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.
J Addict Med. 2009 Mar;3(1):8-18. doi: 10.1097/ADM.0b013e31819a86f7.
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.
肥胖通常与异常的进食行为有关。人类的大脑成像研究表明，多巴胺（DA）调节回路参与病理性进食行为。食物线索会增加纹状体细胞外的 DA，这为 DA 参与食物的非享乐动机特性提供了证据。食物线索也会增加眶额皮质的代谢，表明该区域与食物消费的动机有关。与吸毒成瘾者类似，肥胖者的纹状体 DA D2 受体可用性降低，这可能使肥胖者倾向于寻求食物作为暂时补偿奖励回路刺激不足的手段。肥胖者前额叶区域参与抑制控制的 DA D2 受体减少，也与代谢减少有关，这可能是他们无法控制食物摄入的原因。肥胖者的胃刺激会激活与自我控制、动机和记忆相关的皮质和边缘区域。这些大脑区域在吸毒成瘾者的药物渴望中也会被激活。肥胖者的躯体感觉皮层代谢增加，这表明他们对食物的感官特性更加敏感。肥胖者 DA D2 受体减少，加上对食物美味的敏感性增加，可能使食物成为他们最明显的强化物，使他们面临强迫性进食和肥胖的风险。这些研究结果表明，肥胖和药物成瘾中多个但相似的大脑回路被破坏，并表明旨在改善 DA 功能的策略可能对肥胖的治疗和预防有益。
