Interactions between diet and cognition

7.项目摘要：在过去的60年里，美国的膳食糖消费量急剧上升。 除了与体重增加和有害的代谢结果2-7相关外， 揭示了糖和其它“致肥胖”饮食因素的过度消耗（例如，饱和脂肪酸） 负面影响记忆功能和其他认知过程8，9。特别令人关切的是， 儿童的糖摄入量，他们每天总热量的15-20%来自添加糖 （主要来自含糖饮料，SSB）10，11，是任何年龄组中最高的糖消费者。 青少年和青春期发育阶段是代谢性疾病发病的高度敏感期。 糖摄入过多导致的功能障碍6和新的证据表明，这一时期的发展， 也是一个特别脆弱的时间糖相关的神经认知缺陷12，13。因此， 了解准确的发展时期和认知领域，容易受到过度的影响。 在生命的早期阶段消耗添加的糖。我们在此提供的初步数据显示， 过量食用SSB（11%碳水化合物溶液，以匹配美国通常食用的SSB）在 大鼠从幼年期开始发育，但未在成年早期开始 损害空间记忆功能并增加海马14（一个脑区域）中的神经炎症 传统上与空间和陈述性记忆功能有关，最近与学习方面有关， 食物摄入控制15，16.本提案中提出的其他初步数据提供了对可能的 将早期生活中的糖消耗与依赖于大脑的记忆障碍联系起来的机制， 生活SSB访问深刻地改变了肠道微生物组，并减少了海马体中神经发生的标志物。 拟议的实验将提供机制的洞察力之间的关系，早期生活糖 消费和记忆障碍的照明[1]精确的发展时期和喂养- 相关的记忆过程特别容易受到早期糖摄入的影响，[2] 发育期间饮食因素影响认知的神经生物学机制[3] 干预策略，可以潜在地扭转与过度相关的长期记忆缺陷， 早期的糖摄入量。研究结果将有助于了解潜在的机制 通过这些研究，致肥胖饮食因素影响认知，并可能提供有价值的见解， 逆转或预防不健康饮食因素对大脑的病理影响。

7. Project Summary: Dietary sugar consumption has dramatically risen in the U.S. over the past 60 years 1. In addition to being associated with body weight gain and harmful metabolic outcomes 2-7, emerging evidence reveals that excessive consumption of sugar and other “obesogenic” dietary factors (e.g., saturated fatty acids) negatively impacts memory function and other cognitive processes 8,9. Particularly concerning is the rise in sugar consumption among children, who with ~15-20% of their total daily caloric intake from added sugars (predominantly from sugar-sweetened beverages, SSBs) 10,11, are the highest sugar consumers of any age group. The juvenile and adolescent developmental phases are highly susceptible periods for the onset of metabolic dysfunction resulting from excessive sugar intake 6 and new evidence suggests that this period of development is also a particularly vulnerable time for sugar-related neurocognitive deficits 12,13. Therefore, it is important to understand the precise developmental periods and domains of cognition that are vulnerable to excessive consumption of added sugars during early life periods. Our preliminary data presented herein reveals that excessive consumption of SSBs (11% carbohydrate solution to match commonly consumed SSBs in the U.S.) in rats beginning at the onset of the juvenile period of development but not beginning during early adulthood impairs spatial memory function and increases neuroinflammation in the hippocampus 14, a brain region classically associated with spatial and declarative memory function and more recently with learned aspects of food intake control 15,16. Other preliminary data presented in this proposal offer insight into possible mechanisms linking early life sugar consumption with hippocampal-dependent memory impairments, as early life SSB access profoundly alters the gut microbiome and reduces markers of neurogenesis in the hippocampus. Proposed experiments will provide mechanistic insight into the relationship between early life sugar consumption and memory impairment by illuminating [1] the precise developmental periods and feeding- relevant memory processes that are particularly vulnerable to early life sugar consumption, [2] the underlying neurobiological mechanisms through which dietary factors during development influence cognition, and [3] intervention strategies that can potentially reverse the long-lasting memory deficits associated with excessive early life sugar consumption. Results will contribute toward understanding the underlying mechanisms through which obesogenic dietary factors influence cognition and may provide valuable insight toward reversing or preventing the pathological effects of unhealthy dietary factors on the brain.