代谢与记忆：肥胖症儿童和 1 型糖尿病儿童的α-突触核蛋白水平；与糖毒性、脂毒性和执行功能的关系。
Metabolism and memory: α-synuclein level in children with obesity and children with type 1 diabetes; relation to glucotoxicity, lipotoxicity and executive functions.
机构信息
Department of Pediatrics, Faculty of medicine, Ain shams University, Cairo, Egypt.
Department of Clinical Pathology, Faculty of medicine, Ain shams University, Cairo, Egypt.
出版信息
Int J Obes (Lond). 2022 Nov;46(11):2040-2049. doi: 10.1038/s41366-022-01222-z. Epub 2022 Sep 24.
BACKGROUND/OBJECTIVES: Children with obesity and those with type 1diabetes (T1D) exhibit subtle neurocognitive deficits, the mechanism of which remains unknown. α-synuclein plays a fundamental role in neurodegeneration. Moreover, its role in glucose and lipids metabolism is emerging. This study aims to assess whether α-synuclein is correlated with the degree of neurodegeneration in children with obesity and those with T1D in comparison to healthy controls and correlate it to various neurocognitive and metabolic parameters.
SUBJECTS/METHODS: Forty children with obesity, 40 children with T1D and 40 matched-healthy controls were assessed for anthropometric measurements and blood-pressure. Cognitive evaluation was performed using Stanford-Binet scale and Barkley Deficits in Executive Functioning (EF) Scale-Children and Adolescents. α-synuclein, fasting lipids and glucose were measured with calculation of the homeostatic model of insulin-resistance and estimated-glucose disposal rate.
RESULTS
Children with obesity and those with T1D had significantly higher α-synuclein (p < 0.001) and total EF percentile (p = 0.001) than controls. α-synuclein was negatively correlated to total IQ (p < 0.001 and p = 0.001), and positively correlated with total EF percentile (p = 0.009 and p = 0.001) and EF symptom count percentile (p = 0.005 and p < 0.001) in children with T1D and obesity, respectively. Multivariate-regression revealed that α-synuclein was independently related to age (p = 0.028), diabetes-duration (p = 0.006), HbA1C% (p = 0.034), total IQ (p = 0.013) and EF symptom count percentile (p = 0.003) among children with T1D, and to diastolic blood-pressure percentile (p = 0.013), waist/hip ratio SDS (p = 0.007), total EF percentile (P = 0.033) and EF symptom count percentile (p < 0.001) in children with obesity.
CONCLUSION
α-synuclein could have a mechanistic role in neurocognitive deficit among children with obesity and T1D.
背景/目的：肥胖儿童和 1 型糖尿病（T1D）儿童表现出细微的神经认知缺陷，其机制尚不清楚。α-突触核蛋白在神经退行性变中起着至关重要的作用。此外，其在葡萄糖和脂质代谢中的作用也逐渐显现。本研究旨在评估α-突触核蛋白是否与肥胖儿童和 T1D 儿童的神经退行性程度相关，与健康对照组进行比较，并与各种神经认知和代谢参数相关。
受试者/方法：评估了 40 名肥胖儿童、40 名 T1D 儿童和 40 名匹配的健康对照组的人体测量学测量和血压。使用斯坦福-比奈量表和 Barkley 执行功能缺陷量表-儿童和青少年对认知进行评估。用稳态模型评估胰岛素抵抗和估计葡萄糖处置率来测量α-突触核蛋白、空腹血脂和血糖。
结果
肥胖儿童和 T1D 儿童的α-突触核蛋白明显更高（p<0.001）和总执行功能百分位数（p=0.001）比对照组。α-突触核蛋白与总智商呈负相关（p<0.001 和 p=0.001），与总执行功能百分位数（p=0.009 和 p=0.001）和执行功能症状计数百分位数（p=0.005 和 p<0.001）呈正相关在肥胖和 T1D 儿童中。多元回归显示，α-突触核蛋白与年龄（p=0.028）、糖尿病病程（p=0.006）、HbA1C%（p=0.034）、总智商（p=0.013）和执行功能症状计数百分位数（p=0.003）独立相关在 T1D 儿童中，与舒张压百分位数（p=0.013）、腰围/臀围比值 SDS（p=0.007）、总执行功能百分位数（P=0.033）和执行功能症状计数百分位数（p<0.001）在肥胖儿童中。
结论
α-突触核蛋白在肥胖和 T1D 儿童的神经认知缺陷中可能具有机制作用。
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