Association of adiposity, telomere length and mortality: data from the NHANES 1999-2002.
Association of adiposity, telomere length and mortality: data from the NHANES 1999-2002.
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DOI：
10.1038/ijo.2017.202
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发表时间：
2018-03
期刊：
影响因子：
--
通讯作者：
Bartels SJ
中科院分区：
文献类型：
--
作者：
Batsis JA;Mackenzie TA;Vasquez E;Germain CM;Emeny RT;Rippberger P;Lopez-Jimenez F;Bartels SJ
端粒缩短与年龄和合并症风险相关。我们评估了肥胖、白细胞端粒长度和死亡率之间的关系，以及这种关系是否会随着年龄而改变。采用双能x线吸收测量法（DEXA）的受试者采用1999-2002年全国健康和营养检查调查确定。肥胖分类采用两种体脂定义（BF1%：男性≥25%；女性≥35%；BF2%分别≥28%和≥38%）、体重指数（BMI）和腰围（WC）（男性≥102cm；女性≥88cm）。使用定量聚合酶链反应评估相对于标准参考DNA的端粒长度（T/S比）。加权多变量回归模型评估了端粒长度与肥胖的关系，包括连续和分类（低/正常BF%，低/高WC和标准BMI类别）。确定了端粒长度随年龄和肥胖的差异，随后的模型按年龄分层。比例风险模型根据肥胖状况评估死亡风险。在整个队列和年龄类别（<60岁vs.≥60岁；<70岁vs.≥70岁）中，通过肥胖相互作用检测端粒。我们确定了7827名受试者。平均年龄46.1岁。总端粒长度为1.05±0.01 (SE)，差异有BF1%（低/高：1.12±0.02比1.03±0.02,p<0.001）、BF2%（1.02±0.02比1.11±0.02,p<0.001）、BMI（体重过轻1.08±0.03，正常1.09±0.02，超重1.04±0.02，肥胖1.03±0.02,p<0.001）、WC（低/高1.09±0.02比1.02±0.02,p<0.001）。评价端粒长度与肥胖之间关系的调整β系数（连续测量）为：BF1% （β= - 0.0033±0.0008;p<0.001）、BF2%（- 0.041±0.008;p<0.001）、BMI （β= - 0.025±0.0008;p=0.005）和WC （β= - 0.0011±0.0004;p=0.007）。高BF% （BF1%: β= - 0.035±0.011,p=0.002; BF2%: β= - 0.041±0.008,p<0.001）和WC （β= - 0.035±0.011,p=0.008）与TL呈负相关，按年龄分层，高BF%（- 0.061±0.013）、高BF%（- 0.065±0.01）、bmi -肥胖（- 0.07±0.015）和高WC（- 0.048±0.013）与TL呈显著负相关（p<0.001）。这种关联随着年龄的增长而减弱。在老年参与者中，TL与死亡率呈负相关（HR 0.36[0.27,0.49]），与按BF1%（0.68[0.56,0.81]）、BF2%（0.75[0.65,0.80]）、BMI（0.50[0.42,0.60]）和WC(0.72[0.63,0.83]分类的死亡率呈负相关。未观察到肥胖状态、端粒长度和死亡率之间的相互作用。肥胖与年轻参与者的端粒长度较短有关，这种关系随着年龄的增长而减弱。它并没有缓和与死亡率的关系。
Telomere shortening is associated with age and risk of medical co-morbidity. We assessed the relationship between measures of adiposity, leukocyte telomere length, and mortality and whether it is modified by age. Subjects with dual energy x-ray absorptiometry (DEXA) measures were identified using the National Health and Nutrition Examination Survey 1999–2002. Obesity was categorized using two body fat definitions (BF1%: men≥25%; females ≥35%; BF2% ≥28% and ≥38%, respectively), body mass index (BMI), and waist circumference (WC) (men≥102cm; females≥88cm). Telomere length relative to standard reference DNA (T/S ratio) was assessed using quantitative polymerase chain reaction. Weighted multivariable regression models evaluated the association of telomere length with adiposity, both continuously and categorically (low/normal BF%, low/high WC and standard BMI categories). Differences in telomere length by age and adiposity were ascertained and subsequent models were stratified by age. Proportional hazard models assessed the risk of mortality by adiposity status. A telomere by adiposity interaction was tested in the entire cohort and by age category (<60 vs. ≥60 years; <70 vs. ≥70 years). We identified 7,827 subjects. Mean age was 46.1 years. Overall telomere length was 1.05±0.01 (SE) that differed by BF1% (low/high:1.12±0.02 vs. 1.03±0.02;p<0.001), BF2% (1.02±0.02 vs. 1.11±0.02;p<0.001), BMI (underweight 1.08±0.03; normal 1.09±0.02; overweight 1.04±0.02; obese 1.03±0.02;p<0.001), and WC (low/high 1.09±0.02 vs. 1.02±0.02;p<0.001). Adjusted β-coefficients evaluating the relationship between telomere length and adiposity (measured continuously) were: BF1% (β=−0.0033 ±0.0008;p<0.001), BF2% (−0.041±0.008;p<0.001), BMI (β=−0.025±0.0008;p=0.005), and WC (β=−0.0011±0.0004;p=0.007). High BF% (BF1%: β=−0.035±0.011;p=0.002; BF2%: β=−0.041±0.008; p<0.001) and WC (β=−0.035±0.011;p=0.008) were inversely related to TL. Stratifying by age, high BF1% (−0.061±0.013), BF2% (−0.065±0.01), BMI-obesity (−0.07±0.015) and high WC (−0.048±0.013) were significant (all p<0.001). This association diminished with increasing age. In older participants, TL was inversely related to mortality (HR 0.36 [0.27,0.49], as were those classified by BF1% (0.68 [0.56,0.81]), BF2% (0.75 [0.65,0.80], BMI (0.50 [0.42,0.60]), and WC (0.72 [0.63,0.83]. No interaction was observed between adiposity status, telomere length and mortality. Obesity is associated with shorter telomere length in young participants, a relationship that diminishes with increasing age. It does not moderate the relationship with mortality.
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影响因子：
3.7
作者：
Farzaneh-Far R;Lin J;Epel E;Lapham K;Blackburn E;Whooley MA
通讯作者：
Whooley MA
影响因子：
5
作者：
Houston, Denise K.;Ding, Jingzhong;Kritchevsky, Stephen B.
通讯作者：
Kritchevsky, Stephen B.
影响因子：
4.7
作者：
Batsis, J. A.;Mackenzie, T. A.;Bartels, S. J.
通讯作者：
Bartels, S. J.
影响因子：
8.9
作者：
Mueezzinler, A.;Zaineddin, A. K.;Brenner, H.
通讯作者：
Brenner, H.
DOI：
10.1038/ijo.2015.243
发表时间：
2016-05
期刊：
International journal of obesity (2005)
影响因子：
--
作者：
Batsis JA;Mackenzie TA;Bartels SJ;Sahakyan KR;Somers VK;Lopez-Jimenez F
通讯作者：
Lopez-Jimenez F