Departments of Complex Genetics.
Toxicology, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, Maastricht University, Netherlands.
Am J Clin Nutr. 2018 Sep 1;108(3):453-475. doi: 10.1093/ajcn/nqy107.
Even before the onset of age-related diseases, obesity might be a contributing factor to the cumulative burden of oxidative stress and chronic inflammation throughout the life course. Obesity may therefore contribute to accelerated shortening of telomeres. Consequently, obese persons are more likely to have shorter telomeres, but the association between body mass index (BMI) and leukocyte telomere length (TL) might differ across the life span and between ethnicities and sexes.
A collaborative cross-sectional meta-analysis of observational studies was conducted to investigate the associations between BMI and TL across the life span.
Eighty-seven distinct study samples were included in the meta-analysis capturing data from 146,114 individuals. Study-specific age- and sex-adjusted regression coefficients were combined by using a random-effects model in which absolute [base pairs (bp)] and relative telomere to single-copy gene ratio (T/S ratio) TLs were regressed against BMI. Stratified analysis was performed by 3 age categories ("young": 18-60 y; "middle": 61-75 y; and "old": >75 y), sex, and ethnicity.
Each unit increase in BMI corresponded to a -3.99 bp (95% CI: -5.17, -2.81 bp) difference in TL in the total pooled sample; among young adults, each unit increase in BMI corresponded to a -7.67 bp (95% CI: -10.03, -5.31 bp) difference. Each unit increase in BMI corresponded to a -1.58 × 10(-3) unit T/S ratio (0.16% decrease; 95% CI: -2.14 × 10(-3), -1.01 × 10(-3)) difference in age- and sex-adjusted relative TL in the total pooled sample; among young adults, each unit increase in BMI corresponded to a -2.58 × 10(-3) unit T/S ratio (0.26% decrease; 95% CI: -3.92 × 10(-3), -1.25 × 10(-3)). The associations were predominantly for the white pooled population. No sex differences were observed.
A higher BMI is associated with shorter telomeres, especially in younger individuals. The presently observed difference is not negligible. Meta-analyses of longitudinal studies evaluating change in body weight alongside change in TL are warranted.
即使在与年龄相关的疾病出现之前,肥胖也可能是导致整个生命周期内氧化应激和慢性炎症累积负担的一个因素。因此,肥胖可能导致端粒加速缩短。因此,肥胖者的端粒更短,但体重指数(BMI)与白细胞端粒长度(TL)之间的关联可能因寿命、种族和性别而异。
对观察性研究进行协作横断面荟萃分析,以研究整个生命周期中 BMI 与 TL 之间的关系。
荟萃分析纳入了 87 个独特的研究样本,共包含 146114 名个体的数据。采用随机效应模型,将研究特异性的年龄和性别调整后的回归系数结合起来,其中绝对(碱基对(bp))和相对端粒与单拷贝基因比值(T/S 比值)TL 与 BMI 相关。通过 3 个年龄组(“年轻”:18-60 岁;“中年”:61-75 岁;“老年”:>75 岁)、性别和种族进行分层分析。
在总 pooled 样本中,BMI 每增加一个单位,TL 相应减少-3.99 bp(95%CI:-5.17,-2.81 bp);在年轻成年人中,BMI 每增加一个单位,TL 相应减少-7.67 bp(95%CI:-10.03,-5.31 bp)。在总 pooled 样本中,BMI 每增加一个单位,年龄和性别调整后的相对 TL 的 T/S 比值相应减少-1.58×10(-3)单位(0.16%减少;95%CI:-2.14×10(-3),-1.01×10(-3));在年轻成年人中,BMI 每增加一个单位,T/S 比值相应减少-2.58×10(-3)单位(0.26%减少;95%CI:-3.92×10(-3),-1.25×10(-3))。这些关联主要见于白人 pooled 人群。未观察到性别差异。
较高的 BMI 与较短的端粒相关,尤其是在年轻个体中。目前观察到的差异不容忽视。需要进行前瞻性研究,评估体重随 TL 变化的变化。