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Dietary supplementation with soy isoflavones or replacement with soy proteins prevents hepatic lipid droplet accumulation and alters expression of genes involved in lipid metabolism in rats

机译:饮食中补充大豆异黄酮或大豆蛋白替代物可防止肝脂质滴积累并改变大鼠脂质代谢相关基因的表达

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摘要

Accumulation of hepatic lipid droplet (HLD) is the hallmark pathology of non-alcoholic fatty liver disease (NAFLD). This study examined the effects of soy isoflavones (ISF) and different amounts of soy proteins on the accumulation of HLD, lipid metabolism and related gene expression in rats. Weanling Sprague–Dawley rats were fed diets containing either 20 % casein protein without (D1) or with (D2) supplemental ISF (50 mg/kg diet) or substitution of casein with increasing amounts of alcohol-washed soy protein isolate (SPI, 5, 10, and 20 %; D3, D4, D5) for 90 days. Dietary casein (20 %) induced accumulation of HLD in female, but not in male rats. Both soy proteins and ISF remarkably prevented the formation of HLD. Soy proteins lowered hepatic total cholesterol and triglyceride in a dose-dependent manner. Interestingly, soy proteins but not ISF significantly increased free fatty acids in the liver of the female rats compared to D1. Proteomic analysis showed that at least 3 enzymes involved in lipogenesis were down-regulated and 7 proteins related to fatty acid β-oxidation or lipolysis were up-regulated by soy protein over D1. Additionally, 9 differentially expressed proteins identified were related to amino acid metabolism, 5 to glycolysis and 2 to cholesterol metabolism. Dietary ISF and SPI markedly reduced hepatic-peroxisome-proliferator-activated receptor γ2 (PPARγ2) and fat-specific protein 27 (FSP27) in female rats. Overall, this study has shown that partial or full replacement of dietary casein by soy protein or supplementation with soy ISF can effectively prevent the accumulation of HLD. The potential molecular mechanism(s) involved might be due to suppression of lipogenesis and stimulation of lipolysis and down-regulation of PPARγ2 and FSP27. This suggests that consumption of soy foods or supplements might be a useful strategy for the prevention or treatment of fatty liver diseases.Electronic supplementary materialThe online version of this article (doi:10.1007/s12263-013-0373-3) contains supplementary material, which is available to authorized users.
机译:肝脂质滴(HLD)的积累是非酒精性脂肪肝疾病(NAFLD)的标志性病理。这项研究检查了大豆异黄酮(ISF)和不同数量的大豆蛋白对大鼠HLD积累,脂质代谢和相关基因表达的影响。断奶的Sprague–Dawley大鼠饲喂日粮中含有20%酪蛋白的蛋白质,不含(D1)或(D2)补充ISF(50 mg / kg饮食),或用增加量的酒精洗涤大豆分离蛋白代替的酪蛋白代替(SPI,5 ,10%和20%; D3,D4,D5)持续90天。饮食酪蛋白(20%)诱导雌性HLD积累,但不引起雄性大鼠。大豆蛋白和ISF均显着阻止了HLD的形成。大豆蛋白以剂量依赖的方式降低了肝脏的总胆固醇和甘油三酸酯。有趣的是,与D1相比,大豆蛋白而非ISF显着增加了雌性大鼠肝脏中的游离脂肪酸。蛋白质组学分析表明,与脂肪形成有关的至少3种酶被下调,大豆D1上的大豆蛋白上调了7种与脂肪酸β-氧化或脂解相关的蛋白。此外,鉴定出的9种差异表达蛋白与氨基酸代谢有关,5与糖酵解有关,2与胆固醇代谢有关。饮食中的ISF和SPI可以明显降低雌性大鼠肝过氧化物酶体增殖物激活受体γ2(PPARγ2)和脂肪特异性蛋白27(FSP27)。总的来说,这项研究表明用大豆蛋白部分或全部替代酪蛋白饮食或补充大豆ISF可以有效预防HLD的积累。涉及的潜在分子机制可能是由于抑制脂肪生成和刺激脂解以及下调PPARγ2和FSP27。这表明食用大豆食品或补品可能是预防或治疗脂肪肝疾病的有用策略。电子补充材料本文的在线版本(doi:10.1007 / s12263-013-0373-3)包含补充材料,其中适用于授权用户。

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