Erectile dysfunction is a common problem for more than half of men with diabetes. A recent study from the Brady Urological Institute at Johns Hopkins suggests that an over-supply of a simple blood sugar could be a major cause of erectile dysfunction in diabetic men.

Describing the mechanism of erection, the research team has determined that high glucose in diabetes mellitus is an interrupting factor of this process.

Erection begins when a sexual stimulus activates the enzyme neuronal nitric oxide synthase (nNOS) that causes short-term release of nitric oxide (NO) at the nerve endings in the penis.

This initial release of NO causes short-term and rapid increases in penile blood flow and short-term relaxation of the penile smooth muscle, initiating an erection. The resulting expansion of penile blood vessels and smooth-muscle relaxation allows more blood to flow into the penis. This increased blood flow (shear stress) activates the eNOS in penile blood vessels causing sustained NO release, continued relaxation and full erection.

O-GlcNAc, a blood sugar present in hyperglycemic (high blood sugar) circumstances, hinders this normal chain of events by inhibiting the activation of eNOS, and consequently reducing the release of NO and preventing the smooth muscle in the penis from relaxing. Without this relaxation, there is no shear stress to stoke the production of more NO and therefore, no normal, sustained erection.

This is not the same type of erectile dysfunction seen in non-diabetics, and it is less effectively treated with conventional drugs like Viagra. The mechanism described above stresses the critical importance of vascular function in the erectile response. It may suggest new ways of treating erectile dysfunction by targeting specifically this mechanism in penile erection.