Poulsen Malene W, Bak Monika J, Andersen Jeanette M, Monošík Rastislav, Giraudi-Futin Anne C, Holst Jens J, Nielsen John, Lauritzen Lotte, Larsen Lesli H, Bügel Susanne, Dragsted Lars O
Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, Rolighedsvej 30, 1958, Frederiksberg C, Denmark.
Eur J Nutr. 2014;53(2):661-72. doi: 10.1007/s00394-013-0574-y. Epub 2013 Aug 9.
Advanced glycation end products (AGEs) formed in food during high-heat cooking may induce overeating and inflammation. We investigated whether AGE contents in a single meal affect postprandial appetite and markers of inflammation, endothelial activation, and oxidative stress.
In total, 19 healthy overweight individuals completed a crossover meal test with two meals of identical ingredients prepared by roasting (H-AGE) or steaming (L-AGE), respectively. Postprandial blood samples were analysed for N(ε)-carboxymethyl-lysine (CML), appetite-regulating gut hormones, glucose, insulin, triacylglycerol, and markers of inflammation and endothelial activation. Subjective appetite ratings and subsequent food intake were also assessed, and urine was analysed for CML, methylglyoxal-derived hydroimidazolone (MG-H1), and F2-isoprostanes.
CML content of the H- and L-AGE meals was 5.0 and 2.8 mg, respectively. Plasma CML and urinary CML and MG-H1 tended to be higher after the H-AGE meal. There was no change in subsequent food intake, appetite sensations, or appetite hormone responses between meals, except for the overall ghrelin response, which was higher after the H-AGE meal compared with the L-AGE meal (p = 0.016). There was an increased glycaemic response to the H-AGE meal (p = 0.027) compared with the L-AGE meal. Inflammatory and endothelial activation markers did not differ between meals, but there was an overall effect on endothelial activation (p = 0.021) and on the oxidative marker, F2-isoprostanes, in urine (p = 0.013).
The present study did not show any pronounced effects of AGEs on appetite and markers of inflammation, but did indicate that AGEs may affect postprandial ghrelin, oxidative stress, and glucose responses.
高温烹饪过程中食物形成的晚期糖基化终产物（AGEs）可能会导致暴饮暴食和炎症。我们研究了单餐中的AGE含量是否会影响餐后食欲以及炎症、内皮细胞活化和氧化应激的标志物。
总共19名健康超重个体完成了一项交叉餐试验，分别食用通过烘烤（高AGE）或蒸煮（低AGE）制备的两种成分相同的餐食。分析餐后血样中的N(ε)-羧甲基赖氨酸（CML）、调节食欲的肠道激素、葡萄糖、胰岛素、三酰甘油以及炎症和内皮细胞活化的标志物。还评估了主观食欲评分和随后的食物摄入量，并分析尿液中的CML、甲基乙二醛衍生的氢咪唑酮（MG-H1）和F2-异前列腺素。
高AGE餐和低AGE餐的CML含量分别为5.0毫克和2.8毫克。高AGE餐后血浆CML、尿CML和MG-H1往往更高。餐与餐之间，后续食物摄入量、食欲感觉或食欲激素反应没有变化，但总体而言，高AGE餐后的胃饥饿素反应高于低AGE餐（p = 0.016）。与低AGE餐相比，高AGE餐的血糖反应增加（p = 0.027）。餐与餐之间炎症和内皮细胞活化标志物没有差异，但对内皮细胞活化（p = 0.021）和尿液中的氧化标志物F2-异前列腺素（p = 0.013）有总体影响。
本研究未显示AGEs对食欲和炎症标志物有任何明显影响，但确实表明AGEs可能会影响餐后胃饥饿素、氧化应激和葡萄糖反应。
