Haltia Lauri T, Rinne Juha O, Merisaari Harri, Maguire Ralph P, Savontaus Eriika, Helin Semi, Någren Kjell, Kaasinen Valtteri
Department of Neurology, University of Turku, Turku, Finland.
Synapse. 2007 Sep;61(9):748-56. doi: 10.1002/syn.20418.
Dopamine is known to regulate food intake by modulating food reward via the mesolimbic circuitry of the brain. The objective of this study was to compare the effects of high energy input (i.v. glucose) on striatal and thalamic dopamine release in overweight and lean individuals. We hypothesized that glucose would induce dopamine release and positive ratings (e.g., satiety) in Behavioral Analog Scales, particularly in food-deprived lean subjects. [(11)C]raclopride PET was performed for 12 lean (mean BMI = 22 kg/m(2)) and 12 overweight (mean BMI = 33 kg/m(2)) healthy subjects. Each subject was imaged twice in a blinded counter-balanced setting, after 300 mg/kg i.v. glucose and after i.v. placebo. Dopamine D2 receptor binding potentials (BPs) were estimated. The voxel-based analysis of the baseline scans indicated lower striatal BPs in the overweight group and a negative correlation between BMIs and BPs. Intravenous glucose did not have a significant effect on BPs in overweight or lean subjects (male and female groups combined). However, BP changes were opposite in the two gender groups. In male subjects, significant BP reductions after glucose were seen in the right and left caudate nucleus, left putamen, and right thalamus. In female subjects, increases in BP secondary to glucose were seen in the right caudate nucleus and right and left putamen. The sexually dimorphic effect of glucose was seen in both overweight and lean subjects. Although gender differences were not among the a priori hypotheses of the present study and, therefore, they must be considered to be preliminary findings, we postulate that this observation is a reflection of an interaction between glucose, sex steroids (estrogen), leptin, and dopamine.
众所周知，多巴胺通过调节大脑中脑边缘神经回路的食物奖赏来调节食物摄入量。本研究的目的是比较高能量输入（静脉注射葡萄糖）对超重和瘦个体纹状体和丘脑多巴胺释放的影响。我们假设葡萄糖会诱导多巴胺释放，并在行为模拟量表中产生积极评分（如饱腹感），特别是在食物剥夺的瘦受试者中。对12名瘦（平均BMI = 22 kg/m²）和12名超重（平均BMI = 33 kg/m²）的健康受试者进行了[(11)C]雷氯必利PET检查。在300 mg/kg静脉注射葡萄糖后和静脉注射安慰剂后，每个受试者在双盲平衡设置下进行两次成像。估计多巴胺D2受体结合电位（BPs）。基于体素的基线扫描分析表明，超重组的纹状体BPs较低，且BMI与BPs之间呈负相关。静脉注射葡萄糖对超重或瘦受试者（男性和女性组合并）的BPs没有显著影响。然而，两个性别组的BP变化相反。在男性受试者中，葡萄糖注射后右侧和左侧尾状核、左侧壳核和右侧丘脑的BP显著降低。在女性受试者中，葡萄糖注射后右侧尾状核以及右侧和左侧壳核的BP升高。葡萄糖的性别差异效应在超重和瘦受试者中均可见。尽管性别差异不在本研究的先验假设之中，因此，它们必须被视为初步发现，但我们推测这一观察结果反映了葡萄糖、性类固醇（雌激素）、瘦素和多巴胺之间的相互作用。
