Erectile dysfunction in diabetes is due to defect in brain
March 15, 2007
A new study shed additional
light on how erectile dysfunction (ED) interacts
with diabetes. The study is an additional step
in detection the association between the two
disorder, and may lead to better efficiency
in erectile dysfunction treatments
Sexual dysfunction is a well-recognized
outcome of diabetes mellitus in men. Erectile
dysfunction and the loss of seminal emission
have all been described by such patients. This
study examines induce penile erection, yawning
and stretch in diabetic rats. Male Sprague-Dawley
rats treated with streptozotocin (STZ) to persuade
diabetes were used as they put on display sexual
and behavioral symptoms similar to those found
in diabetic
men with erectile dysfunction.
The researchers focused on
the paraventricular nucleus (PVN) of the hypothalamus,
situated in the brain, an addition center between
the central and peripheral nervous systems.
The site is implicated in numerous functions,
including erectile function and sexual behavior,
and is a primary site within the forebrain that
has been implicated in penile erection. The
investigators also examined central nitric oxide
which plays an significant role in the neurotransmission
of normal penile erection.
Penile erection is a behavioral
reaction that occurs in answer to the administration
of N-methyl-D-aspartic acid within the PVN.
At the same time, self-consciousness of NO synthase
with NG-monomethly-L-argining prevents NMDA-induced
erection. The researchers hypothesized that
the dull NMDA mediated response in diabetes
reflects an impaired NO instrument within the
PVN. The involvement of an NO mechanism in the
NMDA mediated behavioral response was also explored.
Four experiments were conducted.
Experiment one observe the effect of L-NMMA
on NMDA mediated behavioral responses in normal
rats; experiment two measured behavioral responses
to NMDA or sodium nitroprusside (SNP), an NO
donor in both control and diabetic rats; the
third experiment observed the effect of diabetes
on nNOS protein in the PVN; the fourth experiment
measured NMDA mediated behavioral responses
in diabetic rats after restoring the nNOS protein
in the PVN using viral gene transfer.
So the researchers finish
off saying that erectile dysfunction in diabetes
is due to a discriminating imperfection in the
NO mechanisms within the PVN. This defect is
a loss in the synthetic enzyme for the production
of NO within the neurons of the PVN. Restoring
this synthetic enzyme may have a significant
therapeutic value for diabetic patients with
erectile dysfunction.
Source:
http://www.eurekalert.org/pub_releases
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