高温烧烤类食物促进糖尿病心血管粥样硬化
J Am Diet Assoc 2010年6月;
食物中的晚期糖基化终末产物和在饮食中减少糖基化终末产物的实用指南
Jaime Uribarri 1, Sandra Woodruff, Susan Goodman, Weijing Cai, Xue Chen, Renata Pyzik, Angie Yong, Gary E前锋，Helen Vlassara
现代饮食大多经过热处理，因此含有高水平的晚期糖基化终产物(AGEs)。膳食糖基化终末产物(dAGEs)被认为有助于增加氧化应激和炎症，这与最近流行的糖尿病和心血管疾病有关。本报告显著扩展了现有的dAGE数据库，验证了dAGE测试方法，比较了新dAGE形成的烹饪方法和抑菌剂，并介绍了减少日常生活中dAGE消耗的实用方法。根据研究结果，在不同的食物种类中，干热可以促进>形成比未煮熟高出10- 100倍的新dAGE。动物性食品，高脂肪和蛋白质，通常是富年龄和容易在烹饪的新时代形成。相比之下，富含碳水化合物的食物，如蔬菜、水果、全谷类食物和牛奶，即使是在烹饪后，保质期也相对较短。在烹饪过程中，抑制年龄的化合物氨基胍可以防止新dAGEs的形成，而通过湿热烹饪、使用更短的烹饪时间、在更低的温度下烹饪和使用酸性成分如柠檬汁或醋，可以显著减少新dAGEs的形成。新的dAGE数据库为估计dAGE摄取量和指导食物选择以减少dAGE摄取量提供了一个有价值的工具。
2010年美国饮食协会。爱思唯尔出版保留所有权利。J Am Diet Assoc, 2010 Jun;
Advanced glycation end products in foods and a practical guide to their reduction in the diet
Jaime Uribarri 1, Sandra Woodruff, Susan Goodman, Weijing Cai, Xue Chen, Renata Pyzik, Angie Yong, Gary E Striker, Helen VlassaraDivision of Nephrology, Mount Sinai School of Medicine, New York, NY, USA.
Modern diets are largely heat-processed and as a result contain high levels of advanced glycation end products (AGEs). Dietary advanced glycation end products (dAGEs) are known to contribute to increased oxidant stress and inflammation, which are linked to the recent epidemics of diabetes and cardiovascular disease. This report significantly expands the available dAGE database, validates the dAGE testing methodology, compares cooking procedures and inhibitory agents on new dAGE formation, and introduces practical approaches for reducing dAGE consumption in daily life. Based on the findings, dry heat promotes new dAGE formation by >10- to 100-fold above the uncooked state across food categories. Animal-derived foods that are high in fat and protein are generally AGE-rich and prone to new AGE formation during cooking. In contrast, carbohydrate-rich foods such as vegetables, fruits, whole grains, and milk contain relatively few AGEs, even after cooking. The formation of new dAGEs during cooking was prevented by the AGE inhibitory compound aminoguanidine and significantly reduced by cooking with moist heat, using shorter cooking times, cooking at lower temperatures, and by use of acidic ingredients such as lemon juice or vinegar. The new dAGE database provides a valuable instrument for estimating dAGE intake and for guiding food choices to reduce dAGE intake.
2010 American Dietetic Association. Published by Elsevier Inc. All rights reserved.https://pubmed.ncbi.nlm.nih.gov/20497781/
在2型糖尿病患者中 膳食晚期糖基化终产物摄取与动脉硬化和炎症有关
High intake of dietary advanced glycation end-products is associated with increased arterial stiffness and inflammation in subjects with type 2 diabetes.
