首页> 外文期刊>The Journal of Nutritional Biochemistry >Dietary protein restriction induces steatohepatitis and alters leptin/signal transducers and activators of transcription 3 signaling in lactating rats.
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Dietary protein restriction induces steatohepatitis and alters leptin/signal transducers and activators of transcription 3 signaling in lactating rats.

机译:饮食中蛋白质的限制会诱发脂肪性肝炎,并会改变泌乳大鼠的瘦素/信号转导子和转录3信号转导激活剂。

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Dietary protein restriction during lactation affects lipid metabolism and food intake in rats. The goals of this study were to determine the effect of a low-protein diet on a liver damage in lactating rats, to determine whether dietary protein restriction of lactating dams affects the liver health of their offspring and to elucidate the molecular mechanisms underlying the development of hepatic damage. Lactating Sprague-Dawley rats were fed either a control 20% protein diet or an 8% low-protein diet for 11 or 23 days, respectively. After weaning, the offspring were continuously fed either the same control diet or the low-protein diet for an additional 22 days. Feeding a low-protein diet during lactation caused steatohepatitis with severe steatosis, lobular inflammation, ballooning degeneration and fibrosis. Offspring nourished by dams fed a low-protein diet showed simple hepatic steatosis. Combined effects of increased lipogenesis, decreased fatty acid oxidation and impaired very-low-density lipoprotein secretion were responsible for the development of hepatic steatosis. Hepatic up-regulation of genes linked to oxidative stress including nicotinamide adenine dinucleotide phosphate oxidase, inflammation and fibrogenesis supports the development of steatohepatitis in protein-restricted lactating rats. Furthermore, protein-restricted lactating rats showed activation of the leptin/signal transducers and activators of the transcription 3 signaling pathway. Taken together, oxidative stress induced by up-regulation of nicotinamide adenine dinucleotide phosphate oxidase with activation of leptin/signal transducers and activators of the transcription 3 signaling was responsible for development of steatohepatitis in protein-restricted lactating rats. Our findings suggest that protein malnutrition has a potential to induce steatohepatitis/hepatic steatosis in lactating mothers and infants during breast-feeding
机译:哺乳期饮食中蛋白质的限制会影响大鼠的脂质代谢和食物摄入。这项研究的目的是确定低蛋白饮食对泌乳大鼠肝脏损伤的影响,确定饮食对泌乳水坝的蛋白质限制是否会影响其子代的肝脏健康,并阐明其发育的分子机制。肝损害。哺乳期的Sprague-Dawley大鼠分别饲喂20%的对照蛋白质饮食或8%的低蛋白质饮食,持续11天或23天。断奶后,给后代连续喂食相同的对照饮食或低蛋白饮食22天。哺乳期间喂养低蛋白饮食会导致脂肪性肝炎,并伴有严重的脂肪变性,小叶炎症,球囊变性和纤维化。用低蛋白饮食的水坝养育的后代显示出简单的肝脂肪变性。脂肪生成增加,脂肪酸氧化减少和极低密度脂蛋白分泌受损的综合作用是造成肝脂肪变性的原因。肝脏与氧化应激相关的基因的上调,包括烟酰胺腺嘌呤二核苷酸磷酸氧化酶,炎症和纤维化,支持蛋白质受限的泌乳大鼠脂肪性肝炎的发展。此外,蛋白质受限的哺乳期大鼠显示出瘦素/信号转导子和转录3信号通路的激活子的激活。两者合计,由烟酰胺腺嘌呤二核苷酸磷酸氧化酶的上调与瘦素/信号转导子和转录3信号转导子的激活诱导的氧化应激是蛋白质限制性泌乳大鼠脂肪性肝炎的发展。我们的发现表明,蛋白质营养不良可能会在哺乳期的母亲和婴儿中诱发脂肪性肝炎/肝脂肪变性

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