Tissue metabolism and the inflammatory bowel diseases

J Mol Med (Berl). 2017 Sep;95(9):905-913. doi: 10.1007/s00109-017-1544-2. Epub 2017 May 20.

Abstract

The intestinal mucosa provides a selective barrier between the anaerobic lumen and a highly metabolic lamina propria. A number of recent studies indicate that acute inflammation of the mucosa can result in tissue hypoxia and associated shifts in tissue metabolism. The activation of hypoxia-inducible factor (HIF) under these conditions has been demonstrated to function as an endogenous molecular cue to promote resolution of inflammation, particularly through the orchestration of barrier repair toward homeostasis. Given the central role of oxygen in tissue metabolism, ongoing studies have defined metabolic endpoints of HIF stabilization as important biomarkers of disease activity. Such findings make HIF and HIF-associated metabolic pathways particularly attractive therapeutic targets in inflammatory bowel disease (IBD). Here, we review the recent literature related to tissue metabolism in IBD.

Keywords: Hypoxia; Inflammation; Metabolite; Microbiota; Nucleotide.

Publication types

  • Review

MeSH terms

  • Acute Disease
  • Adenosine / metabolism
  • Animals
  • Disease Susceptibility
  • Energy Metabolism*
  • Gastrointestinal Microbiome / immunology
  • Humans
  • Hypoxia / metabolism
  • Hypoxia-Inducible Factor 1 / metabolism
  • Inflammatory Bowel Diseases / etiology*
  • Inflammatory Bowel Diseases / metabolism*
  • Inflammatory Bowel Diseases / pathology
  • Intestinal Mucosa / immunology
  • Intestinal Mucosa / metabolism*
  • Intestinal Mucosa / microbiology
  • Intestinal Mucosa / pathology
  • Organ Specificity
  • Tryptophan / metabolism

Substances

  • Hypoxia-Inducible Factor 1
  • Tryptophan
  • Adenosine