Fructose-Induced Cognitive Dysfunction Is Associated with Increased Oxidative Stress in the Rat Brains

• 作者: En Yabe Hiroe Sakuyama Tomari Shoko Yamakawa Yoshio Uehara Yuri Kintaka
• 来源期刊: 生物科学与医学(英文)
• 学科: 医学
• 关键词: FRUCTOSE COGNITIVE Function Type 2 DIABETES Dahl Rat
• 年，卷（期）: 2018,（10）
• 页码范围: 52-64
• 页数: 13页
• 分类号: R73

摘要

High fructose consumption is a risk factor for diabetes. Type 2 diabetes is associated with cognitive and memory impairment. To determine if fructose intake might affect memory function independently of diabetes development, we investigated the effects of monosaccharides on memory in prediabetic state. We examined whether 2.5% apple juice solution could influence cognitive function in salt-sensitive Dahl rats using passive avoidance methods. Furthermore, we examined the role of monosaccharides intake in cognitive function and oxidative stress in the brain. Four-week consumption of either apple juice or 2.5% fructose did not affect the blood glucose concentrations;however, apple juice, but not fructose, significantly decreased cognitive function compared with that of control rats given water. Second, Wistar rats aged 4 weeks were assigned to four groups given water, or 1.25% glucose, or fructose, or galactose solutions for 11 weeks. The fructose group had only slightly higher blood glucose concentrations than the control group. However, memory function engraved at age of 7 weeks and evaluated for 8 weeks in a passive avoidance test, was significantly decreased in the fructose and galactose groups compared with those in the glucose group. Oxidative stress in the brain, assessed by the tissue malondialdehyde (MDA) content, was significantly increased in the fructose group compared with that in the control group, and the decrease in cognitive function significantly correlated with the MDA content. These findings suggest that long-term apple juice consumption decreases memory function, possibly through an increase in oxidative stress in the brain, in turn induced by fructose overloading. Fructose-induced cognitive dysfunction is likely mediated by mechanisms other than insulin resistance.