Biochemical pathway may link addiction,
compulsive eating
Source: UCSF press release
Date: September 1, 2010
Ezlopitant, a compound known to suppress craving for
alcohol in humans, was shown to decrease consumption of
sweetened water by rodents in a study by researchers at
the Ernest Gallo Clinic and Research Center, which is
affiliated with the University of California, San
Francisco.
“This finding suggests a possible link between the
neurochemical pathways for addiction and compulsive
eating,” says principal investigator Selena Bartlett,
PhD, Director of the Pre-Clinical Development Group at
the Gallo Center.
The study will be published online in PLoS
One on September 1, 2010.
Ezlopitant is an NK1 receptor-antagonist, a class of
drugs that blocks the action of substance P, a
neurotransmitter that is believed to play a role in the
reward system. The reward system is a complex of brain
structures that, among other things, governs craving
for, and addiction to, alcohol and drugs.
“Substance P is released in your brain in response
to certain stimuli, and needs to bind with receptors on
neurons in order to have an effect,” Bartlett
explains. “The NK1 receptor is where it binds, and
ezlopitant prevents that binding.”
In the study, rats given ezlopitant showed
significantly decreased motivation to consume water
sweetened with sugar, water sweetened with saccharin,
and an alcohol solution.
Bartlett believes one possible explanation is that
the NK1 receptor is part of the same reward system that
links compulsive craving for sweets with craving for
drugs and alcohol.
“In other studies, NK1-receptor antagonists have
been shown to decrease craving for alcohol in humans
with alcohol-use disorder,” she says. “In our
study, the decrease in the rats’ consumption of
sweetened water was, in fact, even greater than their
decrease in alcohol consumption. For the first time,
we’ve shown that this receptor might be a target for
compulsive eating. We’re looking at a potentially
promising new approach to addressing pathological food
addiction.
Bartlett notes that her laboratory is focused on the
development of medications for human use, so,
“naturally,” she says, “we’d like to see this
experiment replicated in humans as soon as
possible.”
Co-authors of the study were Pia Steensland of the
Karolinksa Institut, Stockholm, Sweden, and Jeffrey A.
Simms, Carsten K. Nielsen, Joan Holgate, and Jade J.
Bito-Onon of the Preclinical Development Group at the
Gallo Center.
The study was supported by funds from the State of
California for medical research on alcohol and
substance abuse through UCSF, and from the US
Department of Defense.
The UCSF-affiliated Ernest Gallo Clinic and Research
Center is one of the world’s preeminent academic
centers for the study of the biological basis of
alcohol and substance use disorders. Gallo Center
discoveries of potential molecular targets for the
development of therapeutic medications are extended
through preclinical and proof-of-concept clinical
studies.
UCSF is a leading university dedicated to promoting
health worldwide through advanced biomedical research,
graduate-level education in the life sciences and
health professions, and excellence in patient care.
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