http://www.nature.com/ejcn/journal/v67/n3/full/ejcn2012220a.htmlNeste endereco encontra-se o artigo na integra.ReviewEuropean Journal of Clinical Nutrition (2013) 67, 239248; doi:10.1038/ejcn.2012.220; published online 30 January 2013Dietary advanced glycation end-product restriction for the attenuation of insulin resistance, oxidative stress and endothelial dysfunction: a systematic reviewN J Kellow1 and G S Savige11Department of Rural & Indigenous Health, Monash University, Moe, Victoria, AustraliaCorrespondence: NJ Kellow, Department of Rural & Indigenous Health, Monash University, PO Box 975, Moe, Victoria 3833, Australia. E-mail:nicolekellow@live.com.auReceived 12 November 2012; Revised 19 December 2012; Accepted 21 December 2012Advance online publication 30 January 2013Topof pageAbstractThe benefits of advanced glycation end-product (AGE)-restricted diets in humans are unclear. This review aimed to determine the effect of dietary AGE restriction on the inflammatory profiles of healthy adults and adults with diabetes or renal failure. Eight computer databases were searched for controlled feeding trials published in English between January 1997 and December 2012. Human trials were included if at least one group received an AGE-restricted dietary intervention. A total of 12 trials reporting on 289 participants were included in the review. Five trials (42%) were of high methodological quality. Meta-analysis of two long-term (16 week) trials provided evidence favoring an AGE-restricted diet for the reduction of 8-isoprostanes (standardized mean difference 0.9; 95% confidence interval (CI): 0.31.5) and tumor necrosis factor- (1.3; 95% CI: 0.61.9) in healthy adults. Intermediate-term dietary AGE restriction in adults with chronic renal failure reduced serum VCAM-1 (0.9; 95% CI: 0.11.7). Individual trials provided some evidence that long-term dietary AGE restriction reduces HOMA-IR (1.4; 95% CI: 0.32.6) and AGE-modified low-density lipoprotein (2.7; 95% CI: 1.63.9) in adults with type 2 diabetes. Generalisability is limited, as 75% of studies were of less than 6 weeks duration and more than half were of low methodological quality. Evidence quality ranged from low to very low, limiting the conclusions that can be drawn from this review. There is currently insufficient evidence to recommend dietary AGE restriction for the alleviation of the proinflammatory milieu in healthy individuals and patients with diabetes or renal failure. Additional long-term high-quality RCTs with larger sample sizes measuring patient-important outcomes are required to strengthen the evidence supporting the effects of AGE-restricted diets.Keywords: systematic review; advanced glycation end product; dietary AGE restriction; diabetes; inflammation; humans http://www.unileverhealthinstitute.com.br/artigo/produtos-de-glicacao-avancadaProdutos de glicacao avancada (AGEs) sao compostos toxicos formados por meio de uma reacao nao enzimatica entre acucares redutores e proteinas, fosfolipideos ou acidos nucleicos, conhecida como reacao de Maillard. Isto ocorre como parte do metabolismo normal, porem, quando produzidos em excesso, os AGEs promovem estresse oxidativo, inflamacao e alteracao na funcao de proteinas, tornando-se patogenicos. Carboximetilisina (CML) e derivados do metilglioxal (MG) estao entre os mais estudados1. Alem da producao endogena, estas glicotoxinas tambem estao presentes nos alimentos, sendo o processamento (temperatura e metodo de coccao) o principal responsavel pela formacao de AGEs nos alimentos. A exposicao ao calor (alimentos grelhados, fritos, assados e churrasco) gera mais AGEs do que a coccao em temperaturas mais baixas e na presenca de agua (alimentos cozidos em agua ou no vapor)2. Por exemplo, amostras de peito de frango frito apresentam 73.896 U/g de AGEs, enquanto este valor