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Hippocampal neural cell degeneration and memory deficit in high-fat diet-induced postnatal obese rats– exploring the comparable benefits of choline and DHA or environmental enrichment
International Journal of Neuroscience ( IF 1.7 ) Pub Date : 2020-06-04 , DOI: 10.1080/00207454.2020.1773819
Gayathri S Prabhu 1 , Mohandas K G Rao 1 , Kiranmai S Rai 2
Affiliation  

Abstract

Purpose

Childhood obesity increases risk for neural dysfunctions causing learning and memory deficits. The objective of the study is to identify the effects of high fat diet-induced obesity in postnatal period on serum lipids, memory and neural cell survival in hippocampus and compare the role of choline and DHA or environmental enrichment in attenuating the alterations

Materials and methods

21 day postnatal male Sprague Dawley rats were assigned as Normal control [NC] fed normal chow diet, Obesity-induced [OB] fed high fat diet, Obesity-induced fed choline & DHA [OB + CHO + DHA], Obesity-induced environmental enrichment [OB + EE] [n = 8/group]. Memory was assessed using radial arm maze. Subsequently blood was collected for serum lipid analysis and rats were euthanized. 5 µm hippocampal sections were processed for cresyl-violet stain. Surviving neural cells were counted using 100 µm scale.

Results

Memory errors were significantly higher [p < 0.001, 0.01] in OB compared to same in NC rats. Mean number of surviving neural cells in hippocampus of OB was significantly lesser [p < 0.01] compared to same in NC. Interventions in OB + CHO + DHA and OB + EE significantly attenuated [p < 0.01] memory errors and number of surviving neural cells in hippocampus [CA1, CA3 and DG] compared to same in OB. Moreover, hippocampal neural cell survival was found to be inversely related to serum lipid profile in OB group and was attenuated in OB + CHO + DHA and OB + EE rats.

Conclusions

High fat diet-induced postnatal obesity in rats causes CA1/CA3 hippocampal neuro-degeneration and memory deficits. Supplementation of choline and DHA in obese rats attenuates these deficits.



中文翻译:

高脂饮食诱导的产后肥胖大鼠海马神经细胞退化和记忆缺陷——探索胆碱和 DHA 或环境富集的可比益处

摘要

目的

儿童肥胖会增加导致学习和记忆缺陷的神经功能障碍的风险。该研究的目的是确定产后高脂饮食诱导的肥胖对海马血脂、记忆和神经细胞存活的影响,并比较胆碱和 DHA 或环境富集在减轻这些改变中的作用

材料和方法

将出生后 21 天的雄性 Sprague Dawley 大鼠分配为正常对照 [NC] 喂正常食物饮食、肥胖诱导 [OB] 喂高脂肪饮食、肥胖诱导喂食胆碱和 DHA [OB + CHO + DHA]、肥胖诱导环境富集 [OB + EE] [ n  = 8/组]。使用径向臂迷宫评估记忆。随后采集血液进行血脂分析,并对大鼠实施安乐死。对 5 µm 海马切片进行了甲酚紫染色处理。使用 100 µm 规模对存活的神经细胞进行计数。

结果

 与 NC 大鼠相比,OB 中的记忆错误显着更高 [ p < 0.001, 0.01]。 与 NC 相比,OB 海马中存活神经细胞的平均数量显着减少 [ p < 0.01]。与 OB 相比,对 OB + CHO + DHA 和 OB + EE 的干预显着减弱了 [ p  < 0.01] 的记忆错误和海马中存活的神经细胞 [CA1、CA3 和 DG] 的数量。此外,发现海马神经细胞存活与 OB 组的血脂谱呈负相关,并在 OB + CHO + DHA 和 OB + EE 大鼠中减弱。

结论

高脂饮食诱导的大鼠产后肥胖导致 CA1/CA3 海马神经变性和记忆缺陷。在肥胖大鼠中补充胆碱和 DHA 可减轻这些缺陷。

更新日期:2020-06-04
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