Obesity is typically associated with abnormal eating behaviors. Brain imaging studies in humans implicate the involvement of dopamine (DA)-modulated circuits in pathologic eating behavior(s). Food cues increase striatal extracellular DA, providing evidence for the involvement of DA in the nonhedonic motivational properties of food. Food cues also increase metabolism in the orbitofrontal cortex indicating the association of this region with the motivation for food consumption. Similar to drug-addicted subjects, striatal DA D2 receptor availability is reduced in obese subjects, which may predispose obese subjects to seek food as a means to temporarily compensate for understimulated reward circuits. Decreased DA D2 receptors in the obese subjects are also associated with decreased metabolism in prefrontal regions involved in inhibitory control, which may underlie their inability to control food intake. Gastric stimulation in obese subjects activates cortical and limbic regions involved with self-control, motivation, and memory. These brain regions are also activated during drug craving in drug-addicted subjects. Obese subjects have increased metabolism in the somatosensory cortex, which suggests an enhanced sensitivity to the sensory properties of food. The reduction in DA D2 receptors in obese subjects coupled with the enhanced sensitivity to food palatability could make food their most salient reinforcer putting them at risk for compulsive eating and obesity. The results from these studies suggest that multiple but similar brain circuits are disrupted in obesity and drug addiction and suggest that strategies aimed at improving DA function might be beneficial in the treatment and prevention of obesity.
From the Medical Department (GJW, JSF), Brookhaven National Laboratory, Upton, NY; Mount Sinai School of Medicine (GJW, JSF), New York, NY; and National Institute of Drug Abuse/National Institute of Alcohol Abuse and Alcoholism (NDV, PKT), Bethesda, MD.
Received for publication September 16, 2008; accepted December 30, 2008.
Send correspondence and reprint requests to Gene-Jack Wang, MD, Medical Department, Brookhaven National Laboratory, Upton, New York, NY 11973. e-mail: email@example.com
Supported in part by grants from the U.S. Department of Energy OBER (DE-ACO2-76CH00016), the National Institute on Drug Abuse (5RO1DA006891-14, 5RO1DA6278-16, 5R21, DA018457-2), the National Institute on Alcohol Abuse and Alcoholism (RO1AA9481-11 & Y1AA3009), and by the General Clinical Research Center at Stony Brook University Hospital (NIH MO1RR 10710).