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April 19, 2026Journal of Agricultural and Food Chemistry2 citations

Mechanism of Acylated Starch on Barrier Function of Intestinal Organoids Based on Microbiomics and Metabolomics

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HLHui LiYCYanqi ChengXZXuechun Zhang

Key Points

  • To explore how acylated starch affects the intestinal barrier function using an intestinal organoid model.
  • Established TNF-α-induced intestinal organoid damage model.
  • Analyzed fermentation characteristics of acetylated, propionylated, and butyrylated starches.
  • Examined microbiomics and metabolomics effects on gut health.
  • Acylated starch promoted growth of beneficial bacteria like Bifidobacterium adolescentis.
  • It significantly reduced the damage rate of intestinal organoids compared to the model group.
  • MSP and MSB notably increased Muc-2 secretion, improving barrier function.

Abstract

Acylated starch has been demonstrated to benefit the intestinal barrier. This study established a tumor necrosis factor-α (TNF-α)-induced intestinal organoid (IOs) damage model, analyzed the in vitro fermentation characteristics of acetylated starch (MSA), propionylated starch (MSP), and butyrylated starch (MSB) via microbiomics and metabolomics, and investigated their mechanism on intestinal barrier function. The results showed that acylated starch promoted the proliferation of beneficial gut bacteria, including Bifidobacterium adolescentis, and modulated amino acid synthesis and metabolism. Importantly, acylated starch metabolites mitigated the IO barrier damage. On day 8, the damage rate of IOs in the model group was 48.42 ± 5.50%, while those in the MSA, MSP, and MSB groups were 19.22 ± 0.47%, 17.86 ± 1.63%, and 19.35 ± 3.83%, respectively (p < 0.001). Especially, MSP and MSB markedly increased Muc-2 secretion. In conclusion, acylated starch influenced microbiota's metabolites production by modulating gut microbial composition, thereby improving the intestinal barrier.

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Cite This Study

Li et al. (2026) studied this question.

synapsesocial.com/papers/69e47193010ef96374d8de06https://doi.org/10.1021/acs.jafc.6c01815
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