Formula‐derived advanced glycation end products are involved in the development of long‐term inflammation and oxidative stress in kidney of IUGR piglets

Scope Formula‐derived dietary advanced glycation end products (AGEs) may promote programming of inflammation and oxidative stress in the kidney of intrauterine growth retardation (IUGR) piglets. Methods and results IUGR piglets received either a low temperature heated formula ( n = 8) or a high temperature heated formula (HHF: n = 8) or suckled naturally for 3 wk postnatally. Then they were fed with normal ad libitum regular diet. N(ε)‐carboxymethyllysine (CML) was measured in plasma, feces, and formula by HPLC/MS‐MS. CML was detected by immunofluorescence in kidney cells. Target renin–angiotensin—apoptotic, pro‐inflammatory genes—p62 NF‐κB, and soluble receptor of AGE (sRAGE) levels were quantified. Compared with that in controls, free CML and plasma urea increased significantly in the HHF‐fed group at PND36 ( p < 0.05). CML was detected in the nuclei of renal tubular cells of formula‐fed piglets but not in suckled ones. This presence of CML was associated with the activation of the soluble receptor of AGE. AT1, AT2, caspase 3, caspase 8, NF‐κB, p62 NF‐κB, and total protein oxidation in kidney were higher in HHF‐fed group as compared to LHF‐fed group ( p < 0.05). Conclusion Food processes aimed at reducing the concentration of AGEs in infant formula are urgently needed and may be therapeutically relevant for premature and/or IUGR babies.