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Dietary intake of vegetables, folate, and antioxidants and the risk of Barrett's esophagus.蔬菜、叶酸和抗氧化剂的饮食摄入与 Barrett 食管的风险。
Cancer Causes Control. 2013 May;24(5):1005-14. doi: 10.1007/s10552-013-0175-3. Epub 2013 Feb 19.
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Inflammation and Barrett's carcinogenesis.炎症与巴雷特食管癌变。
Pathol Res Pract. 2012 May 15;208(5):269-80. doi: 10.1016/j.prp.2012.03.007. Epub 2012 Apr 27.
3
Advanced glycation end products and diabetic cardiovascular disease.糖基化终产物与糖尿病心血管疾病。
Cardiol Rev. 2012 Jul-Aug;20(4):177-83. doi: 10.1097/CRD.0b013e318244e57c.
4
Dietary fat and meat intakes and risk of reflux esophagitis, Barrett's esophagus and esophageal adenocarcinoma.饮食脂肪和肉类摄入量与反流性食管炎、巴雷特食管和食管腺癌的风险。
Int J Cancer. 2011 Sep 15;129(6):1493-502. doi: 10.1002/ijc.26108.
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Evidence for activation of Toll-like receptor and receptor for advanced glycation end products in preterm birth.早产中 Toll 样受体和晚期糖基化终产物受体激活的证据。
Mediators Inflamm. 2010;2010:490406. doi: 10.1155/2010/490406. Epub 2010 Nov 28.
6
Barrett's esophagus, esophageal and esophagogastric junction adenocarcinomas: the role of diet.巴雷特食管、食管和胃食管交界处腺癌:饮食的作用。
Clin Res Hepatol Gastroenterol. 2011 Jan;35(1):7-16. doi: 10.1016/j.gcb.2010.08.015.
7
Zinc deficiency activates S100A8 inflammation in the absence of COX-2 and promotes murine oral-esophageal tumor progression.锌缺乏会在没有 COX-2 的情况下激活 S100A8 炎症,并促进小鼠口腔食管肿瘤的进展。
Int J Cancer. 2011 Jul 15;129(2):331-45. doi: 10.1002/ijc.25688. Epub 2010 Nov 9.
8
Advanced glycation end products in foods and a practical guide to their reduction in the diet.食品中的晚期糖基化终产物及其饮食中减少摄入的实用指南。
J Am Diet Assoc. 2010 Jun;110(6):911-16.e12. doi: 10.1016/j.jada.2010.03.018.
9
Effects of dietary fiber, fats, and meat intakes on the risk of Barrett's esophagus.膳食纤维、脂肪和肉类摄入与 Barrett 食管风险的关系。
Nutr Cancer. 2009;61(5):607-16. doi: 10.1080/01635580902846585.
10
Zinc replenishment reverses overexpression of the proinflammatory mediator S100A8 and esophageal preneoplasia in the rat.锌补充可逆转大鼠体内促炎介质S100A8的过表达和食管发育异常。
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饮食中肉类、脂肪、动物产品和晚期糖基化终产物的摄入与 Barrett 食管的风险。

Dietary consumption of meat, fat, animal products and advanced glycation end-products and the risk of Barrett's oesophagus.

机构信息

Houston VA Health Services Research and Development Center of Excellence, Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX, USA.

出版信息

Aliment Pharmacol Ther. 2013 Oct;38(7):817-24. doi: 10.1111/apt.12459. Epub 2013 Aug 19.

DOI:10.1111/apt.12459
PMID:23957669
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3811083/
Abstract

BACKGROUND

Advanced glycation end-products (AGEs) are found in high quantity in high-fat foods and meat cooked at high temperature. AGEs have been shown to contribute to chronic inflammation and oxidative stress in humans.

AIM

To investigate the associations between consumption of meat, fat and AGEs, and the risk of Barrett's oesophagus (BO).

METHODS

We conducted a case-control study using data from the patients who were scheduled for elective esophagogastroduodenoscopy (EGD) and from a random sample of patients who were identified at primary care clinics. Daily consumption of meat, fat and Nε-(carboxymethyl) lysine (CML), a major type of AGEs, was derived from the food frequency questionnaire (FFQ). Multivariate logistic regression models were used to estimate the odds ratio (OR) and its 95% confidence interval (CI) for BO.

RESULTS

A total of 151 cases with BO and 777 controls without BO completed the FFQ. The multivariate OR (95% CI) for BO was 1.91 (1.07-3.38) for total meat, 1.80 (1.02-3.16) for saturated fat and 1.63 (0.96-2.76) for CML-AGE, when the highest tertile of intake was compared with the lowest. The association for total meat was attenuated to 1.61 (0.82-3.16), and that for saturated fat to 1.54 (0.81-2.94) after adjusting for CML-AGE.

CONCLUSIONS

Higher consumption of total meat, saturated fat or possibly CML-AGE was associated with an increased risk of Barrett's oesophagus. CML-AGE may partly explain the association between total meat and saturated fat consumption and the risk of Barrett's oesophagus.

摘要

背景

晚期糖基化终产物(AGEs)在高脂肪食物和高温烹饪的肉类中含量很高。AGEs 已被证明会导致人类慢性炎症和氧化应激。

目的

研究肉类、脂肪和 AGEs 的摄入量与 Barrett 食管(BO)风险之间的关联。

方法

我们使用计划接受选择性食管胃十二指肠镜检查(EGD)的患者和初级保健诊所中随机选择的患者的数据进行了病例对照研究。通过食物频率问卷(FFQ)得出每日肉类、脂肪和 Nε-(羧甲基)赖氨酸(CML)的摄入量,CML 是 AGEs 的主要类型之一。使用多变量逻辑回归模型估计 BO 的比值比(OR)及其 95%置信区间(CI)。

结果

共有 151 例 BO 患者和 777 例无 BO 对照者完成了 FFQ。与摄入量最低的 tertile 相比,总肉类、饱和脂肪和 CML-AGE 的多变量 OR(95%CI)分别为 1.91(1.07-3.38)、1.80(1.02-3.16)和 1.63(0.96-2.76)。调整 CML-AGE 后,总肉类的相关性减弱至 1.61(0.82-3.16),饱和脂肪的相关性减弱至 1.54(0.81-2.94)。

结论

总肉类、饱和脂肪或可能的 CML-AGE 摄入量较高与 Barrett 食管的风险增加相关。CML-AGE 可能部分解释了总肉类和饱和脂肪摄入与 Barrett 食管风险之间的关联。