Fatty acid oxidation (FAO) has been implicated in the control of eating since the first demonstration of an increase in food intake in response to intraperitoneal injection of the FAO inhibitor mercaptoacetate (MA). The prevailing view for more than 20 years was that MA stimulates eating by inhibiting hepatic FAO, thus activating a vagal afferent signal from the liver. However, mounting evidence against an effect of hepatic FAO on eating demands an alternative explanation. Here I propose that MA may stimulate eating by inhibiting FAO in enterocytes and present some evidence supporting the idea that changes in enterocyte FAO can affect eating.