Beschreibung:
<jats:title>Abstract</jats:title><jats:p>Dietary advanced glycation end products (AGE) formed during heating of food have gained interest as potential nutritional toxins with adverse effects on inflammation and glucose metabolism. In the present study, we investigated the short-term effects of high and low molecular weight (HMW and LMW) dietary AGE on insulin sensitivity, expression of the receptor for AGE (<jats:italic>RAGE</jats:italic>), the AGE receptor 1 (<jats:italic>AGER1</jats:italic>) and <jats:italic>TNF-α</jats:italic>, F2-isoprostaglandins, body composition and food intake. For 2 weeks, thirty-six Sprague–Dawley rats were fed a diet containing 20 % milk powder with different proportions of this being given as heated milk powder (0, 40 or 100 %), either native (HMW) or hydrolysed (LMW). Gene expression of <jats:italic>RAGE</jats:italic> and <jats:italic>AGER1</jats:italic> in whole blood increased in the group receiving a high AGE LMW diet, which also had the highest urinary excretion of the AGE, methylglyoxal-derived hydroimidazolone 1 (MG-H1). Urinary excretion of <jats:italic>N</jats:italic><jats:sup><jats:italic>ε</jats:italic></jats:sup>-carboxymethyl-lysine increased with increasing proportion of heat-treated milk powder in the HMW and LMW diets but was unrelated to gene expression. There was no difference in insulin sensitivity, F2-isoprostaglandins, food intake, water intake, body weight or body composition between the groups. In conclusion, <jats:italic>RAGE</jats:italic> and <jats:italic>AGER1</jats:italic> expression can be influenced by a high AGE diet after only 2 weeks in proportion to MG-H1 excretion. No other short-term effects were observed.</jats:p>