The effects of tributyrin and tricaproin feeding on rumen and ileum transcriptome
收藏NIAID Data Ecosystem2026-05-10 收录
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https://www.ncbi.nlm.nih.gov/sra/DRP013846
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Feeding tributyrin and/or tricaproin may offer a potential approach to enhance gastrointestinal development and barrier function. In a prior, unpublished study, we observed that calves fed milk replacer containing tributyrin and tricaproin exhibited improved gut permeability, along with enhanced histological characteristics in the rumen papillae and ileum. Similarly, Liu et al. reported that calves fed milk replacer containing 0.2% tributyrin of the total milk replacer demonstrated increased villus heights and villus crypt-to-depth ratios in the jejunum, as well as heightened villus heights in the ileum, compared to calves receiving milk replacer without tributyrin. To gain a more comprehensive understanding of how tributyrin and tricaproin feeding influence gastrointestinal histology development and barrier function, it is essential to uncover the molecular changes occurring within the gastrointestinal tract as a result of this feeding regimen. Nonetheless, the precise mechanisms underlying histological development and barrier function in the rumen and ileum through the administration of tributyrin and tricaproin remain unclear. Therefore, the primary objective of this study is to elucidate the molecular mechanisms by which tributyrin and tricaproin contribute to the improvement of histological development and barrier function in the rumen and ileum. In this investigation, calves were provided with milk replacer containing vegetable oils (negative control), dairy cream (positive control), and a combination of tributyrin and tricaproin. At the end of the fifth week, we conducted a transcriptome analysis of the rumen and ileum tissues in conjunction with their corresponding histology data. Our hypothesis posits that tributyrin and tricaproin in the milk replacer facilitate the expression of genes associated with barrier function, cell proliferation, or cell apoptosis."
创建时间:
2025-09-23



