The Role of Dopamine Deficiency in Obesity

Dopamine, a potent neural transmitter found in the human brain, has been implicated in a variety of reward circuits including eating.  It has been well established that the production of dopamine in the dorsal striatum of the brain markedly increases during feeding in both rodents and humans.  Controlled levels of dopamine production are also required for normal eating behavior.  These finding are consistent with the known role that dopamine plays in the reward circuitry of the brain. 

Given this critical role played by dopamine in relation to eating behavior, it has been suggested that overeating may be a compensation for a diminished function in regard to the reward circuitry dependent upon dopamine levels.  In fact, dopamine receptor deficiency has been reported in studies involving obese patients.  This is certainly consistent with significantly reduced response to food stimuli in individuals suffering from obesity.  Additionally, rats that were purposefully depleted of dopamine receptors demonstrated obsessive feeding behavior.

The physiological mechanism linking incessant high-fat intake to dopamine deficiency has been unclear.   Dr. Luis A. Tellez and his colleagues at the John B Pierce Laboratory in New Haven, CT focused their research in an attempt to elucidate the physiological mechanism linking obesity and dopamine levels in the brain.  In their experimental approach, they administered oleoylethanolamine to mice fed a diet rich in fat.  Oleoylethanolamine is, in fact, a lipid messenger whose production is suppressed in individuals subjected to high-fat dietary intake.  Upon administration of this lipid messenger, the experimental mice demonstrated increased levels of dopamine release.   Exposure of these mice to oleoylethanolamine also reinstated normal eating habits.

From these data, the authors of this report concluded that high-fat dietary intake as evidence of gastrointestinal malfunction seems to play a pivotal role in dopamine deficiency and, most importantly, restoring gut-related lipid messenger may  increase the reward feedback mechanism in regard to the intake of healthier lower-fat food.