Most chronic modern non-transmissible diseases seem to begin as the result of low-grade inflammation extending over prolonged periods of time. The importance of diet as a source of many pro-inflammatory compounds that could create and sustain such a low-grade inflammatory state cannot be ignored, particularly since we are constantly exposed to them during the day. The focus of this review is on specific components of the diet associated with inflammation, specifically advanced glycation end products (AGEs) that form during thermal processing of food. AGEs are also generated in the body in normal physiology and are widely recognized as increased in diabetes, but many people are unaware of the potential importance of exogenous AGEs ingested in food. We review experimental models, epidemiologic data, and small clinical trials that suggest an important association between dietary intake of these compounds and development of an inflammatory and pro-oxidative state that is conducive to chronic diseases. We compare dietary intake of AGEs with other widely known dietary patterns, such as the Mediterranean and the Dietary Approaches to Stop Hypertension (DASH) diets, as well as the Dietary Inflammation Index (DII). Finally, we delineate in detail the pathophysiological mechanisms induced by dietary AGEs, both direct (i.e., non-receptor-mediated) and indirect (receptor-mediated).

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.

The aim of this study was to review the effect of a low advanced glycation end product (AGEs) diet, exercise, and a combination of both on circulating AGE levels as well as on plasma lipids and anthropometric parameters. Forty-three overweight or obese men (body mass index [BMI] >25 kg/m(2)), 30 to 55 y, participated in a 12-wk study and were randomly assigned to one of three groups: low AGE diet, exercise with habitual food intake, or exercise plus low AGE diet. Exercise was for 45 min at 65% to 75% of their maximum heart rate three times a week. We measured somatometric variables (BMI and waist circumference), blood glucose, lipids, and serum AGEs (N(ε)-[Carboxymethyl]Lysine [CML] and methylglyoxal [MG]) at baseline and at 12 wk. Exercise alone was associated with decreased somatometric variables; the low AGE diet had the same effects and decreased serum CML and MG and when combined with exercise reproduced all these effects, but also decreased triacylglycerols and increased high-density lipoprotein. Correlation analysis showed that both changes of CML and MG correlated with changes in dietary AGEs (P < 0.020 and P < 0.038, respectively); change in maximum oxygen consumption correlated inversely with change in weight and triacylglycerols. Regression analyses, including change in dietary AGEs and in dietary calories, showed that change in dietary AGEs was the independent determinant of change in CML (P < 0.020) and MG (P < 0.038). An AGE-restricted diet reduces serum AGE and indices of body fat. The addition of exercise to the restricted diet has the same effects but also improves lipid profile.

Type 2 diabetes mellitus (T2D) is a leading cause of morbidity and mortality in Mexico. Here, we aimed to report incidence rates (IR) of type 2 diabetes in middle-aged apparently-healthy Mexican adults, identify risk factors associated to ID and develop a predictive model for ID in a high-risk population. Prospective 3-year observational cohort, comprised of apparently-healthy adults from urban settings of central Mexico in whom demographic, anthropometric and biochemical data was collected. We evaluated risk factors for ID using Cox proportional hazard regression and developed predictive models for ID. We included 7636 participants of whom 6144 completed follow-up. We observed 331 ID cases (IR: 21.9 per 1000 person-years, 95%CI 21.37–22.47). Risk factors for ID included family history of diabetes, age, abdominal obesity, waist-height ratio, impaired fasting glucose (IFG), HOMA2-IR and metabolic syndrome. Early-onset ID was also high (IR 14.77 per 1000 person-years, 95%CI 14.21–15.35), and risk factors included HOMA-IR and IFG. Our ID predictive model included age, hypertriglyceridemia, IFG, hypertension and abdominal obesity as predictors (Dxy = 0.487, c-statistic = 0.741) and had higher predictive accuracy compared to FINDRISC and Cambridge risk scores. ID in apparently healthy middle-aged Mexican adults is currently at an alarming rate. The constructed models can be implemented to predict diabetes risk and represent the largest prospective effort for the study metabolic diseases in Latin-American population.