Laboratory of Nutrition and Metabolism, Faculty of Medicine of Ribeirao Preto, University of São Paulo, Av. Bandeirantes, 3900, Ribeirao Preto, São Paulo, Brazil; Department of Physical Education, Faculty of Physical Education and Sport, State University of Londrina, Rodovia Celso Garcia Cid, Pr 445 Km 380, Campus Universitário, Londrina, Paraná, Brazil.
Laboratory of Nutrition and Metabolism, Faculty of Medicine of Ribeirao Preto, University of São Paulo, Av. Bandeirantes, 3900, Ribeirao Preto, São Paulo, Brazil.
Life Sci. 2014 Jun 6;105(1-2):43-7. doi: 10.1016/j.lfs.2014.04.015. Epub 2014 Apr 24.
The aim of this study is to examine the effects of taurine supplementation on homocysteine (Hcy) metabolism and liver injury in rats fed a choline-deficient diet.
Thirty rats were divided into three groups (n=10), to receive one of the following diets for 4 weeks: control diet (C), choline-deficient diet (CDD), or choline-deficient diet supplemented with taurine (CDDT). The CDD and the CDDT consisted of AIN-93 without the recommended choline content of 2.5%, and the CDDT was supplemented by the addition of 2.5% taurine.
Four weeks of ingesting a CDD resulted in a significant increase in plasma Hcy (50%) as well as a decrease in liver S-adenosylmethionine (SAM) concentration and S-adenosylmethionine/S-adenosylhomocysteine ratio. No changes were found in plasma methionine and cysteine plasma levels compared to control group. Four weeks of ingesting a CDD also caused a significant (P<0.05) increase in hepatic total fat, hepatic malondialdehyde (MDA), and plasma alanine aminotransferase (ALT) levels. In addition, reduced hepatic glutathione (GSH) levels and reduced/oxidized glutathione ratios (GSH/GSSG) were found in rats fed a CDD compared to controls. Taurine supplementation of the CDD normalized genes involved in the remethylation pathway, BHMT and CHDH, which were impaired by CDD alone. However, taurine supplementation failed to prevent CDD-induced Hcy metabolism disturbances and hepatic injury. Also, taurine added to CDD caused decreased expression of PEMT, CHKa, and CHKb, key genes involved in phosphatidylcholine (PC) synthesis and liver fat accumulation.
Taurine supplementation failed to ameliorate impaired Hcy metabolism and liver injury caused by CDD intake.
本研究旨在探讨牛磺酸补充对胆碱缺乏饮食喂养大鼠同型半胱氨酸（Hcy）代谢和肝损伤的影响。
将 30 只大鼠随机分为 3 组（n=10），分别给予以下 4 种饮食中的一种喂养 4 周：对照饮食（C）、胆碱缺乏饮食（CDD）或胆碱缺乏饮食添加牛磺酸（CDDT）。CDD 和 CDDT 由不含推荐的 2.5%胆碱的 AIN-93 组成，CDDT 通过添加 2.5%牛磺酸进行补充。
摄入 CDD 4 周可显著增加血浆 Hcy（50%），降低肝脏 S-腺苷甲硫氨酸（SAM）浓度和 S-腺苷甲硫氨酸/S-腺苷同型半胱氨酸比值。与对照组相比，血浆蛋氨酸和半胱氨酸水平无变化。摄入 CDD 4 周还可显著增加肝总脂肪、肝丙二醛（MDA）和血浆丙氨酸氨基转移酶（ALT）水平（P<0.05）。此外，与对照组相比，CDD 喂养大鼠的肝谷胱甘肽（GSH）水平降低，还原/氧化谷胱甘肽比值（GSH/GSSG）降低。CDD 单独喂养可损害参与再甲基化途径的 BHMT 和 CHDH 基因，而 CDD 中添加牛磺酸可使这些基因正常化。然而，牛磺酸补充未能预防 CDD 引起的 Hcy 代谢紊乱和肝损伤。此外，牛磺酸添加到 CDD 中会降低参与磷脂酰胆碱（PC）合成和肝脂肪积累的关键基因 PEMT、CHKa 和 CHKb 的表达。
牛磺酸补充未能改善 CDD 摄入引起的 Hcy 代谢紊乱和肝损伤。
