Dietary advanced glycation end products restriction diminishes inflammation markers and oxidative stress in patients with type 2 diabetes mellitus.

The augmented consumption of dietary advanced glycation end products (dAGEs) has been associated with increased oxidative stress and inflammation, however, there is insufficient information over the effect on insulin resistance. The objective of the present study is to investigate the effect of dAGEs restriction on tumor necrosis factor-α (TNF-α), malondialdehyde, C-reactive protein (CRP), and insulin resistance in DM2 patients. We carried out a randomized 6 weeks prospective study in two groups of patients: subjects with a standard diet (n = 13), vs low dAGEs (n = 13). At the beginning and the end of study, we collected anthropometric measurements, and values of circulating glucose, HbA1c, lipids, insulin, serum AGEs, CRP, TNF-α and malondialdehyde. Anthropometric measurements, glucose, and lipids were similar in both groups at base line and at the end of the study. Estimation of basal dAGEs was similar in both groups; after 6 weeks it was unchanged in the standard group but in the low dAGEs group decreased by 44% (p<0.0002). Changes in TNF-α levels were different under standard diet (12.5 ± 14.7) as compared with low dAGEs (-18.36 ± 17.1, p<0.00001); changes in malondialdehyde were different in the respective groups (2.0 ± 2.61 and -0.83 ± 2.0, p<0.005) no changes were found for insulin levels or HOMA-IR. In conclusion, The dAGEs restriction decreased significantly TNF-α and malondialdehyde levels.