Interactions between diet and cognition

7.项目摘要：在过去的60年里，美国的食糖消费量急剧上升1。 除了与体重增加和有害代谢结果2-7有关外，新的证据 揭示了过量摄入糖和其他“肥胖”饮食因素(如饱和脂肪酸) 对记忆功能和其他认知过程有负面影响8，9.尤其令人担忧的是 儿童的糖摄入量，他们每天总卡路里摄入量的15%-20%来自添加糖 (主要来自含糖饮料，SSB)10，11，是所有年龄段中含糖量最高的人群。 少年和青少年发育阶段是新陈代谢开始的高度敏感时期。 糖摄入量过多导致的功能障碍6和新证据表明，这一发育期 这也是糖类相关神经认知缺陷的特别易患时期12，13。 了解易受过度影响的认知的确切发展阶段和领域 在生命的早期阶段摄入添加糖。我们在此提供的初步数据显示， 过量摄入SSB(11%的碳水化合物溶液以匹配美国常用的SSB)在……里面 大鼠从幼年发育期开始，但不是在成年早期开始 损害空间记忆功能并增加大脑区域海马区14的神经炎症 经典地与空间和陈述性记忆功能相关，最近与学习的方面有关 食物摄取控制15，16。本提案中提出的其他初步数据提供了对 早期生命糖摄入量与海马区依赖记忆损害的联系机制 LIFE 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。 拟议中的实验将提供对早期生命糖之间关系的机械洞察 通过阐明精确的发育期和摄食来损害消耗和记忆。 相关的记忆过程特别容易受到早期生活中糖类摄入的影响，[2]潜在的 发育过程中饮食因素影响认知的神经生物学机制[3] 干预策略，潜在地可以扭转与过量相关的长期记忆缺陷 早期生活中的糖类消费。这些结果将有助于理解潜在的机制 肥胖饮食因素通过这些因素影响认知，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.