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首页> 外文期刊>The Journal of Nutritional Biochemistry >Dairy milk proteins attenuate hyperglycemia-induced impairments in vascular endothelial function in adults with prediabetes by limiting increases in glycemia and oxidative stress that reduce nitric oxide bioavailability
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Dairy milk proteins attenuate hyperglycemia-induced impairments in vascular endothelial function in adults with prediabetes by limiting increases in glycemia and oxidative stress that reduce nitric oxide bioavailability

机译：乳制品蛋白质通过限制糖血症和氧化应激的增加，减少血管内皮功能的高血糖内皮功能损伤，降低一氧化氮生物利用度

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Postprandial hyperglycemia (PPH) transiently impairs vascular endothelial function (VEF) in an oxidative stress-dependent manner by decreasing nitric oxide (NO center dot) bioavailability. Dairy milk and its proteins attenuate PPH, but whether this improves VEF is unknown. We hypothesized that dairy milk, mediated by its whey and/or casein proteins, improves VEF by attenuating PPH-induced oxidative stress that otherwise decreases NO center dot bioavailability. A randomized, cross-over trial was conducted in adults with prediabetes (n=23) who ingested glucose (75 g, GLU) alone or with 473 mL of non-fat dairy milk (MILK) or isonitrogenous (16.5 g) amounts of whey (WHEY) or casein (CASEIN) in 473 mL of water. Prior to and at 30 min intervals for 180 min postprandially, we assessed brachial artery flow-mediated dilation (FMD) and measured biomarkers of glycemic control, oxidative stress, and NO center dot homeostasis. FMDAUC decreased to the greatest extent during GLU, which was similarly improved in dairy trials. Compared with GLU, AUCs for glucose, malondialdehyde, F-2-isoprostanes, methylglyoxal, and endothelin-1 were similarly lower in dairy trials. Plasma arginine and NO center dot metabolites were greater but methylated arginine metabolites were lower in dairy trials compared with GLU. Postprandial insulin, lipids, and tetrahydrobiopterin redox status did not differ among trials. Thus, dairy milk, mediated by its whey and casein proteins, attenuates PPH-mediated impairments in VEF by limiting oxidative stress. This improves NO center dot bioavailability to the vascular endothelium by increasing arginine availability and limiting competitive inhibition on NO center dot biosynthesis by asymmetric dimethylarginine. These findings support observational studies that dairy milk lowers cardiovascular disease risk. (C) 2018 Elsevier Inc. All rights reserved.
机译：通过减少一氧化氮（无中心点）生物利用度，黄芪高血糖（PPH）瞬时损害血管内皮功能（VEF）以氧化应激依赖性方式。乳制品及其蛋白质衰减PPH，但这是否改善了VEF是未知的。我们假设由其乳清和/或酪蛋白介导的乳制品通过衰减PPH诱导的氧化应激而改善VEF，否则否则不降低中心点生物利用度。随机交叉试验在具有预先摄取葡萄糖（N = 23）的成人中，单独摄取葡萄糖（75g，Glu）或用473ml非脂肪乳制乳（牛奶）或异源（16.5g）乳清量的乳清剂（乳清）或酪蛋白（酪蛋白）在473ml水中。在后期和30分钟的间隔之前，我们在后造成的180分钟之前，我们评估了血管动脉流动介导的扩张（FMD）和测量的血糖控制，氧化应激和NO中枢稳态的测量生物标志物。 FMDAUC在Glu期间的最大程度上减少，在乳制品试验中类似地改善。与Glu相比，葡萄糖，丙二醛，F-2-异丙醇，甲基甘油和内皮素-1的AUC在乳制品试验中类似地降低。与Glu相比，血浆精氨酸和NO中的中央点代谢物更大但甲基化精氨酸代谢物较低。餐后胰岛素，脂质和四氢替辛替司氧化还原状态在试验中没有差异。因此，由其乳清和酪蛋白介导的乳制品通过限制氧化应激而衰减VEF中的PPH介导的损伤。这通过通过增加精氨酸可用性和限制不对称二甲基碱的中央点生物合成的竞争性抑制来改善对血管内皮的中心点生物利用度。这些发现支持乳制品降低心血管疾病风险的观察研究。 （c）2018年Elsevier Inc.保留所有权利。

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