Advanced glycation end products could play an important role of the progression of diabetic nephropathy via epigenetic changes.

众所周知，围产期营养过剩会增加日后肾损伤的易感性。虽然营养过剩，如高晚期糖基化终产物（AGEs）饮食，可能导致肾损伤的进展，在以后的生活中的确切机制仍有待阐明。从出生后第1天到第16周，与正常喂养（NF）的雄性后代相比，高AGEs喂养（高脂肪饮食和高果糖水：HFF）母亲所生的雄性后代血清脂联素水平降低。生后4周HFF组血清MDA水平较NF组明显升高。16周时HFF尿白蛋白增加，细胞外基质积聚增加。此外，HFF在16周时显著上调肾脏中TGF-β的蛋白表达。与NF相比，HFF的肌酐清除率降低。我们目前的数据表明，高AGEs饮食可通过氧化应激和脂联素的减少加重雄性后代在以后的生活中的肾损伤。

Overnutrition during perinatal period is known to increase susceptibility to renal injury later in life. Although the precise mechanisms why overnutrition,such as high advanced glycation end products(AGEs) diet,could cause the progression of renal injury later in life remain to be elucidated. Male offspring born to high AGEs fed(high fat diet and high fructose water: HFF) mothers had decreased serum adiponectin compared with male offspring born to normal fed(NF) from day 1 after birth to week 16. HFF had increased serum MDA compared with NF from week 4 after birth. Urinary albumin was increased and enhanced extracellular matrix accumulation was observed in HFF at 16 week. Moreover,HFF significantly upregulated protein expression of TGF-b in the kidney at 16 week. HFF had decreased creatinine clearance compared with NF. Our present data suggest that high AGEs diet could exacerbate renal injury via the oxidative stress and the decrease of adiponectin in male offspring later in life.