A gut lipid messenger links excess dietary fat to dopamine deficiency

Luis A. Tellez, Sara Medina, Wenfei Han, Jozelia G. Ferreira, Paula Licona-Limón, Xueying Ren, Tu Kiet T. Lam, Gary J. Schwartz, Ivan E. De Araujo

Research output: Contribution to journalArticlepeer-review

226 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)800-802
Number of pages3
Issue number6147
StatePublished - 2013

ASJC Scopus subject areas

  • General


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