Does Accumulation of Advanced Glycation End Products Contribute to the Aging Phenotype?

Abstract

Based on these data, we propose that accumulation of AGEs accelerate the multisystem functional decline that occurs with aging, and therefore contribute to the aging phenotype. Exposure to AGEs can be reduced by restriction of dietary intake of AGEs and drug treatment with AGE inhibitors and AGE breakers. Modification of intake and circulating levels of AGEs may be a possible strategy to promote health in old age, especially because most Western foods are processed at high temperature and are rich in AGEs.

Thermal stability of collagen in naturally ageing and in vitro glycated rabbit tissues

“…An issue still discussed is whether stabilization of collagen fibres by AGEs formation resulting from an excess of sugars follows a similar pattern as that seen in normal ageing [10][11][12]21].…”

“…AGEs were found in all types of connective tissue, both in healthy ageing and in diabetic ones, and it is believed that glycation plays a main role in their ageing and disease-associated dysfunctions [8][9][10][11][12].…”

The application of information theory for the estimation of old-age multimorbidity

“…Among the biomarkers, following the above functional measurements, the highest NMI value was found for glucose at admission and discharge -0.05372 and 0.0441, respectively. This may emphasize the important role of glycation as a fundamental mechanism of aging for the emergence of multiple aging-related diseases (Semba et al 2010). Incidentally, the recently quite famous TAME studyBTargeting Aging with Metformin^that aims to reduce age-related multimorbidity by intervening into its underlying aging process, utilizes the well-known antidiabetic biguanide drug-metformin, which is a Bglucophage^with a primary function of reducing glucose and the corresponding glycation (Hall 2015;Newman et al 2016).…”

Formação de produtos da reação de Maillard em carne bovina (<i>Semimembranosus</i>) submetida a diferentes técnicas de cocção

“…Também, foi relatado que seus níveis estão aumentados no sangue e no colágeno da pele de pacientes com diabetes, comparado com indivíduos saudáveis (DYER et al, 1993;MIURA et al, 2003) 3) A interação entre os AGEs e seu receptor ativa sinais de transdução e induz resposta inflamatória. A interação AGE-RAGE (recepetor de AGE) ativa o fator nuclear-B, aumentando a transcrição para citocinas pró-inflamatórias (IL-1, IL-6), TNF-α, e moléculas de adesão como endotelina -1, VCAM-1 e selectina E (figura 6), e consequentemente, promove o stress oxidativo, trombogênese, inflamação vascular e angiogênese, eventos diretamente relacionados a complicações macro e microvasculares do diabetes (HUTTUNEN et al, 1999;HUANG et al, 2001;WAUTIER et al, 2001;HARJA et al, 2008;SEMBA et al, 2010).…”