儿童肥胖会加速生物衰老:氧化压力是否与此有关?
Branko Subošić1,2, Vera Zdravković3,4, Maja Ješić3,4
1Biochemical Laboratory, University Children's Hospital, Tiršova 10, Belgrade, Serbia.
The British journal of nutrition
|May 13, 2024
概括
缩短的端粒,细胞衰老的标志物,与儿童的肥胖有关. 这项研究发现,肥胖与增加的氧化应激和较短的端粒长度相关,表明生物衰老加速.
科学领域:
- 儿科内分泌学 儿科内分泌学
- 老年学是一门学科.
- 生物化学 生物化学
背景情况:
- 肥胖是一种复杂的疾病,涉及生化,遗传和氧化还原不平衡.
- 由端粒长度表明的细胞衰老是健康状况的潜在生物标志物.
研究的目的:
- 为了研究白细胞相对端粒长度 (rLTL) 和肥胖与瘦身儿童的代谢/减氧状态之间的关联.
- 通过各种生物标志物的主要成分分析 (PCA) 来识别肥胖的预测因素.
主要方法:
- 对110名肥胖儿童和42名瘦身儿童和青少年进行比较研究.
- 测量白细胞相对端粒长度 (rLTL).
- 用PCA和后勤回归分析对代谢和氧化还原状态生物标志物的分析,包括C反应蛋白和总氧化剂状态 (TOS),使用PCA和后勤回归.
主要成果:
- 与瘦孩子相比,肥胖儿童的RLTL显著较短 (P < 0.01).
- rLTL与TOS (斯皮尔曼的 ρ = -0.365,P < 0.001) 和C反应蛋白 (斯皮尔曼的 ρ = -0.363,P < 0.001) 有负相关性.
- 来自PCA的抗氧化因子评分是BMI>30 kg/m2 (OR: 1.66,P = 0.029) 的最强预测因素.
结论:
- 儿童的肥胖与加速的生物衰老有关,以短端粒为证.
- 氧化应激在与肥胖相关的细胞衰老中起着重要作用.
- 由于肥胖而引起的细胞平衡障碍可能会先于明显的疾病表现.
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