Xu Li, Huang Danping, Hu Qiaolin, Wu Jing, Wang Yizhen, Feng Jie
Key Laboratory of Molecular Animal Nutrition, Ministry of Education, College of Animal Sciences, Zhejiang University,Hangzhou310029,People's Republic of China.
Br J Nutr. 2015 Jun 28;113(12):1835-43. doi: 10.1017/S0007114515001130. Epub 2015 Apr 29.
To assess the effects of betaine on hepatic lipid accumulation and investigate the underlying mechanism, thirty-two male Sprague-Dawley rats weighing 100 (sd 2·50) g were divided into four groups, and started on one of four treatments: basal diet, basal diet with betaine administration, high-fat diet and high-fat diet with betaine administration. The results showed that no significant difference of body weight was found among experimental groups. Compared with high-fat diet-fed rats, a betaine supplementation decreased (P< 0·05) hepatic TAG accumulation induced by high-fat diet, which was also supported by hepatic histology results. Additionally, hepatic betaine-homocysteine methyltransferase concentration [corrected] as well as its mRNA abundance and lecithin level were found increased (P< 0·05) by betaine supplementation in both basal diet-fed rats and high-fat diet-fed rats. Betaine administration in high-fat diet-fed rats exhibited a higher (P< 0·05) concentration [corrected] of hepatic carnitine palmitoyltransferase 1 (CPT1) compared with high-fat diet-fed rats. High-fat diet inhibited (P< 0·05) the gene expression of hepatic PPARα and CPT1. However, betaine administration in high-fat diet-fed rats elevated (P< 0·05) the gene expression of PPARα and CPT1. Moreover, concentration, gene and protein expressions of hepatic fibroblast growth factor 21 (FGF21) were increased (P< 0·05) in response to betaine administration in high-fat diet group; meanwhile the gene expression of hepatic AMP-activated protein kinase was increased (P< 0·05) as well. The results suggest that betaine administration enhanced hepatic lipid export and fatty acid oxidation in high-fat diet-fed rats, thus effectively alleviating fat accumulation in the liver.
为评估甜菜碱对肝脏脂质蓄积的影响并探究其潜在机制,将32只体重为100(标准差2.50)g的雄性斯普拉格 - 道利大鼠分为四组,并开始接受以下四种处理之一:基础饮食、给予甜菜碱的基础饮食、高脂饮食和给予甜菜碱的高脂饮食。结果显示,各实验组之间体重无显著差异。与高脂饮食喂养的大鼠相比,补充甜菜碱可降低(P<0.05)高脂饮食诱导的肝脏三酰甘油(TAG)蓄积,肝脏组织学结果也支持这一点。此外,在基础饮食喂养的大鼠和高脂饮食喂养的大鼠中,补充甜菜碱均使肝脏甜菜碱 - 同型半胱氨酸甲基转移酶浓度[校正后]及其mRNA丰度和卵磷脂水平升高(P<0.05)。与高脂饮食喂养的大鼠相比,高脂饮食喂养的大鼠给予甜菜碱后肝脏肉碱棕榈酰转移酶1(CPT1)浓度[校正后]更高(P<0.05)。高脂饮食抑制(P<0.05)肝脏过氧化物酶体增殖物激活受体α(PPARα)和CPT1的基因表达。然而,高脂饮食喂养的大鼠给予甜菜碱后PPARα和CPT1的基因表达升高(P<0.05)。此外,高脂饮食组给予甜菜碱后,肝脏成纤维细胞生长因子21(FGF21)的浓度、基因和蛋白表达均升高(P<0.05);同时肝脏腺苷酸活化蛋白激酶的基因表达也升高(P<0.05)。结果表明,给予甜菜碱可增强高脂饮食喂养大鼠的肝脏脂质输出和脂肪酸氧化,从而有效减轻肝脏脂肪蓄积。