Antioxidant status and expression of inflammatory genes in gut and liver of piglets fed different dietary methionine concentrations

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Methionine (Met) is one of the first‐limiting amino acids in pig diets and often has to be supplemented to prevent an undersupply of this essential amino acid and to meet total sulphur amino acid requirements for maintenance and growth. Besides its role as a proteinogenic amino acid, however, Met is also the principal methyl donor in mammalian cells and is a precursor for synthesis of polyamines, which are involved in cell proliferation, and for glutathione (GSH), the major intracellular antioxidant in mammals (Bauchart‐Thevret et al., 2009a). It has been shown that sulphur amino acid‐free diets decreased not only plasma Met concentrations and body weight gains, but also reduced intestinal epithelial growth and tissue GSH concentrations (Bauchart‐Thevret et al., 2009b). Interestingly, Met was preferentially utilized for protein synthesis and methylation reactions, but less so for Met catabolism via the transsulphuration pathway which generates, amongst others, GSH, which reduces oxidative stress due to its antioxidant function (Bauchart‐Thevret et al., 2009b). In addition, polyamine levels and the antioxidant status of the gut were positively affected in piglets when Met supplementation was increased above requirements (Chen et al., 2014). Oxidative stress results when levels of reactive oxygen species (ROS) increase and is counteracted by the antioxidant defence system where the key transcription factor nuclear factor (erythroid‐derived 2)‐like 2 (Nrf2), the master regulator of the antioxidant response, plays a crucial role (Morgan and Liu, 2011; Buelna‐Chontal and Zazueta, 2013). In addition, under conditions of oxidative stress, the nuclear factor ‘kappa‐light‐chain‐enhancer’ of activated B‐cells (NF‐κB), the master regulator of inflammation, is activated to prevent further oxidative damage and promote cellular survival or, sometimes, apoptosis (Morgan and Liu, 2011; Buelna‐Chontal and Zazueta, 2013). So far, however, it is unknown how suboptimal concentrations of dietary Met affect the antioxidant defence system. A modification of the oxidant/antioxidant balance may impair the ability of the antioxidant defence system to protect tissues and body fluids from damage by oxidants like ROS and to support immune cell function (Puertollano et al., 2011). In addition, the impact of dietary Met on inflammation‐ and antioxidant‐related molecular pathways has not been investigated so far. Therefore, the objective of this study was to investigate the effects of dietary concentrations of sulphur‐containing amino acids equivalent to 80%, 90% and 100% of requirements for maintenance and growth on gut morphology, gene expression of Nrf2 and NF‐κB target genes, and on concentrations of antioxidants and lipid peroxidation products in gut and liver of weaned piglets. We hypothesized that feeding suboptimal dietary Met concentrations reduce GSH concentrations and activate gene expression of Nrf2 and NF‐κB target genes in gut and liver of piglets.
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