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Probiotics stimulate liver and plasma protein synthesis in piglets with dextran sulfate-induced colitis and macronutrient restriction

机译:益生菌可刺激硫酸葡聚糖诱导的结肠炎和大量营养物质限制的仔猪肝脏和血浆蛋白合成

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摘要

Adequate nutrition and probiotics have each been shown to reduce the severity of colitis, but their impact on hepatic and gastrointestinal protein metabolism has not been studied. Our objective was to determine whether maintaining adequate nutrition compared with administering probiotics affected protein synthesis, colon histopathology, and oxidative stress in our macronutrient-restricted piglet model of colitis. Piglets (n = 8/group) receiving dextran sulfate to induce colitis were randomized to 3 treatment groups: macronutrient restricted (MR); macronutrient restricted with VSL #3 probiotics (MRP), or well nourished (WNC). An additional 8 piglets served as healthy references for comparative purposes given the unique nature of the experimental model. A primed, constant infusion of the tracer L-[ring-(2)H(5)]phenylalanine was performed in colitis piglets after 14 d to determine the fractional synthesis rates of proteins in small intestinal mucosa, colon, and liver and of plasma proteins (total protein, fibrinogen, albumin). Colon histopathology and oxidative stress were also assessed. Compared with MR piglets, both WNC and MRP piglets had higher protein synthesis rates in liver and plasma protein pools. However, only adequate nutrition increased protein synthesis in the colon and decreased colitis severity. Whereas probiotics did not stimulate gastrointestinal protein synthesis or reduce colitis severity, a still-unidentified signaling mechanism between the gut and liver seems to be responsible for the probiotic-induced increase in liver protein and plasma protein synthesis. These data underscore the importance of maintaining nutrient intake in pediatric patients with gastrointestinal disease. A strategy for correcting compromised nutrition seems to be more beneficial for reducing damage during colitis than using probiotics only.
机译:每种营养和益生菌均能减轻结肠炎的严重程度,但尚未研究其对肝和胃肠道蛋白质代谢的影响。我们的目标是确定在我们的大型营养限制型仔猪结肠炎模型中,与施用益生菌相比,维持足够的营养是否会影响蛋白质合成,结肠组织病理学和氧化应激。将接受硫酸葡聚糖诱导结肠炎的仔猪(n = 8 /组)随机分为3个治疗组:大量营养限制型(MR);富含VSL#3益生菌(MRP)或营养丰富(WNC)的大量营养素。鉴于实验模型的独特性,另外有8头仔猪作为健康参考,用于比较。 14天后在结肠炎仔猪中进行示踪剂L- [ring-(2)H(5)]苯丙氨酸的恒定输注,以确定小肠粘膜,结肠,肝脏和血浆中蛋白质的分数合成速率蛋白质(总蛋白质,纤维蛋白原,白蛋白)。还评估了结肠组织病理学和氧化应激。与MR仔猪相比,WNC和MRP仔猪在肝脏和血浆蛋白库中的蛋白质合成率更高。但是,只有足够的营养才能增加结肠中的蛋白质合成,并降低结肠炎的严重程度。尽管益生菌不会刺激胃肠道蛋白质的合成或降低结肠炎的严重程度,但肠道和肝脏之间仍未确定的信号传导机制似乎是由益生菌引起的肝脏蛋白质和血浆蛋白质合成增加的原因。这些数据强调了在患有胃肠疾病的小儿患者中维持营养摄入的重要性。与仅使用益生菌相比,纠正营养不良的策略似乎对减少结肠炎期间的损害更为有益。

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