Department of Internal Medicine, VU University Medical Centre, Amsterdam, The Netherlands.
EMGO+ Institute for Health and Care Research, VU University Medical Centre, Amsterdam, The Netherlands.
Hum Brain Mapp. 2017 Oct;38(10):5069-5081. doi: 10.1002/hbm.23715. Epub 2017 Jul 17.
Obesity is related to altered functional connectivity of resting state brain networks that are involved in reward and motivation. It is unknown to what extent these associations reflect genetic confounding and whether the obesity-related connectivity changes are associated with differences in dietary intake. In this study, resting state functional MRI was performed after an overnight fast in 16 female monozygotic twin pairs (aged 48.8 ± 9.8 years) with a mean BMI discordance of 3.96 ± 2.1 kg/m (range 0.7-8.2). Functional connectivity of the salience, basal ganglia, default mode and anterior cingulate-orbitofrontal cortex networks was examined by independent component analysis. Dietary intake was assessed using 3-day 24-hour recalls. Results revealed that within the basal ganglia network, heavier versus leaner co-twins have decreased functional connectivity strength in bilateral putamen (P < 0.05, FWE-corrected). There were no differences in connectivity in the other networks examined. In the overall group, lower functional connectivity strength in the left putamen was correlated with higher intake of total fat (P < 0.01). It was concluded that, after eliminating genetic effects, overweight is associated with lower resting state functional connectivity in bilateral putamen in the basal ganglia network. The association between lower putamen connectivity and higher fat intake suggests an important role of the putamen in appetitive mechanisms. The cross-sectional nature of our study cannot discriminate cause and consequence, but the findings are compatible with an effect of lower putamen connectivity on increased BMI and associated higher fat intake. Hum Brain Mapp 38:5069-5081, 2017. © 2017 Wiley Periodicals, Inc.
肥胖与参与奖励和动机的静息状态大脑网络的功能连接改变有关。目前尚不清楚这些关联在多大程度上反映了遗传混杂,以及与肥胖相关的连接变化是否与饮食摄入的差异有关。在这项研究中,对 16 对女性同卵双胞胎(年龄 48.8±9.8 岁)进行了一夜禁食后的静息状态功能磁共振成像检查,这些双胞胎的平均 BMI 差异为 3.96±2.1 kg/m(范围为 0.7-8.2)。通过独立成分分析检查了突显、基底神经节、默认模式和前扣带皮层-眶额皮层网络的功能连接。使用 3 天 24 小时回忆法评估饮食摄入。结果显示,在基底神经节网络中,与较瘦的同卵双胞胎相比,较重的同卵双胞胎双侧壳核的功能连接强度降低(P<0.05,经 FWE 校正)。在其他检查的网络中没有发现连接差异。在整个组中,左壳核的功能连接强度越低,总脂肪摄入量越高(P<0.01)。结论是,在消除遗传效应后,超重与基底神经节网络中双侧壳核的静息状态功能连接降低有关。壳核连接降低与脂肪摄入增加之间的关联表明壳核在食欲机制中起着重要作用。本研究的横断面性质不能区分因果关系,但研究结果与壳核连接降低导致 BMI 增加和相关脂肪摄入增加的假设相符。人类大脑映射 38:5069-5081,2017。©2017 年 Wiley 期刊公司。