据英国《每日邮报》5月17日报道，美国加州大学学者近日在《生理学期刊》(Journal of Physiology)发表文章称，多吃含高果糖添加剂的食物会使人变笨，导致记忆力等大脑功能下降。
据报道，该文作者对老鼠进行了对比试验，一组老鼠的食物中添加高含果糖的玉米糖浆，另一组老鼠饮食正常。在试验之初，研究者让老鼠走带有路标的迷宫，在两组老鼠进食6周后，研究者测试老鼠回忆走迷宫路线的能力，发现食用高含糖食物的一组老鼠反应缓慢，大脑功能有所下降。该文章作者之一费尔南多·戈麦斯·皮尼拉(Professor Fernando Gomez-Pinilla)教授描述食用高糖食物的一组老鼠：“它们的脑细胞发送信号出现问题，使其难以清晰思考并想起过去走过的路线。”
皮尼拉称，长期饮食高含果糖的食物会影响大脑学习和记忆的能力。然而好消息是，吃坚果和鱼类(如鲑鱼)能平衡糖类食物的影响。此类食物含有N-3不饱和脂肪酸，该物质能减少高糖食物的负面作用。
据悉，试验中价格低廉的玉米糖浆高含果糖，比普通蔗糖甜6倍，但它是诸如软饮料这样的加工食品常用的原料。皮尼拉教授称，他们所说的果糖并非水果中天然含有的果糖，而是加工食品中作为添加剂、甜味剂的高果糖玉米糖浆。
据报道，此前有众多关于果糖因引起肥胖、糖尿病、脂肪肝等问题有害身体的研究，但这一关于糖类影响大脑功能的研究尚属首例。
‘Metabolic syndrome' in the brain: deficiency in omega-3 fatty acid exacerbates dysfunctions in insulin receptor signalling and cognition
Rahul Agrawal and Fernando Gomez-Pinilla
We pursued studies to determine the effects of the metabolic syndrome (MetS) on brain, and the possibility of modulating these effects by dietary interventions. In addition, we have assessed potential mechanisms by which brain metabolic disorders can impact synaptic plasticity and cognition. We report that high-dietary fructose consumption leads to an increase in insulin resistance index, and insulin and triglyceride levels, which characterize MetS. Rats fed on an n-3 deficient diet showed memory deficits in a Barnes maze, which were further exacerbated by fructose intake. In turn, an n-3 deficient diet and fructose interventions disrupted insulin receptor signalling in hippocampus as evidenced by a decrease in phosphorylation of the insulin receptor and its downstream effector Akt. We found that high fructose consumption with an n-3 deficient diet disrupts membrane homeostasis as evidenced by an increase in the ratio of n-6/n-3 fatty acids and levels of 4-hydroxynonenal, a marker of lipid peroxidation. Disturbances in brain energy metabolism due to n-3 deficiency and fructose treatments were evidenced by a significant decrease in AMPK phosphorylation and its upstream modulator LKB1 as well as a decrease in Sir2 levels. The decrease in phosphorylation of CREB, synapsin I and synaptophysin levels by n-3 deficiency and fructose shows the impact of metabolic dysfunction on synaptic plasticity. All parameters of metabolic dysfunction related to the fructose treatment were ameliorated by the presence of dietary n-3 fatty acid. Results showed that dietary n-3 fatty acid deficiency elevates the vulnerability to metabolic dysfunction and impaired cognitive functions by modulating insulin receptor signalling and synaptic plasticity.
文献链接：https://jp.physoc.org/content/590/10/2485.abstract?sid=aff346dc-da16-4ca9-b73b-4bfca4dddb0f
