Department of Endocrinology and Metabolism, Academic Medical Center, Amsterdam, Netherlands.
Department of Nuclear Medicine, Academic Medical Center, Amsterdam, Netherlands.
Metabolism. 2018 Aug;85:325-339. doi: 10.1016/j.metabol.2017.09.007. Epub 2017 Sep 29.
Obesity results from an imbalance between energy intake and expenditure, and many studies have aimed to determine why obese individuals continue to (over)consume food under conditions of caloric excess. The two major "neurotransmitter hypotheses" of obesity state that increased food intake is partially driven by decreased dopamine-mediated reward and decreased serotonin-mediated homeostatic feedback in response to food intake. Using molecular neuroimaging studies to visualize and quantify aspects of the central dopamine and serotonin systems in vivo, recent PET and SPECT studies have also implicated alterations in these systems in human obesity. The interpretation of these data, however, is more complex than it may appear. Here, we discuss important characteristics and limitations of current radiotracer methods and use this framework to comprehensively review the available human data on central dopamine and serotonin in obesity. On the basis of the available evidence, we conclude that obesity is associated with decreased central dopaminergic and serotonergic signaling and that future research, especially in long-term follow-up and interventional settings, is needed to advance our understanding of the neuronal pathophysiology of obesity in humans.
肥胖是由于能量摄入和消耗之间的不平衡引起的，许多研究旨在确定为什么肥胖者在热量过剩的情况下继续（过度）摄入食物。肥胖的两个主要“神经递质假说”表明，食物摄入的增加部分是由多巴胺介导的奖励减少和对食物摄入的血清素介导的体内平衡反馈减少驱动的。使用分子神经影像学研究来可视化和量化体内中央多巴胺和血清素系统的各个方面，最近的 PET 和 SPECT 研究也表明这些系统的改变与人类肥胖有关。然而，对这些数据的解释比表面上看起来要复杂。在这里，我们讨论了当前示踪剂方法的重要特征和局限性，并使用这个框架全面回顾了肥胖症中中枢多巴胺和血清素的现有人类数据。根据现有证据，我们得出的结论是，肥胖与中枢多巴胺能和血清素能信号的减少有关，需要进行未来的研究，特别是在长期随访和干预环境中，以增进我们对人类肥胖的神经元病理生理学的理解。
