Brain dopamine and obesity
Brain dopamine and obesity
复制标题
DOI：
10.1016/s0140-6736(00)03643-6
复制
发表时间：
2001-02-03
期刊：
影响因子：
168.9
通讯作者：
Fowler, JS
中科院分区：
文献类型：
--
作者：
Wang, GJ;Volkow, ND;Fowler, JS
背景导致病理性暴饮暴食和肥胖的行为背后的大脑机制知之甚少。多巴胺，一种调节食物奖赏特性的神经递质，可能与此有关。为了验证这一假设，肥胖的人有异常的大脑多巴胺活动，我们测量了多巴胺D-2受体在brain.Methods脑多巴胺D-2受体的可用性测定与正电子发射断层扫描（PET）和[C-11]雷氯必利（放射性配体的多巴胺D-2受体）。Bmax/Kd（纹状体与小脑中分布体积的比值减1）被用作多巴胺D-2受体可用性的量度。结果：10名肥胖者纹状体多巴胺D-2受体的利用率（2.47 [SD 0.36]）显著低于对照组（2.99 [0.41]; p小于或等于0.0075）。在肥胖个体中，体重指数（BMI）与D-2受体的测量值呈负相关（r=0.84; p ≤ 0.002）; D-2值最低的个体具有最大的BMI。相比之下，无论是全脑还是纹状体代谢肥胖个体和对照组之间的差异，表明纹状体D-2受体的减少是不是由于放射性示踪剂delivery.Interpretation的系统性减少多巴胺D-2受体的可用性在肥胖个体中的比例下降，他们的BMI。多巴胺调节动机和奖励回路，因此肥胖个体的多巴胺缺乏可能使病理性进食永久化，作为补偿这些回路激活减少的手段。旨在改善多巴胺功能的策略可能对肥胖个体的治疗有益。
Background The cerebral mechanisms underlying the behaviours that lead to pathological overeating and obesity are poorly understood. Dopamine, a neurotransmitter that modulates rewarding properties of food, is likely to be involved. To test the hypothesis that obese individuals have abnormalities in brain dopamine activity we measured the availability of dopamine D-2 receptors in brain.Methods Brain dopamine D-2 receptor availability was measured with positron emission tomography (PET) and [C-11]raclopride (a radioligand for the dopamine 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 receptor 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 lower in the ten obese individuals (2.47 [SD 0.36]) than in controls (2.99 [0.41]; p less than or equal to0.0075). In the obese individuals body mass index (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 had 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 radiotracer delivery.Interpretation The availability of dopamine D-2 receptor was decreased in obese 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 activation of these circuits. Strategies aimed at improving dopamine function may be beneficial in the treatment of obese individuals.