心血管疾病杂志2017年11月27(11):978-984。doi:10.1016 / j.numecd.2017.06.014。Epub 2017年7月8日。
Di Pino A1, Currenti W1, Urbano F1, Scicali R1, Piro S1, Purrello F2, Rabuazzo AM1。
作者信息
摘要
背景和目的:
现代饮食中含有从加工方法中衍生出来的高级糖基化终产物(dAGEs)，在促进动脉粥样硬化风险方面发挥了关键作用。在这项横断面研究中，我们研究了dAGE摄入量、动脉僵硬度、炎症情况和大量营养成分之间的关系。
方法和结果:
对85例2型糖尿病患者的动脉僵硬度、羧基甲基赖氨酸、内源性内分泌受体(esRAGE)、高敏感性C反应蛋白(hs-CRP)、S100A12和宏量营养素摄入量进行了评价。受试者根据达歌消费分层分为两组:高、低dAGEs摄入量(≥或< 15.000 kU /天,分别)。高摄入dAGEs(n = 45)显示更高的增大,增大指数和脉搏波速度(采集)相比,这些学科dAGEs的摄入量较低(18±5.4 vs 12.2±6.3毫米汞柱,P < 0.05;38.3±5.4 vs 29.3±10%;9.2±1.4米/秒和7.9±1.7,P < 0.05,分别)。高dAGE摄入量的受试者hs-CRP较高[0.42 (0.18-0.54)vs 0.21 (0.14-0.52) mg/dL, P < 0.05，而esRAGE血浆水平较低[0.16 (0.23-0.81)vs 0.2 (0.14-0.54) ng/dL, P < 0.05]。简单回归分析显示dAGEs与脂肪摄入量存在相关性。多因素分析表明，增加、收缩压(BP)与dAGE消耗之间存在独立的联系;BMI和esRAGE是PWV的主要决定因素。
结论:
我们的数据表明，长期高dAGE饮食可能导致血管功能障碍和炎症激活，导致2型糖尿病患者出现血管并发症。检验这一假设可能代表了未来研究的方向。
关键词:
心血管疾病;膳食高级糖基化终端产品;炎症;晚期糖基化终产物可溶性受体;2型糖尿病High intake of dietary advanced glycation end-products is associated with increased arterial stiffness and inflammation in subjects with type 2 diabetes.
Nutr Metab Cardiovasc Dis. 2017 Nov;27(11):978-984. doi: 10.1016/j.numecd.2017.06.014. Epub 2017 Jul 8.
Abstract
BACKGROUND AND AIMS:
Modern diets are high in advanced glycation end-products (dAGEs), derived from processing methods, exerting a pivotal role in promoting atherosclerotic risk. In this cross-sectional study we investigate the relationship between dAGE intake, arterial stiffness, inflammatory profile and macronutrient composition, in subjects with type 2 diabetes without overt cardiovascular disease.
METHODS AND RESULTS:
Arterial stiffness, carboxy-methyl-lysine, endogenous secretory receptor for AGEs (esRAGE), high sensitivity C reactive protein (hs-CRP), S100A12 and macronutrient intake were evaluated in 85 subjects with type 2 diabetes. The subjects were stratified into two groups according to dAGE consumption: high and low dAGE intake (≥ or <15.000 kU/day, respectively). Subjects with high dAGE intake (n = 45) showed a higher augmentation, augmentation index and pulse wave velocity (PWV) compared with those subjects with low dAGE intake (18 ± 5.4 vs 12.2 ± 6.3 mmHg, P < 0.05; 38.3 ± 5.4 vs 29.3 ± 10%; 9.2 ± 1.4 m/sec vs 7.9 ± 1.7, P < 0.05, respectively). hs-CRP were higher in subjects with high dAGE intake [0.42 (0.18-0.54) vs 0.21 (0.14-0.52) mg/dL, P < 0.05] whereas esRAGE plasma levels were lower [0.16 (0.23-0.81) vs 0.2 (0.14-0.54) ng/dL, P < 0.05]. Simple regression analysis showed a correlation between dAGEs and fat intake. Multivariate analysis showed an independent association between augmentation, systolic blood pressure (BP) and dAGE consumption; BMI and esRAGE were the major determinants of PWV.
CONCLUSIONS:
Our data suggests that a chronic high dAGE diet could lead to a vascular dysfunction and inflammatory activation, contributing to the development of vascular complications in subjects with type 2 diabetes. Testing this hypothesis may represent a direction of future research.
Copyright © 2017 The Italian Society of Diabetology, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition, and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.
KEYWORDS:
Cardiovascular disease; Dietary advanced glycation end-products; Inflammation; Soluble receptor for advanced glycation endproducts; Type 2 diabetes
- PMID:
- 28958695
- DOI:
- 10.1016/j.numecd.2017.06.014
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