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首页> 外文期刊>American Journal of Physiology >Transcription profiling in the liver of undernourished male rat offspring reveals altered lipid metabolism pathways and predisposition to hepatic steatosis
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Transcription profiling in the liver of undernourished male rat offspring reveals altered lipid metabolism pathways and predisposition to hepatic steatosis

机译：营养不良雄性大鼠后代肝脏的转录谱揭示了脂质代谢途径和肝脏脂肪变性的改变

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Clinical and animal studies have reported an association between low birth weight and the development of nonalcoholic fatty liver disease (NAFLD) in offspring. Using a model of prenatal maternal 70% food restriction diet (FR30) in the rat, we previously showed that maternal undernu-trition predisposes offspring to altered lipid metabolism in adipose tissue, especially on a high-fat (HF) diet. Here, using microarray-based expression profiling combined with metabolic, endocrine, biochemical, histological, and lipidomic approaches, we assessed whether FR30 procedure sensitizes adult male offspring to impaired lipid metabolism in the liver. No obvious differences were noted in the concentrations of triglycerides, cholesterol, and bile acids in the liver of 4-mo-old FR30 rats whichever postweaning diet was used. However, several clues suggest that offspring's lipid metabolism and steatosis are modified by maternal undernutrition. First, lipid composition was changed (i.e., higher total saturated fatty acids and lower elaidic acid) in the liver, whereas larger triglyceride droplets were observed in hepatocytes of undernourished rats. Second, FR30 offspring exhibited long-term impact on hepatic gene expression and lipid metabolism pathways on a chow diet. Although the transcrip-tome profile was globally modified by maternal undernutrition, cholesterol and bile acid biosynthesis pathways appear to be key targets, indicating that FR30 animals were predisposed to impaired hepatic cholesterol metabolism. Third, the FR30 protocol markedly modifies hepatic gene transcription profiles in undernourished offspring in response to postweaning HF. Overall, FR30 offspring may exhibit impaired metabolic flexibility, which does not enable them to properly cope with postweaning nutritional challenges influencing the development of nonalcoholic fatty liver.
机译：临床和动物研究报道了低出生体重与后代非酒精性脂肪肝病（NAFLD）之间的关联。在大鼠中使用产前母体70％的食物限制性饮食（FR30），我们以前表明母体undernu-histitib在脂肪组织中改变了改变脂质代谢的后代，特别是在高脂肪（HF）饮食中改变脂质代谢。在这里，使用基于微阵列的表达分析与代谢，内分泌，生化，组织学和脂质化方法相结合，我们评估了FR30程序是否使成年男性后代敏感到肝脏中的脂质代谢受损。在使用后切换饮食的4-Mo-you的FR30大鼠肝脏中，甘油三酯，胆固醇和胆汁酸的浓度没有明显差异。然而，若干线索表明，后代的脂质代谢和脂肪变性被孕产妇的损益。首先，在肝脏中改变脂质组合物（即，较高的总饱和脂肪酸和低级蛋白酸），而在营养不良大鼠的肝细胞中观察到较大的甘油三酯液滴。其次，FR30后代对肝脏基因表达和脂质代谢途径进行了长期影响。虽然通过孕产妇的欠育术，但经过孕产妇的概况，但胆固醇和胆汁酸生物合成途径似乎是关键目标，表明FR30动物被倾向于肝胆固醇代谢受损。第三，FR30方案显着改变营养不良后代的肝基因转录曲线，响应后两种HF。总的来说，FR30后代可能表现出损害的代谢灵活性，这并不能使它们能够适当地应对影响非酒精性脂肪肝的发育的切换营养挑战。

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