Collaborative Research Centre 1052 'Obesity Mechanisms', Leipzig University Medical Center, Leipzig, Germany.
Department of Neurology, MaxPlanck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany.
J Neuroendocrinol. 2020 Dec;32(12):e12917. doi: 10.1111/jne.12917. Epub 2020 Dec 3.
Obesity is associated with alterations in dopaminergic transmission and cognitive function. Rodent studies suggest that diets rich in saturated fat and refined sugars (HFS), as opposed to diets diets low in saturated fat and refined sugars (LFS), change the dopamine system independent of excessive body weight. However, the impact of HFS on the human brain has not been investigated. Here, we compared the effect of dietary dopamine depletion on dopamine-dependent cognitive task performance between two groups differing in habitual intake of dietary fat and sugar. Specifically, we used a double-blind within-subject cross-over design to compare the effect of acute phenylalanine/tyrosine depletion on a reinforcement learning and a working memory task, in two groups that are on opposite ends of the spectrum of self-reported HFS intake (low vs high intake: LFS vs HFS group). We tested 31 healthy young women matched for body mass index (mostly normal weight to overweight) and IQ. Depletion of peripheral precursors of dopamine reduced the working memory specific performance on the operation span task in the LFS, but not in the HFS group (P = 0.016). Learning from positive- and negative-reinforcement (probabilistic selection task) was increased in both diet groups after dopamine depletion (P = 0.049). As a secondary exploratory research question, we measured peripheral dopamine precursor availability (pDAP) at baseline as an estimate for central dopamine levels. The HFS group had a significantly higher pDAP at baseline compared to the LFS group (P = 0.025). Our data provide the first evidence indicating that the intake of HFS is associated with changes in dopamine precursor availability, which is suggestive of changes in central dopamine levels in humans. The observed associations are present in a sample of normal to overweight participants (ie, in the absence of obesity), suggesting that the consumption of a HFS might already be associated with altered behaviours. Alternatively, the effects of HFS diet and obesity might be independent.
肥胖与多巴胺传递和认知功能的改变有关。啮齿动物研究表明，富含饱和脂肪和精制糖的饮食（HFS）与低饱和脂肪和精制糖的饮食（LFS）相比，会改变多巴胺系统，而与体重过度无关。然而，HFS 对人类大脑的影响尚未得到研究。在这里，我们比较了两组习惯性饮食脂肪和糖摄入量不同的人群中，饮食性多巴胺耗竭对多巴胺依赖认知任务表现的影响。具体来说，我们使用双盲、自身交叉设计比较了急性苯丙氨酸/酪氨酸耗竭对强化学习和工作记忆任务的影响，这两组人群在自我报告的 HFS 摄入量（低与高摄入量：LFS 与 HFS 组）处于两个极端。我们测试了 31 名健康的年轻女性，她们的体重指数（主要是正常体重到超重）和智商相匹配。外周多巴胺前体耗竭降低了 LFS 组在操作跨度任务中的工作记忆特定表现，但在 HFS 组中没有（P = 0.016）。在两种饮食组中，多巴胺耗竭后，从正强化和负强化中学习（概率选择任务）增加（P = 0.049）。作为一个次要的探索性研究问题，我们在基线时测量了外周多巴胺前体可用性（pDAP），作为中枢多巴胺水平的估计值。HFS 组的 pDAP 基线水平明显高于 LFS 组（P = 0.025）。我们的数据首次提供了证据表明，HFS 的摄入与多巴胺前体可用性的变化有关，这表明人类中枢多巴胺水平发生了变化。在正常到超重的参与者（即没有肥胖）样本中观察到了这些关联，这表明 HFS 的消费可能已经与行为改变有关。或者，HFS 饮食和肥胖的影响可能是独立的。
