The surgery for morbid obesity reduces the release of neurotransmitter dopamine, which in turn decreased sugar-seeking behavior in mice that had the surgery, researchers report Nov. 19 in the journal Cell Metabolism.
The authors say weight loss might be achieved by bariatric surgeries because they prevent nutrient signals generated in the upper intestine from reaching the reward’s brain circuitry.
“We hope our work will provide new insights into how different bariatric interventions may lead to a diverse repertoire of behavioral modifications,” said Yale’s Ivan de Araujo of the John B. Pierce Laboratory, senior author of the study. “Ultimately we would like to clarify the mechanisms by which these surgeries benefit behavior, so that less invasive and more affordable therapies may develop.”
Subjects who undergo bariatric surgery to treat obesity or diabetes report changes in food preferences but scientists have been unclear exactly why. So scientists mimicked a form of bariatric surgery in mice conditioned to seek sugar by connecting the stomach to a lower part of the intestine, bypassing the upper small intestine. The authors hypothesized that this gastrointestinal rerouting would lead to changes in dopamine release in the dorsal striatum, a neurochemical event associated with calorie intake. They found that dopamine release in the dorsal striatum region of the brain was reduced.
Mice who underwent this surgery did not continue to seek sweet rewards, unlike animals that had not had the procedure. When researchers activated the dorsal striatum in these mice, the cravings for sugar returned, reversing the behavioral effects of the surgery.
De Araujo said it would be wrong to conclude that the mechanisms of bariatric surgery have been fully explained, and that more research needed to be done to definitively determine why bariatric surgeries tend to reduce calorie intake in subjects.
Wenfei Han of the Pierce Laboratory and Tongji University in Shanghai, China is lead author of the study.
The research was funded by the National Institutes of Health.
Contact Bill Hathaway [email protected] 203-432-1322