Effects of a Low-Protein Diet on Plasma Amino Acid and Homocysteine Levels and Oxidative Status in Rats

被引:13
作者
Deminice, Rafael [1 ]
Portari, Guilherme Vannucchi [1 ]
Marchini, Julio Sergio [1 ]
Vannucchi, Helio [1 ]
Jordao, Alceu Afonso [1 ]
机构
[1] Univ Sao Paulo, Fac Med Ribeirao Preto, Lab Nutr & Metab, BR-14049900 Ribeirao Preto, SP, Brazil
关键词
Protein malnutrition; Methyl balance; Homocysteine; Glutathione; LOW-CASEIN DIET; CREATINE SUPPLEMENTATION; METABOLISM; METHIONINE; LIVER; HYPERHOMOCYSTEINEMIA; MALNUTRITION; DETERMINANT; DEFICIENT; CYSTEINE;
D O I
10.1159/000218707
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background/Aims: Transmethylation reactions and antioxidant metabolism are linked by transsulfuration, where homocysteine (Hcy) is converted to cysteine and reduced glutathione (GSH). Low protein intake can modulate the balance of this metabolic reaction. The aim of the present investigation was to study the effect of a low-protein diet on Hcy metabolism by monitoring levels of the amino acids involved in these pathways, and relating these levels to GSH levels and lipid peroxidation in rats. Methods: Sixteen rats were divided into 2 groups: control (C; standard AIN-93 diet, 20% protein) and low-protein diet (LPD; 8% protein diet). Rats in both groups were placed on the diets for 28 days. Results: A significant reduction (p < 0.05) in plasma Hcy concentration was found in LPD rats (0.16 +/- 0.04 mu mol/mg protein) versus C rats (0.25 +/- 0.03 mu mol/mg protein). Methionine levels were not significantly different between the 2 groups (C: 1.24 +/- 0.22 mu mol/mg protein; LPD: 1.03 +/- 0.27 mu mol/mg protein). A significant reduction (p ! 0.05) in hepatic GSH concentrations (C: 44 8 10 mu mol/mg protein; LPD: 17.4 +/- 4.3 mu mol/mg protein) was accompanied by an increase in lipid peroxidation (C: 0.13 +/- 0.01 mu mol/mg protein; LPD: 0.17 +/- 0.02 mu mol/mg protein; r = -0.62, p < 0.01). Conclusion: Hcy levels were reduced under a low-protein diet, resulting in modulated methyl balance and reduced GSH formation leading to increased susceptibility of hepatic cells to oxidative events. Copyright (C) 2009 S. Karger AG, Basel
引用
收藏
页码:202 / 207
页数:6
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