June 20, 2012 in Neuroscience Researchers from Boston
University School of Medicine (BUSM) have demonstrated in experimental models
that blocking the Sigma-1 receptor, a cellular protein, reduced binge eating
and caused binge eaters to eat more slowly. The research, which is published
online in Neuropsychopharmacology, was led by Pietro Cottone, PhD, and
Valentina Sabino, PhD, both assistant professors in the pharmacology and
psychiatry departments at BUSM. Binge eating disorder, which affects
approximately 15 million Americans, is believed to be the eating disorder that
most closely resembles substance dependence. In binge eating subjects, normal
regulatory mechanisms that control hunger do not function properly. Binge
eaters typically gorge on "junk" foods excessively and compulsively
despite knowing the adverse consequences, which are physical, emotional and
social in nature. In addition, binge eaters typically experience distress and
withdrawal when they abstain from junk food. The researchers developed an
experimental model of compulsive binge eating by providing a sugary, chocolate
diet only for one hour a day while the control group was given a standard
laboratory diet. Within two weeks, the group exposed to the sugary diet
exhibited binge eating behavior and ate four times as much as the controls. In
addition, the experimental binge eaters exhibited compulsive behavior by
putting themselves in a potentially risky situation in order to get to the
sugary food while the control group avoided the risk. The researchers then
tested whether a drug that blocks the Sigma-1 receptor could reduce binge
eating of the sugary diet. The experimental data showed the drug successfully
reduced binge eating by 40 percent, caused the binge eaters to eat more slowly
and blocked the risky behavior. The abnormal, risky behavior exhibited by the binge
eating experimental group suggested to the researchers that there could be
something wrong with how decisions were made. Because evaluation of risks and
decision making are functions executed in the prefronto-cortical regions of the
brain, the researchers tested whether the abundance of Sigma-1 receptors in
those regions was abnormal in the binge eaters. They found that Sigma-1
receptor expression was unusually high in those areas, which could explain why
blocking its function could decrease both compulsive binge eating and risky
behavior. "These findings suggest that the Sigma-1 receptor may contribute
to the neurobiological adaptations that cause compulsive-like eating, opening
up a new potential therapeutic treatment target for binge eating disorder,"
said Cottone, who also co-directs the Laboratory of Addictive Disorders at BUSM
with Sabino. Journal reference: Neuropsychopharmacology
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