González L, Corvalán C, Pereira A, Kain J, Garmendia M L, Uauy R
Institute of Nutrition and Food Technology (INTA), University of Chile, Santiago, Chile.
1] Institute of Nutrition and Food Technology (INTA), University of Chile, Santiago, Chile [2] The London School of Hygiene and Tropical Medicine, London, UK.
Int J Obes (Lond). 2014 Oct;38(10):1299-304. doi: 10.1038/ijo.2014.97. Epub 2014 Jun 9.
Early adiposity rebound (AR <5 years) has been consistently associated with increased obesity risk, but its relationship with metabolic markers is less clear; in addition, the biologic mechanisms involved in these associations have not been established.
The objective of this study was to assess the association between timing of AR and metabolic status at age 7 years, evaluating the potential role of adiposity, adipose functionality and skeletal maturation in this association.
We estimated the age of AR from the body mass index (BMI) trajectories from 0 to 7 years in 910 children from the Growth and Obesity Chilean Cohort Study (GOCS). At 7 years, we measured waist circumference (WC) and blood glucose, insulin, triglycerides and high-density lipoprotein-cholesterol levels and constructed a metabolic risk score. We also measured percent fat mass (adiposity), plasma concentrations of leptin and adiponectin (adipose functionality) and bone age using wrist ultrasound (skeletal maturation).
We found that 44% of the children had an AR <5 years. Earlier AR was associated with larger WC (β: 5.10 (95% confidence interval (CI): 4.29-5.91)), higher glucose (β: 1.02 (1.00-1.03)), insulin resistance (β Homeostatic Model Assessment: 1.06 (1.03-1.09)), triglycerides (β: 10.37 (4.01-6.73)) and adverse metabolic score (β: 0.30 (0.02-0.37)). Associations decreased significantly if adiposity was added to the models (i.e. β WC: 0.85 (0.33-1.38)) and, to a lesser extent, when adipokines (i.e. β WC: 0.73 (0.14-1.32)) and skeletal maturation (i.e. β WC: 0.65 (0.10-1.20)) were added.
In GOCS children, AR at a younger age predicts higher metabolic risk at 7 years; these associations are mostly explained by increased adiposity, but adipose dysfunction and accelerated skeletal maturation also have a role.
早期肥胖反弹(年龄<5岁)一直与肥胖风险增加相关,但其与代谢标志物的关系尚不清楚;此外,这些关联背后的生物学机制尚未明确。
本研究旨在评估肥胖反弹时间与7岁时代谢状态之间的关联,评估肥胖、脂肪功能和骨骼成熟度在该关联中的潜在作用。
我们根据智利生长与肥胖队列研究(GOCS)中910名儿童0至7岁的体重指数(BMI)轨迹估算肥胖反弹年龄。在7岁时,我们测量了腰围(WC)、血糖、胰岛素、甘油三酯和高密度脂蛋白胆固醇水平,并构建了代谢风险评分。我们还测量了体脂百分比(肥胖程度)、血浆瘦素和脂联素浓度(脂肪功能)以及使用手腕超声测量骨龄(骨骼成熟度)。
我们发现44%的儿童肥胖反弹年龄<5岁。较早的肥胖反弹与更大的腰围(β:5.10(95%置信区间(CI):4.29 - 5.91))、更高的血糖(β:1.02(1.00 - 1.03))、胰岛素抵抗(β稳态模型评估:1.06(1.03 - 1.09))、甘油三酯(β:10.37(4.01 - 6.73))和不良代谢评分(β:0.30(0.02 - 0.37))相关。如果在模型中加入肥胖程度,这些关联会显著降低(即β腰围:0.85(0.33 - 1.38)),在较小程度上,加入脂肪因子(即β腰围:0.73(0.14 - 1.32))和骨骼成熟度(即β腰围:0.65(0.10 - 1.20))时也是如此。
在GOCS儿童中,较小年龄的肥胖反弹预示着7岁时更高的代谢风险;这些关联主要由肥胖程度增加解释,但脂肪功能障碍和骨骼成熟加速也起到一定作用。