The endothelial functional is impaired by advanced glycation end products (AGE) in eutrophic and obese healthy adults

Background: An endogenous increase in advanced glycation products (AGE - advanced glycation end product) has been correlated with coronary artery disease (CAD) for some time, but the role of exogenous AGEs consumed through foods with any degree of processing that involves temperature increase, has not yet been fully elucidated. We aimed to verify if the dietary intake of AGE (dAGE) and the formation of fluorescent AGE in the skin correlate with the presence of endothelial dysfunction and subclinical atherosclerosis during the aging process.

Design: Observational, quantitative, descriptive cross-sectional study

Methods: 30 adults (age 54 + 9.7 years; non-smokers, without diabetes mellitus (DM), and without coronary artery disease were stratified by Body Mass Index (BMI) range (normal weight <25 Kg/m2, between 25 and 29.9 Kg/m2 overweight and obesity >30 Kg/m2), and evaluated about dietary intake and AGE formation and cardiovascular parameters related to endothelial function, and subclinical atherosclerosis. We used Carotid Doppler Ultrasound to calculate intimal medial thickness (IMT), flow-mediated dilation (FMD) to verify endothelial function, Skin Autofluorescence (SAF) AGE reading to measure AGE formation. We collected 03 24-hour dietary recalls on different days to calculate dietary AGE intake.

Results: dAGE and SAF was homogeneous in the 3 evaluated groups (eutrophic = 17743 + 6088 kU/day ; 3,0 + 0,7 AU , overweight = 20555 + 4901 kU/day ; 2,7 + 0,5 AU, obese = 18424 + 8778 kU/day; 2,7 + 0,7 AU; p=0.63; p=0,58). dAGE was inversely correlated with the FMD in the eutrophic group (r=-0.679, p<0.05). SAF was inversely orreated with FD in the obesegroup (r=-0,662, p= <0,05).

Conclusion: In healthy elderly, higher dietary AGE and the fluorescent AGE in the skin are independently associated with endothelial dysfunction, suggesting a contribution to the atherosclerosis process.