Researchers have found that one particular simple sugar, present in increased levels in diabetics, interferes with the chain of events needed to achieve and maintain erection and can lead to permanent penile impairment over time.
Previous research had shown that diabetic erectile dysfunction was partially due to an interruption in an enzyme that starts the chain of vascular events leading to an erection. The Hopkins team suspected O-GlcNAc, a blood sugar present in hyperglycaemic circumstances, to be that interrupting factor.
"We were interested to determine whether high glucose in diabetes mellitus modifies the endothelial nitric oxide synthase (eNOS) enzyme, which is responsible for the achievement and maintenance of erection," says Biljana Musicki, Ph.D., lead investigator of the study and a research associate in the Brady Urological Institute.
"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," Musicki explains.
O-GlcNAc hinders the 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.
The team also found that in comparison with the controls, diabetic rats' erectile response was 30 percent lower, full erections were 40 percent smaller and these erections took 70 percent longer to achieve.
The study emphasises the reduced blood vessel function present in patients with diabetes. "The mechanism we describe here 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," notes Musicki.
MEDICA.de; Source: Johns Hopkins Medical Institutions