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Metabolic Modeling Uncovers Complex Host-Microbiome Dysregulation in IBD

  • Researchers have uncovered a complex, multi-layered deregulation of metabolic interactions between the human host and its microbiome in inflammatory bowel disease (IBD).
  • The study utilized advanced metabolic modeling to reveal the intricate biochemical crosstalk disrupted during IBD, offering new insights into the disease's pathogenesis.
  • Metabolic perturbations driving chronic intestinal inflammation were highlighted, pointing towards new avenues for precision therapy in IBD.
  • The research mapped the metabolic exchanges between the host's cells and gut microbiome, crucial for regulating metabolism, immune function, and mucosal homeostasis.
  • Noteworthy perturbations were observed in pathways involving short-chain fatty acid biosynthesis, amino acid metabolism, and bile acid transformations in IBD patients.
  • The study revealed altered biosynthesis of immune-signaling metabolites in IBD, contributing to dysregulated inflammation in affected individuals.
  • Host mitochondrial metabolism showed significant alterations, indicating a bidirectional metabolic derangement that exacerbates epithelial barrier breakdown in IBD.
  • Personalized metabolic network reconstructions were emphasized, allowing for patient-specific metabolic perturbations mapping and tailored precision medicine interventions.
  • Advanced computational methods integrating host and microbial data transcend traditional microbiome analyses, providing insights into disease mechanisms relevant to IBD.
  • The study's implications range from novel diagnostic biomarkers to microbiome-targeted therapies, revolutionizing IBD management with a focus on metabolic modulation.

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