Prenatal high sucrose intake affected learning and memory of aged rat offspring with abnormal oxidative stress and NMDARs/Wnt signaling in the hippocampus.

Prenatal high sucrose intake affected learning and memory of aged rat offspring with abnormal oxidative stress and NMDARs/Wnt signaling in the hippocampus.
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产前高蔗糖摄入量影响海马氧化应激和 NMDARs/Wnt 信号异常的老年大鼠后代的学习和记忆

DOI:
10.1016/j.brainres.2017.05.022
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发表时间:
2017-08-15
期刊:
影响因子:
2.9
通讯作者:
Sun M
Sun M
中科院分区:
医学3区
文献类型:
--
作者:
He A;Zhang Y;Yang Y;Li L;Feng X;Wei B;Zhu D;Liu Y;Wu L;Zhang L;Xu Z;Sun M

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母亲营养过剩可能会使后代容易患上肥胖、2 型糖尿病和其他成人疾病。本研究调查了产前高蔗糖(HS)饮食对老年大鼠后代认知能力的长期影响。对照组和 HS 组之间的空腹血糖浓度没有差异。然而,糖耐量试验异常的HS后代的空腹血浆胰岛素和胰岛素抵抗指数值显着升高。与对照组相比,HS后代表现出逃避潜伏期和到平台的游泳路径长度增加,并且在目标象限中的时间和穿过平台的次数减少。 HS组Grin2b/NR2B、Wnt2、Wnt3a和β-catenin蛋白活性形式表达减少,Dickkopf相关蛋白1表达增加。此外,HS组海马脂质过氧化生物标志物硫代巴比妥酸反应物、烟酰胺腺嘌呤二核苷酸磷酸氧化酶2和超氧化物歧化酶1水平显着升高,过氧化氢酶活性降低。结果表明,产前 HS 诱导的代谢变化会导致老年大鼠后代认知缺陷,这可能是由于 N-甲基-D-天冬氨酸受体/Wnt 信号传导和海马氧化应激的改变所致。
Maternal over-nutrition may predispose offspring to obesity, type 2 diabetes and other adult diseases. The present study investigated long-term impact of prenatal high sucrose (HS) diets on cognitive capabilities in aged rat offspring. The fasting plasma glucose concentration did not differ between the control and HS groups. However, the fasting plasma insulin and insulin resistance index values were significantly increased in HS offspring that showed abnormal glucose tolerance test. HS offspring exhibited increased escape latency and swimming path length to the platform, and reduced time in the target quadrant and the number of crossing the platform, as compared with the control group. The expression of Grin2b/NR2B, Wnt2, Wnt3a and active form of β-catenin protein were decreased, and Dickkopf-related protein 1 was increased in the HS group. In addition, the levels of lipid peroxidation biomarker thiobarbituricacid reactive substance, nicotinamide adenine dinucleotide phosphate oxidases 2 and superoxide dismutase 1 were significantly increased, and the activity of catalase was decreased in the hippocampus in the HS group. The results demonstrate that prenatal HS-induced metabolic changes cause cognitive deficits in aged rat offspring, probably due to altered N-methyl-D-aspartate receptors/Wnt signaling and oxidative stress in the hippocampus.
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