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首页> 外文学位 >Feeding Soy Protein Isolate and/or Omega-3 Polyunsaturated Fatty Acids on the Spleen-Liver Axis in a Female Rat Model of Autosomal Recessive Polycystic Kidney Disease with Liver Steatosis.
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Feeding Soy Protein Isolate and/or Omega-3 Polyunsaturated Fatty Acids on the Spleen-Liver Axis in a Female Rat Model of Autosomal Recessive Polycystic Kidney Disease with Liver Steatosis.

机译：在常染色体隐性隐性多囊肾病伴肝脏脂肪变性的雌性大鼠模型中，在脾肝轴上饲喂大豆分离蛋白和/或Omega-3多不饱和脂肪酸。

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摘要

ABSTRACT Feeding Soy Protein Isolate and/or Omega-3 Polyunsaturated Fatty Acids on the Spleen-Liver Axis in a Female Rat Model of Autosomal Recessive Polycystic Kidney Disease with Liver Steatosis Lauren Brooke Gibson Autosomal recessive polycystic kidney disease (ARPKD) is a congenital hepatorenal fibrocystic syndrome with a mortality rate of 30% during the first year of life. The most common extra-renal manifestation of ARPKD is liver disease with a greater rate in females due to their higher estrogen levels. Abnormal spleen enlargement (splenomegaly) has been found to occur in 60% of ARPKD patients. In the absence of effective medications to treat the hepatic and splenic complications of ARPKD, diet offers a potentially efficacious, safe, and cost-effective therapy option. Soy protein isolate (SPI) has been shown to reduce cyst proliferation associated with its anti-estrogenic and anti-inflammatory actions. Omega-3 polyunsaturated fatty acids (n-3 PUFAs) have anti-inflammatory effects and influence mediators of de novo lipogenesis (DNL) through up-regulation of beta-oxidation. Young (age 28 days) female PCK rats, an orthologous animal model of ARPKD, were randomly assigned to one of four diets (n=12/group) and fed for 12 weeks. Diet groups consisted of 1) casein + corn oil (Casein + CO), 2) casein + soybean oil (Casein + SO), 3) soy protein isolate + soybean oil (SPI + SO), or 4) soy protein isolate + a 1:1 soybean: salmon oil blend (SPI + SB) rich in long chain n-3 PUFAs. Unexpectedly, SPI + SB fed rats had the highest histological evidence of hepatic steatosis (p=0.003) suggesting non-alcoholic fatty liver disease (NAFLD). NAFLD is the leading cause of chronic liver disease in adults and children consuming Westernized diets. The SPI + SB group also had increased (p=0.03) inflammation and up-regulated (p=0.03) expression of fibrosis related genes suggesting progression of NAFLD to non-alcoholic steatohepatitis (NASH). The spleen was also significantly (P=0.02) elongated in the SPI+SB fed group compared to the Casein + CO and Casein + SO groups. However, spleen weight was not significantly different among diet. We hypothesize the spleen-liver axis is responsible for the development of steatosis and fibrosis in our rats. Given the close anatomical proximity of the spleen to the liver bioactive compounds produced by the spleen such as splenic fatty acids, inflammatory and immune genes can directly access the liver via the splenic and portal veins. The objective of this study was to determine the effect of SPI and/or n-3 PUFAs on splenic DNL, lipolysis, inflammatory response, and immune gene expression. Results of DNL gene expression and splenic fatty acid content of DNL fatty acids were not significantly different among diet groups. Rats fed the SPI+SB diet containing the highest (P<0.001) dietary eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) exhibited the highest (P<0.001) splenic EPA and DHA, and the lowest (P=0.03) splenic arachidonic acid (AA) showing diet did effect the spleen with potentially anti-inflammatory effects. However, no significant differences in gene expression regulating inflammation or immunity were found among dietary treatment groups. Based on our results we concluded that diet had no effect on splenomegaly and splenomegaly did not significantly contribute to the development of liver steatosis in a female PCK rat model.
机译：摘要：在常染色体隐性多囊性肾脏病伴肝脂肪变性的雌性大鼠模型中，在脾肝轴上饲喂大豆分离蛋白和/或Omega-3多不饱和脂肪酸Lauren Brooke Gibson常染色体隐性隐性多囊性肾病（ARPKD）是先天性肝肾纤维囊性疾病生命的第一年，其死亡率为30％。 ARPKD最常见的肾外表现是肝脏疾病，由于雌激素水平较高，女性发病率更高。已发现60％的ARPKD患者出现异常的脾肿大（脾肿大）。在缺乏有效的药物来治疗ARPKD的肝脾并发症时，饮食提供了一种潜在有效，安全且具有成本效益的治疗选择。大豆分离蛋白（SPI）已被证明可减少与其抗雌激素和抗炎作用相关的囊肿增生。 Omega-3多不饱和脂肪酸（n-3 PUFA）具有抗炎作用，并通过上调β-氧化作用影响新生脂肪形成（DNL）的介质。将年轻（年龄28天）的雌性PCK大鼠（ARPKD的直系同源动物模型）随机分配到四种饮食（n = 12 /组）中的一种中，喂养12周。饮食组包括1）酪蛋白+玉米油（酪蛋白+ CO），2）酪蛋白+大豆油（酪蛋白+ SO），3）大豆分离蛋白+大豆油（SPI + SO）或4）大豆分离蛋白+ a 1：1大豆：富含长链n-3 PUFA的鲑鱼油混合物（SPI + SB）。出乎意料的是，用SPI + SB喂养的大鼠具有最高的肝脂肪变性的组织学证据（p = 0.003），提示非酒精性脂肪肝（NAFLD）。在食用西餐的成人和儿童中，NAFLD是导致慢性肝病的主要原因。 SPI + SB组还具有增加的炎症（p = 0.03）和纤维化相关基因的表达上调（p = 0.03），这表明NAFLD已发展为非酒精性脂肪性肝炎（NASH）。与酪蛋白+ CO和酪蛋白+ SO组相比，SPI + SB喂养组的脾脏也显着延长（P = 0.02）。然而，饮食之间的脾脏重量没有显着差异。我们假设脾肝轴是导致大鼠脂肪变性和纤维化的原因。考虑到脾脏与脾脏在解剖学上的紧密联系，例如脾脏脂肪酸，炎症和免疫基因可以通过脾脏和门静脉直接进入肝脏。这项研究的目的是确定SPI和/或n-3 PUFA对脾脏DNL，脂解，炎症反应和免疫基因表达的影响。饮食组之间DNL基因表达的结果和DNL脂肪酸的脾脂肪酸含量没有显着差异。喂养含有最高（P <0.001）膳食二十碳五烯酸（EPA）和二十二碳六烯酸（DHA）的SPI + SB饮食的大鼠表现出最高（P <0.001）的脾EPA和DHA，最低（P = 0.03）的脾花生四烯酸饮食中的乙酸（AA）确实对脾脏有潜在的消炎作用。然而，在饮食治疗组之间，在调节炎症或免疫力的基因表达上没有发现显着差异。根据我们的结果，我们得出结论，饮食对脾肿大没有影响，而脾肿大在雌性PCK大鼠模型中对肝脂肪变性的发展没有显着贡献。

著录项

  • 作者

    Gibson, Lauren.;

  • 作者单位

    West Virginia University.;

  • 授予单位 West Virginia University.;
  • 学科 Nutrition.;Molecular biology.
  • 学位 M.S.
  • 年度 2016
  • 页码 79 p.
  • 总页数 79
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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