首页> 外文期刊>The British Journal of Nutrition >Parenteral and enteral feeding in preterm piglets differently affects extracellular matrix proteins, enterocyte proliferation and apoptosis in the small intestine.
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Parenteral and enteral feeding in preterm piglets differently affects extracellular matrix proteins, enterocyte proliferation and apoptosis in the small intestine.

机译:早产仔猪的肠胃外和肠内喂养对小肠细胞外基质蛋白,肠上皮细胞增殖和凋亡的影响不同。

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The preterm intestine is immature and responds differently to total parenteral nutrition (TPN) and enteral nutrition, compared with the term intestine. We hypothesised that in preterms, diet composition and feeding route affect mucosal morphology, enterocyte mitosis and apoptosis, and the distribution of laminin-1, fibronectin and collagen IV (extracellular matrix proteins (ECMP)). Preterm piglets (93.5 % of gestation) were delivered via caesarean section and birth weight-matched allocated to one of the four experimental groups: the piglets were either euthanised immediately after delivery, after 3 d of TPN or after 2 d enteral feeding with colostrum or milk formula, following 3 d of TPN. We combined immunohistochemistry, image analysis and stereological measurements to describe the intestinal mucosal layer. No significant changes occurred after 3 d of TPN. Feeding colostrum or milk replacer for 2 d after TPN was associated with an increased crypt depth. Only enteral feeding with colostrum resulted in an increased villus height and mitotic index. Neither TPN nor enteral feeding changed the distribution pattern of ECMP or the occurrence of bifid crypts. The immature distribution pattern of ECMP in TPN-fed piglets, coupled with unchanged enterocyte mitosis and apoptosis indices, illustrates that feeding preterm pigs 3 d TPN does not lead to mucosal atrophy. Despite the invariable distribution of ECMP, colostrum was associated with crypt hyperplasia resulting in an increased villus height. These data illustrate that some mechanisms regulating cell turnover are immature in preterms and may in part explain the abnormal gut responses to TPN and enteral feeding in prematurely born pigs.
机译:与术语肠相比,早产肠还不成熟,对总肠胃外营养(TPN)和肠内营养的反应不同。我们假设在早产时,饮食组成和进食途径会影响粘膜形态,肠细胞有丝分裂和细胞凋亡,以及层粘连蛋白-1,纤连蛋白和胶原蛋白IV(细胞外基质蛋白(ECMP))的分布。早产仔猪(妊娠率为93.5%)通过剖腹产分娩,出生体重匹配分配给四个实验组之一:在分娩后,TPN 3天后或初乳经肠饲喂2天后对仔猪实施安乐死。 TPN 3天后的牛奶配方。我们结合免疫组织化学,图像分析和体视学测量来描述肠粘膜层。 TPN 3天后无明显变化。 TPN后饲喂初乳或代乳粉2 d与隐窝深度增加有关。仅肠饲喂初乳会增加绒毛高度和有丝分裂指数。 TPN和肠内喂养均未改变ECMP的分布方式或双隐窝的发生。在TPN饲喂的仔猪中ECMP的未成熟分布模式,以及未改变的肠细胞有丝分裂和凋亡指数,说明饲喂3 d TPN的早产仔猪不会导致粘膜萎缩。尽管ECMP分布不变,但初乳与隐窝增生相关,导致绒毛高度增加。这些数据表明,一些调节细胞更新的机制在早产中还不成熟,可能部分解释了早产猪对TPN和肠内喂养的异常肠道反应。

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