Müezzinler Aysel, Mons Ute, Dieffenbach Aida Karina, Butterbach Katja, Saum Kai-Uwe, Schick Matthias, Stammer Hermann, Boukamp Petra, Holleczek Bernd, Stegmaier Christa, Brenner Hermann
Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany; Network Aging Research (NAR), University of Heidelberg, Heidelberg, Germany.
Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Exp Gerontol. 2016 Feb;74:1-8. doi: 10.1016/j.exger.2015.11.019. Epub 2015 Nov 30.
Telomere length (TL) has been proposed as a biomarker of ageing, which might be used to identify individuals at higher risk of age-related diseases. Obesity is a well-known risk factor for several diseases. This study aims to analyse the associations of BMI with TL and the rate of TL change in older adults.
Leukocyte TL (LTL) was measured by quantitative PCR in blood samples of 3600 older adults aged 50-75 years obtained at the baseline examination of a population-based cohort study in Germany. For longitudinal analyses, measurements were repeated in blood samples obtained at 8-year follow-up from 1000 participants. Multivariate linear regression models were used to estimate associations of BMI with LTL and changes in LTL over time.
LTL was inversely associated with age (r = -0.090, p < 0.0001). BMI and LTL associations varied according to age (p for interaction = 0.021). BMI was significantly inversely associated with LTL in those younger than 60 years (-6 basepairs per 1 kg/m(2) difference in BMI). In particular, weight gain during adulthood was inversely associated with LTL in a dose-response manner in this age group, with those having gained ≥ 30 kg having significantly shorter telomeres (-209 basepairs) than those who maintained their weight. No clear patterns were observed between any of BMI-related variables and the rate of LTL change.
Our cross-sectional analysis supports suggestions that weight gain during adulthood and obesity may contribute to shorter telomere length below 60 years of age, but this relationship could not be shown longitudinally.
端粒长度（TL）已被提议作为衰老的生物标志物，可用于识别患年龄相关疾病风险较高的个体。肥胖是多种疾病的公认风险因素。本研究旨在分析老年人中体重指数（BMI）与TL的关联以及TL变化率。
在德国一项基于人群的队列研究的基线检查中，对3600名年龄在50 - 75岁的老年人的血样进行定量PCR测量白细胞端粒长度（LTL）。对于纵向分析，在1000名参与者8年随访时采集的血样中重复测量。使用多变量线性回归模型来估计BMI与LTL的关联以及LTL随时间的变化。
LTL与年龄呈负相关（r = -0.090，p < 0.0001）。BMI与LTL的关联因年龄而异（交互作用p = 0.021）。在60岁以下人群中，BMI与LTL显著负相关（BMI每相差1 kg/m²，LTL减少6个碱基对）。特别是，在该年龄组中，成年期体重增加与LTL呈剂量反应负相关，体重增加≥30 kg者的端粒长度（-209个碱基对）显著短于体重维持不变者。未观察到任何与BMI相关的变量与LTL变化率之间有明确模式。
我们的横断面分析支持以下观点，即成年期体重增加和肥胖可能导致60岁以下人群的端粒长度缩短，但纵向未能证实这种关系。
