Noble Emily E, Kanoski Scott E
Department of Biological Sciences, Human and Evolutionary Biology Section, University of Southern California, Los Angeles, CA, USA.
Curr Opin Behav Sci. 2016 Jun;9:7-14. doi: 10.1016/j.cobeha.2015.11.014.
Obesogenic dietary factors, such as simple sugars and saturated fatty acids, have been linked to memory impairments and hippocampal dysfunction. Recent evidence suggests that the brain may be particularly vulnerable to the effects of obesogenic diets during early life periods of rapid growth, maturation, and brain development. Investigations utilizing rodent models indicate that early life exposure to "high fat diets" (40-65% kcal derived from fat) or simple sugars (sucrose or high fructose corn syrup) can impair hippocampus-dependent learning and memory processes. In some cases, these deficits occur independent of obesity and metabolic derangement and can persist into adulthood despite dietary intervention. Various neurobiological mechanisms have been identified that may link early life consumption of obesogenic dietary factors with hippocampal dysfunction, including increased neuroinflammation and reduced neurotrophin mediated regulation of neurogenesis and synaptic plasticity. Age, duration of exposure, and dietary composition are key variables contributing to the interaction between early life diet and cognitive dysfunction, however, more research is needed to unravel the precise critical windows of development and causal dietary factors.
致肥胖的饮食因素，如单糖和饱和脂肪酸，已被证明与记忆障碍和海马体功能紊乱有关。最近的证据表明，在快速生长、成熟和大脑发育的早期阶段，大脑可能特别容易受到致肥胖饮食的影响。利用啮齿动物模型进行的研究表明，早年接触“高脂肪饮食”（40%-65%的热量来自脂肪）或单糖（蔗糖或高果糖玉米糖浆）会损害依赖海马体的学习和记忆过程。在某些情况下，这些缺陷的出现与肥胖和代谢紊乱无关，并且尽管进行了饮食干预，仍可能持续到成年期。已经确定了各种神经生物学机制，这些机制可能将早年摄入致肥胖饮食因素与海马体功能紊乱联系起来，包括神经炎症增加以及神经营养因子介导的神经发生和突触可塑性调节减少。年龄、接触时间和饮食组成是导致早年饮食与认知功能障碍之间相互作用的关键变量，然而，还需要更多的研究来揭示发育的精确关键期和因果饮食因素。
