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Title
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Birthweight determines intestinal microvasculature development and alters endothelial nitric oxide synthase density in young piglets
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Author
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Abstract
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| Blood supply to enterocytes dictates intestinal health and nutrient absorption. These two aspects are impaired in low birthweight (LBW) piglets, but whether the perfusion to intestinal tissues is implicated as well is still unknown. Thus, structural changes in the microvasculature of LBW and normal birthweight (NBW) piglets were investigated during early postnatal development. Additionally, the presence of endothelial nitric oxide synthase (eNOS) in the intestinal mucosa was assessed given its important role to assure perfusion. A total of 22 pigs (11 LBW and 11 NBW) were sacrificed at days 0, 3, 8 and 19 of life. Body weight and intestinal length were recorded and a piece of the small intestine was sampled for immunohistochemical analysis of von Willebrand Factor (vWF, an endothelial cell marker) and eNOS. LBW piglets had a relatively (to body weight) longer intestine than their NBW counterparts. Age did not affect microvasculature, which was more abundant (85% larger vWF-positive area) in NBW than LBW pigs. However, an interaction age*BW was observed for eNOS-IR, showing that eNOS presence peaked in NBW piglets on the first day of life and subsequently decreased. This pattern was not observed in LBW piglets. The less abundant intestinal endothelial mass and the different pattern of eNOS expression observed in LBW piglets suggests microcirculation as a contributing factor in the impaired digestive functioning and gut health of LBW pigs. However, revealing whether the origin of this alteration is prenatal or postnatal, for example due to a lower milk intake, needs further study. |
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Language
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English
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Source (journal)
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Anatomia, histologia, embryologia : journal of veterinary medicine: series C. - Berlin
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Publication
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Hoboken
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Wiley
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2020
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ISSN
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0340-2096
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DOI
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10.1111/AHE.12534
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Volume/pages
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8 p.
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ISI
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000509820900001
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Pubmed ID
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31995241
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Full text (Publisher's DOI)
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Full text (publisher's version - intranet only)
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