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Advanced glycation end products (AGEs) are implicated in β-cell oxidant stress. Diet-derived AGE (dAGE) are shown to contribute to end-organ toxicity attributed to diabetes. To assess the role of dAGE on type 1 diabetes, NOD mice were exposed to a high-AGE diet (H-AGE) and to a nutritionally similar diet with approximate fivefold-lower levels of [N.sup.ζ]-carboxymethyllysine (CML) and methylglyoxal-derivatives (MG) (L-AGE). Suppression of serum CML and MG in L-AGE-fed mice was marked by suppression of diabetes (H-AGE mice >94% vs. L-AGE mice 33% in founder [[F].sub.0], 14% in [F.sub.1], and 13% in [F.sub.2] offspring, P < 0.006) and by a delay in disease onset (4-month lag). Survival for L-AGE mice was 76 vs. 0% after 44 weeks of H-AGE mice. Reduced insulitis in L-AGE versus H-AGE mice (P < 0.01) was marked by GAD- and insulin-unresponsive pancreatic interleukin (IL)-4-positive CD4+ cells compared with the GAD and insulin-responsive interferon (IFN)-γ-positive T-cells from H-AGE mice (P < 0.005). Splenocytes from L-AGE mice consisted of GAD- and insulin-responsive IL-10-positive CD4+ cells compared with the IFN-γ-positive T-cells from H-AGE mice (P < 0.005). Therefore, high AGE intake may provide excess antigenic stimulus for T-cell-mediated diabetes or direct β-cell injury in NOD mice; both processes are ameliorated by maternal or neonatal exposure to L-AGE nutrition., Insulin-dependent diabetes (type 1 diabetes) is an autoimmune disease resulting from T-cell-mediated destruction of pancreatic islet β-cells (1). However, the initial events of this process are incompletely understood. While both [...]

In adults a decrease in exogenous glucose supply is fully compensated by an increase in endogenous production. In preterm infants hypoglycemia is a frequent complication, especially in infants [is less [...]