Department of Anatomy, Melaka Manipal Medical College [Manipal campus], Manipal Academy of Higher Education, Manipal, Karnataka, India.
Department of Physiology, Melaka Manipal Medical College [Manipal campus], Manipal Academy of Higher Education, Manipal, Karnataka, India.
Int J Neurosci. 2021 Nov;131(11):1066-1077. doi: 10.1080/00207454.2020.1773819. Epub 2020 Jun 4.
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.
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] [ = 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.
Memory errors were significantly higher [ < 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 [ < 0.01] compared to same in NC. Interventions in OB + CHO + DHA and OB + EE significantly attenuated [ < 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.
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.
儿童肥胖会增加神经功能障碍的风险,导致学习和记忆缺陷。本研究的目的是确定产后高脂肪饮食诱导的肥胖对血清脂质、记忆和海马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。
21 天龄雄性 Sprague Dawley 大鼠被分为正常对照组(NC),给予正常饲料;肥胖诱导组(OB),给予高脂肪饮食;肥胖诱导加胆碱和 DHA 组(OB+CHO+DHA);肥胖诱导加环境富集组(OB+EE)[每组 8 只]。使用放射臂迷宫评估记忆。随后采集血液进行血清脂质分析,处死大鼠。对 5μm 海马切片进行 Cresyl-violet 染色。使用 100μm 标尺计数存活的神经细胞。
OB 组的记忆错误明显高于 NC 组[<0.001,0.01]。OB 组海马存活神经细胞的平均数量明显少于 NC 组[<0.01]。OB+CHO+DHA 和 OB+EE 干预显著降低了 OB 组的记忆错误和海马[CA1、CA3 和 DG]存活神经细胞的数量[<0.01]。此外,在 OB 组中发现海马神经细胞存活与血清脂质谱呈负相关,并在 OB+CHO+DHA 和 OB+EE 大鼠中减弱。
大鼠产后高脂肪饮食诱导的肥胖导致 CA1/CA3 海马神经退行性变和记忆缺陷。在肥胖大鼠中补充胆碱和 DHA 可减轻这些缺陷。