Maternally transmitted and food-derived glycotoxins: a factor preconditioning the young to diabetes?

Proinflammatory advanced glycation end products (AGEs) found in thermally processed foods correlate with serum AGEs (sAGEs) and promote type 1 and type 2 diabetes in mice. Herein we assess the relationship of maternal blood and food AGEs to circulating glycoxidants, inflammatory markers, and insulin levels in infants up to age 1 year.

AGEs (N(ε)-carboxymethyllysine [CML] and methylglyoxal derivatives) were tested in sera of healthy mothers in labor (n = 60), their infants, and infant foods. Plasma 8-isoprostane, fasting glucose, insulin, leptin, and adiponectin levels were assessed in 12-month-old infants.

Significant correlations were found between newborn and maternal serum CML (sCML) (r = 0.734, P = 0.001) serum methylglyoxal derivatives (sMGs) (r = 0.593, P = 0.001), and 8-isoprostanes (r = 0.644, P = 0.001). Infant adiponectin at 12 months negatively correlated with maternal sCML (r = -0.467, P = 0.011), whereas high maternal sMGs predicted higher infant insulin or homeostasis model assessment (P = 0.027). Infant sAGEs significantly increased with the initiation of processed infant food intake, raising daily AGE consumption by ∼7.5-fold in year 1.

Maternal blood and food-derived AGEs prematurely raise AGEs in children to adult norms, preconditioning them to abnormally high oxidant stress and inflammation and thus possibly to early onset of disease, such as diabetes.