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April 12, 2010
Drug Abuse and Obesity Share Brain Mechanism
Some brain mechanisms that contribute to drug addiction in humans also play a role in compulsive eating and the development of obesity in rats, according to a new study. If true in people, the finding may open doors to new approaches for reducing obesity.
Both compulsive eating and drug addiction have been previously linked to a problem in the brain’s reward system. In both cases, overconsumption can trigger a gradual increase in what scientists call the "reward threshold"—that is, over time, more of a palatable, high-fat food or a reinforcing drug is needed to satisfy the craving. Studies have implicated a brain signaling molecule called dopamine in this process. Paul M. Johnson and Dr. Paul J. Kenny of the Scripps Research Institute’s Florida campus set out to further investigate these relationships in rats. Their work was partly funded by NIH’s National Institute on Drug Abuse (NIDA).
The researchers examined 3 groups of male rats over a 40-day period. All the rats had unlimited access to standard chow. Two of the groups also had access to high-fat "cafeteria" foods for short (1-hour) or long (18-23 hours) periods each day. The foods included bacon, sausage, cheesecake, pound cake, frosting and chocolate. After 40 days, all the rats were denied access to the high-fat foods. The researchers observed the feeding behaviors of each group and measured their caloric intake and weight gain. They also directly measured the rats' brain reward circuits for reward thresholds. Their results appeared in the online version of Nature Neuroscience on March 28, 2010.
Rats with extended access to the cafeteria diet, the researchers found, gained a significant amount of weight compared to the other groups. Their total caloric intake was almost twice that of the other groups, and nearly all their calories came from the high-fat cafeteria foods. The restricted-access rats ate about the same number of calories as the chow-only rats, but they developed binge-like feeding behavior, consuming about 66%, of their daily calories in their hour of access to the cafeteria diet. These rats also gained some weight relative to the chow-only group, but the difference wasn't statistically significant.
As the extended-access rats became more obese, their brain reward thresholds gradually rose. These elevated reward thresholds persisted for at least 2 weeks after access to the cafeteria diet was withdrawn.
The researchers next examined type 2 dopamine receptors (D2R), which have been shown to play a key role in addiction, in a core region of the brain’s reward circuits. As the rats became obese, their levels of D2R in the area decreased, similar to drops seen in humans addicted to drugs like cocaine or heroin.
When the researchers genetically knocked down D2Rs, rats with extended access to the cafeteria diet quickly developed higher reward thresholds and showed compulsive eating behaviors. Even when the rats were conditioned to expect a shock, those with extended access to the cafeteria diet weren't discouraged from eating.
"Hopefully, this study will change the way people think about eating," Johnson says. "It demonstrates how just the availability of junk food can trigger overconsumption and obesity."
"The results of this study could provide insight into a mechanism for obesity," Kenny says. "It's possible that drugs developed to treat addiction may also benefit people who are habitual overeaters."