Mehdad A, Campos N A, Arruda S Fernandes, Siqueira E Machado de Almeida
Azadeh Mehdad, Laboratory of Molecular biophysic, Instituto of Biology, Dep. Cellular Biology, University of Brasilia (UnB) Brazil,
J Nutr Health Aging. 2015 Oct;19(8):846-54. doi: 10.1007/s12603-015-0541-9.
Considering that phenotype related to iron overload associated with pathological conditions differs from that caused by dietary iron excess, our study set out to evaluate the impact of dietary iron restriction and dietary iron supplementation on oxidative stress and functional outcome in adult, healthy rats.
adult rats were divided into the three groups and fed diets containing 10, 35 or 350 mg/kg iron (restricted-diet, control-diet and supplemented- diet groups, respectively) for 78 days. Hematological variables, fasting blood glucose, hepatic enzyme activity and C-reactive protein levels were analyzed. Iron and glycogen concentrations in liver and skeletal muscle were determined. The extent of tissue damage caused by either dietary iron restriction or iron supplementation was accessed by measuring malondialdehyde, carbonyl, NADPH oxidase, glutathione peroxidase, glutathione reductase and glutathione-s-transferase in various tissues. The mRNA expression levels of insulin receptor, glucose transporter 4 and p53 were also determined.
Fasting blood glucose values trended toward a decrease by dietary iron restriction, moreover, hepatic glycogen content decreased with concomitant increases in skeletal muscle. In addition, dietary iron restriction resulted in a twofold increase in mRNA expression of Insr and fourfold increase in Glut4 expression in skeletal muscle. Although the dietary iron restriction did not affect body iron status, it caused hepatic low oxidative damages. However, high liver NADPH oxidase activity and increased levels of protein oxidation in muscle were observed. Chronic feeding of high iron diet induces iron overload and resulted in elevated levels of stress markers in tissues.
Dietary iron deprivation may improve insulin receptor and glucose transporter transcription in muscle; however, our results show that dietary iron restriction can prevent and/or promote oxidative damage in a tissue-specific manner, emphasizing the importance of maintaining optimal iron intake.
鉴于与病理状况相关的铁过载表型不同于饮食中铁过量所致的表型，我们的研究旨在评估饮食中铁限制和铁补充对成年健康大鼠氧化应激和功能结局的影响。
将成年大鼠分为三组，分别给予含铁量为10、35或350mg/kg的饮食（分别为限制饮食组、对照饮食组和补充饮食组），持续78天。分析血液学变量、空腹血糖、肝酶活性和C反应蛋白水平。测定肝脏和骨骼肌中的铁和糖原浓度。通过测量各种组织中的丙二醛、羰基、NADPH氧化酶、谷胱甘肽过氧化物酶、谷胱甘肽还原酶和谷胱甘肽 - S - 转移酶，评估饮食中铁限制或铁补充所造成的组织损伤程度。还测定了胰岛素受体、葡萄糖转运蛋白4和p53的mRNA表达水平。
饮食中铁限制使空腹血糖值呈下降趋势，此外，肝脏糖原含量降低，同时骨骼肌糖原含量增加。此外，饮食中铁限制导致骨骼肌中Insr的mRNA表达增加两倍，Glut4表达增加四倍。虽然饮食中铁限制不影响机体铁状态，但会导致肝脏低氧化损伤。然而，观察到肝脏NADPH氧化酶活性高以及肌肉中蛋白质氧化水平升高。长期喂食高铁饮食会导致铁过载，并导致组织中应激标志物水平升高。
饮食中铁缺乏可能改善肌肉中胰岛素受体和葡萄糖转运蛋白的转录；然而，我们的结果表明，饮食中铁限制可以以组织特异性方式预防和/或促进氧化损伤，强调了维持最佳铁摄入量的重要性。
