Obesity and inflammation markers in relation to leukocyte telomere length in a cross-sectional study of persons with Barrett's esophagus.
Obesity and inflammation markers in relation to leukocyte telomere length in a cross-sectional study of persons with Barrett's esophagus.
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DOI：
10.1186/s40608-015-0063-3
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Vaughan TL
中科院分区：
文献类型：
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作者：
Hardikar S;Song X;Risques RA;Montine TJ;Duggan C;Blount PL;Reid BJ;Anderson GL;Kratz M;White E;Vaughan TL
端粒缩短与年龄增长、男性性别和生活方式因素（如肥胖和吸烟）有关。炎症也与细胞衰老有关，并可能促进慢性疾病如肥胖症和糖尿病中的端粒缩短。然而，人们对肥胖和炎症的标志物与白细胞端粒长度（LTL）之间的关系知之甚少。采用定量聚合酶链反应测定了1995年至2009年间295例Barrett食管（BE）患者外周血白细胞的LTL。生活方式变量的数据，包括肥胖和吸烟，收集在人的采访。在储存的血液样品中测量肥胖（瘦素、脂联素）、糖尿病（葡萄糖、胰岛素）、炎症（C-反应蛋白、白细胞介素-6、表面肿瘤坏死因子受体（sTNFR）I和II）和氧化应激（F2-异前列腺素）的生物标志物。我们使用线性和逻辑回归模型，对可能的混杂因素进行了调整，在横断面分析中研究了这些协变量与LTL之间的关联。LTL与年龄（r =-0.30，p < 0.001）、性别（女性r = 0.14，p = 0.01）显著相关，与香烟包年呈负相关（r =-0.11，p = 0.04）。对于sTNF-RI最高三分位数的参与者，具有短LTL的几率显著更高（根据年龄、性别、吸烟和肥胖调整的比值比= 2.19; 95%CI 1.00-4.85，p趋势= 0.02）。LTL与任何其他生活方式因素（包括吸烟或肥胖）或其他炎症、肥胖/糖尿病相关生物标志物测量均无显著相关性。在BE患者中，年龄增加、男性、吸烟史和sTNF-RI水平与LTL缩短相关，但LTL与其他炎症标志物或肥胖指标之间无相关性。为了进一步建立肥胖、炎症标志物和LTL之间的潜在关系，需要进行更大规模的纵向研究。
Telomere shortening is associated with increasing age, male gender and lifestyle factors such as obesity and smoking. Inflammation has also been implicated in cellular senescence and may promote telomere shortening in chronic conditions such as obesity and diabetes. However, little is known about the relationship between markers of obesity and inflammation, and leukocyte telomere length (LTL). LTL was measured using quantitative polymerase chain reaction in peripheral leukocytes from 295 individuals diagnosed with Barrett’s esophagus (BE) between 1995 and 2009. Data on lifestyle variables including obesity and smoking were collected at in-person interviews. Biomarkers of obesity (leptin, adiponectin), diabetes (glucose, insulin), inflammation (C-reactive protein, Interleukin-6, surface tumor necrosis factor receptor (sTNFR) I & II) and oxidative stress (F2-isoprostanes) were measured in stored blood samples. We examined associations between these covariates and LTL in a cross-sectional analysis using linear and logistic regression models, adjusting for possible confounders. LTL was significantly associated with age (r = −0.30, p < 0.001), gender (r = 0.14 for females, p = 0.01) and inversely associated with cigarette pack-years (r = −0.11, p = 0.04). Odds of having short LTL were significantly higher for participants in the highest tertile for sTNF-RI (Odds ratio adjusted for age, gender, smoking, and obesity = 2.19; 95 % CI 1.00–4.85, p-trend = 0.02). LTL was not significantly associated with any other lifestyle factors, including smoking or obesity, or other inflammation-, obesity-/diabetes-related biomarkers measured. Increasing age, male gender, smoking history, and sTNF-RI levels were associated with short LTL among persons with BE but no correlations were observed between LTL and other inflammatory markers or measures of obesity. Larger longitudinal studies are necessary in order to further establish the potential relationships between obesity, inflammation markers and LTL.