10 research outputs found

    193 Characterisation of poor gastrointestinal tract development in gilt progeny

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    Progeny of primiparous sows (gilts) have poor production performance compared to those of multiparous sows. This has been attributed to underlying biological events that occur early in life. We specifically focused on the development of the gastrointestinal tract (GIT) and its function in sow vs gilt progeny (SP vs GP) reared under commercial conditions. Piglet tissues were harvested at birth, at 24 h, and pre- and post-weaning (28 v 29 d) and used to quantify GIT integrity. All data were analysed using Genstat V18 for the effects of parity (sow vs gilt) in birth (0 vs 24 h) and weaning (pre- vs post) cohorts. GIT integrity was quantified from freshly excised tissue in Ussing chambers for transepithelial electrical resistance (TER) and macromolecule permeability (FD4; labelled 4kD dextran). Permeability was measured in stomach, colon, jejunum and ileum. Over the 24-h neonatal period, TER was significantly reduced in the stomach and colon (P = 0.048 and 0.003 respectively) with GP having lower stomach TER than SP (P = 0.015). TER increased in the jejunum and ileum over the 24-h neonatal period (P = 0.004 and 0.002 respectively). An interactive effect of parity and time on ileum FD4 was observed (P = 0.043) where FD4 in SP ileum decreased over the 24-h neonatal period and FD4 in GP ileum increased over the 24-h period (P = 0.043). Jejunum FD4 was significantly higher in GP than SP over the 24-h neonatal period (P = 0.048). An interactive effect of parity and time was observed in the colon over the weaning period where TER increased in SP but decreased in GP (P = 0.005). Stomach TER decreased over the weaning period in both GP and SP (P = 0.013). Jejunum and ileum TER decreased over the weaning period (P = 0.003 and 0.057 respectively). Ileum FD4 was higher in GP than SP over the weaning period (P = 0.037). These findings reflect a reduction in GIT development in GP compared with SP, and gut leakiness may be an underlying reason for poorer production performance and increased morbidity of GP

    Metallothioneins in Drug Resistance

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