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首页> 外文期刊>The Journal of Nutritional Biochemistry >Maternal betaine supplementation attenuates glucocorticoid-induced hepatic lipid accumulation through epigenetic modification in adult offspring rats
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Maternal betaine supplementation attenuates glucocorticoid-induced hepatic lipid accumulation through epigenetic modification in adult offspring rats

机译:母体甜菜碱补充通过成人后代大鼠的表观遗传改性衰减糖皮质激素诱导的肝脂积累

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摘要

There are lots of reports about alleviation of NAFLD by dietary supplements of betaine. However, it remains unclear whether maternal betaine supplementation can also ameliorate NAFLD in offspring. Hence, twenty pregnant rats were fed with a basal diet with or without betaine (1%), and then the female offspring rats were raised at 3 months of age followed by 3 weeks of physiological saline or dexamethasone in a dose of 0.1 mg/kg body mass every day via intraperitoneal injection. In this study, maternal betaine supplementation significantly (P&.05) reduced the increase of hepatic triglycerides concentration in dexamethasone-induced rats, which is associated with the expression of hepatic lipogenic genes (ACCT, FASN and SCD1). Moreover, the hypomethylation of lipogenic genes in dexamethasone-induced rats were reserved by prenatal betaine exposure. Furthermore, the increase of hepatic GR or SP1 content in dexamethasone-injected rats were significantly decreased (P&.05), which were in line with the binding of GR or SP1 to lipogenic genes, in betaine-exposed rats. Together, these results suggest that maternal betaine supplementation attenuates dexamethason-induced fatty liver in the female adult offspring rats, which may be attributed to DNA methylation and GR or SP1-mediated the regulation of lipogenic genes. (C) 2017 Elsevier Inc. All rights reserved.
机译:甜菜碱补充剂有很多关于减轻NAFLD的报道。然而,仍然目前还不清楚母性甜菜碱是否补充剂也可以在后代改善NAFLD。因此,用或没有甜菜碱(1%)的基础饮食喂养20只怀孕大鼠,然后在3个月的时间内提高雌性后代大鼠,然后在0.1mg / kg的剂量下进行3周的生理盐水或地塞米松每天通过腹膜内注射体重。在该研究中,母体甜菜碱补充了显着的(P& .05)降低了地塞米松诱导的大鼠中肝甘油三酯浓度的增加,这与肝脂肪生成基因(ACCT,FASN和SCD1)的表达相关。此外,通过产前甜菜碱暴露保留了地塞米松诱导的大鼠脂质基因的低甲基化。此外,肝脏注射大鼠肝脏GR或SP1含量的增加显着降低(P& .05),其与GR或SP1与脂质基因的结合为甜菜碱暴露大鼠。这些结果表明,母体甜菜碱补充剂在女性成人后代大鼠中衰减了地塞米仑诱导的脂肪肝,其可归因于DNA甲基化和GR或SP1介导的脂原基因的调节。 (c)2017年Elsevier Inc.保留所有权利。

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