Department of Psychology, University of Pennsylvania, Philadelphia, PA, USA.
Université Paris Diderot, Sorbonne Paris Cité, BFA CNRS UMR 8251, Paris, France; Modern Diet and Physiology Research Center, New Haven, CT, USA.
Trends Cogn Sci. 2017 May;21(5):372-384. doi: 10.1016/j.tics.2017.03.004. Epub 2017 Mar 31.
Recent work highlights the importance of genetic variants that influence brain structure and function in conferring risk for polygenic obesity. The neurotransmitter dopamine (DA) has a pivotal role in energy balance by integrating metabolic signals with circuits supporting cognitive, perceptual, and appetitive functions that guide feeding. It has also been established that diet and obesity alter DA signaling, leading to compulsive-like feeding and neurocognitive impairments. This raises the possibility that genetic variants that influence DA signaling and adaptation confer risk for overeating and cognitive decline. Here, we consider the role of two common gene variants, FTO and TaqIA rs1800497 in driving gene × environment interactions promoting obesity, metabolic dysfunction, and cognitive change via their influence on DA receptor subtype 2 (DRD2) signaling.
最近的研究强调了影响大脑结构和功能的遗传变异在多基因肥胖风险中的重要性。神经递质多巴胺（DA）通过将代谢信号与支持认知、感知和食欲功能的回路整合在一起，在能量平衡中起着关键作用，这些回路指导进食。此外，饮食和肥胖会改变 DA 信号，导致强迫性进食和神经认知障碍。这就提出了这样一种可能性，即影响 DA 信号传递和适应的遗传变异会增加暴饮暴食和认知能力下降的风险。在这里，我们考虑了两种常见的基因变异，即 FTO 和 TaqIA rs1800497，它们通过影响多巴胺受体亚型 2（DRD2）信号，在促进肥胖、代谢功能障碍和认知变化的基因×环境相互作用中所起的作用。
