Brain dopamine and obesity

Background The cerebral mechanisms underlying the behaviours that lead to p athological overeating and obesity are poorly understood. Dopamine, a neuro transmitter that modulates rewarding properties of food, is likely to be in volved. To test the hypothesis that obese individuals have abnormalities in brain dopamine activity we measured the availability of dopamine D-2 recep tors in brain. Methods Brain dopamine D-2 receptor availability was measured with positron emission tomography (PET) and [C-11]raclopride (a radioligand for the dopa mine D-2 receptor). Bmax/Kd (ratio of the distribution volumes in striatum to that in cerebellum minus 1) was used as a measure of dopamine D-2 recept or availability. Brain glucose metabolism was also assessed with 2-deoxy-2[ F-18]fluoro-D-glucose (FDG). Findings Striatal dopamine D-2 receptor availability was significantly lowe r in the ten obese individuals (2.47 [SD 0.36]) than in controls (2.99 [0.4 1]; p less than or equal to0.0075). In the obese individuals body mass inde x (BMI) correlated negatively with the measures of D-2 receptors (r=0.84; p less than or equal to0.002); the individuals with the lowest D-2 values ha d the largest BMI. By contrast, neither whole brain nor striatal metabolism differed between obese individuals and controls, indicating that striatal reductions in D-2 receptors were not due to a systematic reduction in radio tracer delivery. Interpretation The availability of dopamine D-2 receptor was decreased in o bese individuals in proportion to their BMI. Dopamine modulates motivation and reward circuits and hence dopamine deficiency in obese individuals may perpetuate pathological eating as a means to compensate for decreased activ ation of these circuits. Strategies aimed at improving dopamine function ma y be beneficial in the treatment of obese individuals.