Alkan Işınsu, Altunkaynak Berrin Zuhal, Gültekin Güldal İnal, Bayçu Cengiz
Dept of Basic Medical Sciences, Dentistry Faculty, Nevşehir Hacı Bektaş Veli University, Nevşehir Turkey.
Depts of Histology and Embryology and Physiology Departments, Medical Faculty, Istanbul Okan University, İstanbul, Turkey.
J Chem Neuroanat. 2021 Jul;114:101947. doi: 10.1016/j.jchemneu.2021.101947. Epub 2021 Mar 22.
Obesity, which has become one of the main health problems, results from irregular and unhealthy nutrition. In particular, an increase in the intake of high-fat foods leads to obesity and associated disorders. It is noteworthy to specify that obese individuals have memory problems. This study aims to examine the effects of high-fat diet on hippocampus, with stereological, histopathological methods and STRING bioinformatic tool.
Female Adult Sprague Dawley rats (n = 20) were equally divided into control (CONT) and high-fat diet (HFD) groups. The control group was given standard rat pellet feed, while the high-fat diet group was fed with a 40 % fat content for 2 months. Following the feeding program, rats were sacrificed. The collected blood samples were analyzed biochemically to determine the level of oxidative stress while performing a stereological and histopathological examination of the brain tissues. Functional protein-protein networks for BDNF, C-Fos, CAT, LPO, SOD and MPO by gene ontology (GO) enrichment analysis were evaluated.
The number of neurons decreased in the HFD group compared to the CONT group. Damage to the histological structure of the hippocampus region; such as degenerate neurons, damaged mitochondria and extended cisterns of the endoplasmic reticulum was observed. Although C-Fos level and oxidative stress parameters increased in HFD group, BDNF level decreased. While BDNF and C-Fos were observed in pathways related to neuron death, oxidative stress and memory, BDNF was pronounced in the mitochondria, and C-Fos in the endoplasmic reticulum.
This study shows that changes in both BDNF and C-Fos levels in obesity due to high-fat diet increase oxidative stress and cause neuron damage in the hippocampus.
肥胖已成为主要的健康问题之一，是由不规律和不健康的营养所致。特别是，高脂肪食物摄入量的增加会导致肥胖及相关疾病。值得注意的是，肥胖个体存在记忆问题。本研究旨在采用体视学、组织病理学方法及STRING生物信息学工具，研究高脂饮食对海马体的影响。
将成年雌性Sprague Dawley大鼠（n = 20）平均分为对照组（CONT）和高脂饮食组（HFD）。对照组给予标准大鼠颗粒饲料，而高脂饮食组喂食脂肪含量为40%的饲料，持续2个月。按照喂养方案进行喂养后，处死大鼠。对采集的血样进行生化分析，以确定氧化应激水平，同时对脑组织进行体视学和组织病理学检查。通过基因本体（GO）富集分析评估BDNF、C-Fos、CAT、LPO、SOD和MPO的功能蛋白质-蛋白质网络。
与CONT组相比，HFD组神经元数量减少。观察到海马体区域的组织结构受损，如神经元退变、线粒体损伤和内质网池扩张。虽然HFD组C-Fos水平和氧化应激参数升高，但BDNF水平降低。虽然BDNF和C-Fos在与神经元死亡、氧化应激和记忆相关的通路中被观察到，但BDNF在线粒体中明显，C-Fos在内质网中明显。
本研究表明，高脂饮食导致的肥胖中BDNF和C-Fos水平的变化会增加氧化应激，并导致海马体神经元损伤。
