatment of ED, and that the cost of these treatments are higher as well. Taken together, even without the advent of new pharmacological agents, current data justified a combination of intensive glucose and blood pressure that has the potential to reduce the risk of ED in men with type 1 diabetes.

DOI: 10.3978/j.issn.2223-4683.2012.s259

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