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Wisconsin Study Links Carbohydrate Overeating to Opiate Reaction

Madison, Wisconsin - Stimulating the same brain receptors that respond to opiate drugs (such as morphine or heroin) triggers rats to binge on carbohydrates, further evidence that eating disorders share certain biological pathways with drugs of abuse.

 

Brian Baldo in labPrior research has established the important role of brain opiates in feeding. However, the current study is the first to identify opiate-sensitive "hot spots" in frontal brain structures charged with higher-level reasoning.

 

This finding may hint at why poorly modulated food or drug intake is so difficult to control.

 

"These findings may help us better understand emotional eating and loss of restraint that are present during certain eating disorders," says Dr. Brian Baldo, the study's author and an assistant professor of psychiatry at the University of Wisconsin School of Medicine and Public Health. "They could also suggest some potential drug pathways for treatment."

 

The research was published today in the March edition of the Journal of Neuroscience. Baldo and colleagues stimulated the ventromedial prefrontal cortex (vmPFC) of the rats with a substance called DAMGO - a synthetic equivalent of an opioid peptide normally produced in the brain. These chemicals, known as endorphins (endogenous morphine, the "brain's own opiates") are naturally triggered by pleasurable activities.

 

"They can trigger a sense of reward and this modifies behavior," Baldo said. He explained that while previous research had shown this effect in other regions of the brain - such as the hypothalamus and nucleus accumbens - no one had looked to see if the opioids also affected the prefrontal cortex, a crucial site for high-level cognition and impulse control.

 

When stimulated in the prefrontal cortex with DAMGO, the rats became hyperactive, and then gorged on food. The researchers tried stimulating other receptors and regions of the cortex, and using other peptides, but none produced this highly specific response.

 

The DAMGO stimulation did not induce the rats to drink water more heavily, even when they were thirsty. Nor did it matter if the rats were well-fed or hungry - all gorged on food when stimulated with DAMGO.

 

In a second round of experiments, the researchers tried to see if the DAMGO-stimulated rats preferred a specific type of tasty food, either high-fat rat chow or high-carbohydrate rat food. All the rats, even those who normally preferred high-fat food, greatly preferred carbohydrates during the DAMGO-induced binges.

 

While the findings are novel, Baldo says they make sense in the context of clinical reports that the opiate-blocking drug, naltrexone, curbs food bingeing and reduces drug cravings in addicts. Furthermore, the frontal parts of the brain often show aberrant activity in drug addicts and patients with eating disorders. The DAMGO stimulation may mimic situations in which triggers such as stress release opioid peptides in the prefrontal cortex, and thereby induce disordered eating.

 

"This suggests that μ-opioid receptors, and other pathways that communicate with the prefrontal cortex mu-opioid system, could be targets for drug development. This could lead to novel medications to treat eating disorders," Baldo says.

 

Members of Baldo's team include Ken Sadeghian and Jesus Mena, a graduate student in the UW-Madison Neuroscience Training Program. Their research was supported by a grant from the National Institute of Mental Health.



Date Published: 03/02/2011

News tag(s):  researchbrainobesitypsychiatryneurosciences

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Last updated: 03/14/2011
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