氧化应激对肥胖儿童认知功能的影响

Samet Özer, İlknur Bütün, Hasan Bozkurt
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Neurocognitive functions including the Visual Memory Test, Finger Tapping Test, Memory Test, Symbol Digit Coding, Stroop Test, Continuous Performance Test, and Shifting Attention Test were evaluated with the battery tests of Central Nervous System Vital Signs (CNSVS) via computer. Malondialdehyde (MDA) and protein carbonyl (PC) were analyzed to determine the oxidative stress. After 10 hours overnight fast, blood samples were collected to determine Fasting glucose, total cholesterol, triglyceride, low-density lipoprotein, high-density lipoprotein, liver enzymes aspartate aminotransferase and alanine aminotransferase by using methods. \nResults: MDA and PC levels in obese children were founs significantly higher (0.78±0.16 µmol/L;198.30±84.45 nmol/mL) than the controls (0.5±0.10 µmol/L; 125.35±43.52 nmol/mL) (P<0.001). All of the cognitive performance domains were statistically significantly different between the study and control groups. 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摘要

研究目的本研究旨在评估肥胖引起的氧化应激与肥胖儿童认知功能代谢变化之间的关系。研究方法研究对象包括 33 名肥胖儿童和青少年(8-18 岁),以及 33 名年龄和性别相似的健康儿童。根据土耳其儿童体重指数(BMI)曲线,儿童被诊断为肥胖。根据土耳其儿童体重指数曲线,考虑到其性别和年龄,超过第 95 百分位数的患者被称为肥胖儿童。肥胖儿童不包括与任何综合症或疾病相关的肥胖儿童。神经认知功能包括视觉记忆测试、手指敲击测试、记忆测试、符号数字编码、斯特罗普测试、连续表现测试和注意力转移测试,并通过计算机进行中枢神经系统生命体征(CNSVS)测试。分析丙二醛(MDA)和蛋白质羰基(PC)以确定氧化应激。空腹 10 小时后,采集血液样本,用方法测定空腹血糖、总胆固醇、甘油三酯、低密度脂蛋白、高密度脂蛋白、肝酶天冬氨酸氨基转移酶和丙氨酸氨基转移酶。结果显示肥胖儿童的 MDA 和 PC 水平(0.78±0.16 µmol/L;198.30±84.45 nmol/mL)明显高于对照组(0.5±0.10 µmol/L;125.35±43.52 nmol/mL)(P<0.001)。研究组和对照组的所有认知表现领域在统计学上都有显著差异。神经认知指标与 MDA 和 PC 水平之间存在统计学意义上的明显相关性。结论必须对肥胖儿童的认知功能进行评估。氧化应激升高可能是导致肥胖儿童认知能力低下的原因。不过,这项针对肥胖儿童认知能力的研究应得到大型研究小组的支持。
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Effect of oxidative stress on cognitive functions in children with obesity
Objectives: This study aims to evaluate the relationship between the oxidative stress induced by obesity and metabolic changes in the cognitive functions of obese children. Methods: Thirty-three obese children and adolescents (age: 8-18); and 33 healthy children similar in terms of age and gender were enrolled. Children were diagnosed with obesity according to the Turkish children's body mass index (BMI) curves. Patients over the 95th percentile in terms of Turkish children's BMI curves considering their genders and age were called obese children. Obese children were excluded whose obesity was related to any syndrome or disease. Neurocognitive functions including the Visual Memory Test, Finger Tapping Test, Memory Test, Symbol Digit Coding, Stroop Test, Continuous Performance Test, and Shifting Attention Test were evaluated with the battery tests of Central Nervous System Vital Signs (CNSVS) via computer. Malondialdehyde (MDA) and protein carbonyl (PC) were analyzed to determine the oxidative stress. After 10 hours overnight fast, blood samples were collected to determine Fasting glucose, total cholesterol, triglyceride, low-density lipoprotein, high-density lipoprotein, liver enzymes aspartate aminotransferase and alanine aminotransferase by using methods. Results: MDA and PC levels in obese children were founs significantly higher (0.78±0.16 µmol/L;198.30±84.45 nmol/mL) than the controls (0.5±0.10 µmol/L; 125.35±43.52 nmol/mL) (P<0.001). All of the cognitive performance domains were statistically significantly different between the study and control groups. A statistically significant correlation was found between neurocognitive indexes and MDA and PC levels. Conclusions: Obese children's cognitive functions must be evaluated. Elevated oxidative stress may be the reason for the bad cognitive performance in children with obesity. However, this cognitive performance study in obese children should be supported with large study groups.
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