Journal
SCIENCE
Volume 341, Issue 6147, Pages 800-802Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1239275
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Funding
- Yale Clinical and Translational Science Award [UL1RR024139]
- NIH [DC009997, DK085579, DK020541, DK026687]
- Ajinomoto USA
- Instituto de Ciencia y Tecnologia del Distrito Federal (Mexico) [BI10-164]
- China Scholarship Council (CSC) [201206260072]
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Excessive intake of dietary fats leads to diminished brain dopaminergic function. It has been proposed that dopamine deficiency exacerbates obesity by provoking compensatory overfeeding as one way to restore reward sensitivity. However, the physiological mechanisms linking prolonged high-fat intake to dopamine deficiency remain elusive. We show that administering oleoylethanolamine, a gastrointestinal lipid messenger whose synthesis is suppressed after prolonged high-fat exposure, is sufficient to restore gut-stimulated dopamine release in high-fat-fed mice. Administering oleoylethanolamine to high-fat-fed mice also eliminated motivation deficits during flavorless intragastric feeding and increased oral intake of low-fat emulsions. Our findings suggest that high-fat-induced gastrointestinal dysfunctions play a key role in dopamine deficiency and that restoring gut-generated lipid signaling may increase the reward value of less palatable, yet healthier, foods.
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