Dietary cysteine alleviates sucrose-induced oxidative stress and insulin resistance

Dietary cysteine alleviates sucrose-induced oxidative stress and insulin resistance
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DOI:
10.1016/j.freeradbiomed.2007.01.006
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发表时间:
2007-04-01
影响因子:
7.4
通讯作者:
Huneau, Jean-Francois
Huneau, Jean-Francois
中科院分区:
医学1区
文献类型:
--
作者:
Blouet, Clemence;Mariotti, Francois;Huneau, Jean-Francois

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促进氧化应激的饮食有利于葡萄糖稳态的损害。在这种情况下,增加半胱氨酸的摄入量可能是有益的,通过维持谷胱甘肽的状态。我们研究了饮食半胱氨酸对高蔗糖(HS)饮食大鼠氧化应激和葡萄糖稳态的影响。将大鼠分配给标准饮食或HS饮食6周,其中蛋白质来源是富含α-乳白蛋白的乳清浓缩物(富含半胱氨酸的蛋白质)或单独的总乳蛋白或每千克食物补充有5.8或20 g N-乙酰半胱氨酸。通过血液和组织谷胱甘肽和羰基水平评估,增加半胱氨酸摄入量可预防HS诱导的氧化应激。与此同时,HS诱导的葡萄糖耐受不良,餐后血糖控制受损,以及肌肉和肝脏胰岛素诱导的胰岛素受体底物1和Akt活化减少,通过增加饮食半胱氨酸水平来预防,这是一个主要的原始发现。令人非常感兴趣的是,观察到补充半胱氨酸的所有有益效果都可以通过食用富含半胱氨酸的蛋白质来复制。这些数据表明,增加半胱氨酸摄入量限制HS诱导的葡萄糖稳态损害,并表明这些影响是由氧化应激减少介导的。(c)2007年爱思唯尔公司All rights reserved.
Diets that promote oxidative stress favor impairment in glucose homeostasis. In this context, increasing the cysteine intake may be beneficial by maintaining glutathione status. We have investigated the effects of dietary cysteine on oxidative stress and glucose homeostasis in rats fed a high-sucrose (HS) diet. Rats were assigned for 6 weeks to a standard diet or to HS diets in which the protein source was either an alpha-lactalbumin-rich whey concentrate (a cysteine-rich protein) or the total milk proteins alone or supplemented with 5.8 or 20 g N-acetylcysteine per kilogram of food. Increasing the cysteine intake prevented HS-induced oxidative stress, as assessed by blood and tissue glutathione and carbonyl levels. At the same time, the HS-induced glucose intolerance, impaired postprandial glycemic control, and decrease in muscle and liver insulin-induced activation of insulin receptor substrate 1 and Akt were prevented by increasing the level of dietary cysteine, a major original finding. Of great interest was the observation that all beneficial effects of cysteine supplementation were duplicated by the consumption of a cysteine-rich protein. These data show that increasing the cysteine intake limits HS-induced impairment of glucose homeostasis and suggest that these effects are mediated by a reduction in oxidative stress. (c) 2007 Elsevier Inc. All rights reserved.