The weight-loss drug sibutramine may work by changing the way two particular brain regions respond to mouth-watering junk foods, a new study suggests. Though sibutramine has been criticized for posing health risks, researchers say the new findings could be used to inform the development of future drugs.
Overweight individuals who took the drug saw a decrease in the activity of their hypothalamus and amydala — two brain regions thought to play roles in appetite regulation and eating behavior — when they viewed pictures of appetizing, high-calorie foods.
Interestingly, the drugs’ effect on the brain differed from that of fullness — when participants were full, a different brain region, called the ventral striatum, showed reduced activity in response to the appetizing foods. This suggests the way the drug curbs eating is different from the way being full limits eating, said study researcher Paul Fletcher, of the University of Cambridge in the United Kingdom.
The study will be published tomorrow (Oct. 27) in The Journal of Neuroscience.
Sibutramine and the brain
Sibutramine, known by the brand name Meridia, is an anti-obesity drug that was approved by the U.S. Food and Drug Administration in 1997 after studies found it could reduce body weight by at least 5 percent in obese individuals. However, it was taken off the market this month because a study found it was linked to an increased risk of heart attack and stroke.
Scientists know sibutramine blocks the transmission of certain chemical signals in the nervous system, but it’s not clear how this blockage leads to changes in eating behavior.
Fletcher and his colleagues had 28 overweight individuals, ages 18 to 45, take either sibutramine or a placebo for two weeks. Toward the end of the treatment, they scanned the participants’ brains twice — once after fasting, and once after eating. During the scans, participants viewed images of high-calorie foods, such as chocolate, and low-calorie foods, such as broccoli. This experiment was repeated in a second round, and the participants took the opposite treatment from what they had during the initial two weeks.
High-calorie foods activated many areas of the brain in the participants who were on the placebo. But while on the drug, they had decreased activity in their hypothalamus and amydala when they looked at these images, regardless of whether they had eaten or were full.
Moreover, the participants who had the greatest reductions in activity in these regions were those who tended to lose more weight and eat less while on the drug, the researchers said.
How does it work?
It’s not clear how reductions in activity of the hypothalamus and amydala act to change eating behavior. But it’s possible that activation of these regions may reflect how highly someone values something, and changing this brain circuitry with a drug “makes the foods less compelling and less likely to overcome a person’s willpower,” Fletcher told MyHealthNewsDaily.
The study was funded by GlaxoSmithKline, the Wellcome Trust, the Bernard Wolfe Health Neuroscience Fund, among others.
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