Table 1.
Role in intestinal homoeostasis | Mechanisms | Outcome |
Anti-inflammatory function | Inhibits histone deacetylases | Pro-inflammatory mediators (TNF-alpha, IL-2, IL-6, IL-8) |
Inhibits NF-kB pathway | Anti-inflammatory mediators (IL-10) | |
Energy source | 90% of butyrate taken up by colonocytes for β-oxidation | Butyrate is the primary energy source for colonocytes |
Protective against colon cancer | Inhibits histone deacetylases (Dachas) |
Apoptosis of colon cancer cells |
Induces cell cycle arrest | Proliferation of colon cancer cells | |
Enhance epithelial barrier function and defence against pathogens | Increased expression of MUC2 gene | Mucin production |
Regulates tight junctional proteins | Antimicrobial peptide production | |
Intestinal epithelial permeability | ||
Anti-diarrhetic | Stimulates Na+ and Cl− coupled transport systems Inhibits secretion of Cl− |
Sodium, chloride, potassium and water absorption in colon |
A summary of the effects of butyrate on gut homoeostasis. The different roles of butyrate in gut homoeostasis are outlined with a description of the mechanisms and outcomes for each role. Blue arrow direction indicates an increase or decrease.