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低碳水化合物饮食与糖尿病和非糖尿病大鼠的氧化应激

Low-carbohydrate diet and oxidative stress in diabetic and nondiabetic rats.

作者信息

Kamuren Zipporah T, Sanders Ruth, Watkins John B

机构信息

Department of Medical Pharmacology, Faculty of Health Science, Moi University, Eldoret, Kenya.

出版信息

J Biochem Mol Toxicol. 2006;20(5):259-69. doi: 10.1002/jbt.20142.

DOI:10.1002/jbt.20142
PMID:17009256
Abstract

Hyperglycemia of diabetes has been implicated in increased tissue oxidative stress, with consequent development of secondary complications. Thus, stabilizing glucose levels near normal levels is of utmost importance. Because diet influences glycemic control, this study investigated whether a low-carbohydrate (5.5%) diet confers beneficial effects on the oxidative status of the heart, kidney, and liver in diabetes. Male and female normal and diabetic rats were fed standard chow (63% carbohydrates) or low-carbohydrate diet for 30 days. Elevated glucose, HbA(1c), and alanine and aspartate aminotransferases in diabetic animals were reduced or normalized by the low-carbohydrate diet. While diabetes increased cardiac activities of glutathione peroxidase and catalase, low-carbohydrate diet normalized cardiac glutathione peroxidase activity in diabetic animals, and reduced catalase activity in females. Diabetic rats fed low-carbohydrate diet had altered activities of renal glutathione reductase and superoxide dismutase, but increased renal glutathione peroxidase activity in diabetic animals was not corrected by the test diet. In the liver, diabetes was associated with a decrease in catalase activity and glutathione levels and an increase in glutathione peroxidase and gamma-glutamyltranspeptidase activities. Decreased hepatic glutathione peroxidase activity and lipid peroxidation were noted in diet-treated diabetic rats. Overall, the low-carbohydrate diet helped stabilize hyperglycemia and did not produce overtly negative effects in tissues of normal or diabetic rats.

摘要

糖尿病患者的高血糖与组织氧化应激增加有关,进而导致继发性并发症的发生。因此,将血糖水平稳定在接近正常水平至关重要。由于饮食会影响血糖控制,本研究调查了低碳水化合物(5.5%)饮食是否对糖尿病大鼠的心脏、肾脏和肝脏的氧化状态产生有益影响。雄性和雌性正常及糖尿病大鼠分别喂食标准饲料(碳水化合物含量63%)或低碳水化合物饮食30天。低碳水化合物饮食可降低或使糖尿病动物升高的血糖、糖化血红蛋白、丙氨酸转氨酶和天冬氨酸转氨酶恢复正常。虽然糖尿病会增加心脏中谷胱甘肽过氧化物酶和过氧化氢酶的活性,但低碳水化合物饮食可使糖尿病动物心脏中的谷胱甘肽过氧化物酶活性恢复正常,并降低雌性动物的过氧化氢酶活性。喂食低碳水化合物饮食的糖尿病大鼠肾脏中谷胱甘肽还原酶和超氧化物歧化酶的活性发生了改变,但试验饮食并未纠正糖尿病动物肾脏中升高的谷胱甘肽过氧化物酶活性。在肝脏中,糖尿病与过氧化氢酶活性和谷胱甘肽水平降低以及谷胱甘肽过氧化物酶和γ-谷氨酰转肽酶活性增加有关。在接受饮食治疗的糖尿病大鼠中,肝脏谷胱甘肽过氧化物酶活性降低和脂质过氧化减少。总体而言,低碳水化合物饮食有助于稳定高血糖,且对正常或糖尿病大鼠的组织未产生明显的负面影响。

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