Butyrate

Butyrate

Names
IUPAC name butanoate
Identifiers
CAS Number	461-55-2
ChemSpider	94582
Jmol 3D model	Interactive image
PubChem	104775
InChI InChI=1S/C4H8O2/c1-2-3-4(5)6/h2-3H2,1H3,(H,5,6)/p-1 Key: FERIUCNNQQJTOY-UHFFFAOYSA-M
SMILES [O-]C(=O)CCC
Properties
Chemical formula	C4H7O2^−
Molar mass	87.098 g mol^−1
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
Infobox references

Butyrate (also known as butanoate) is the traditional name for the conjugate base of butyric acid (also known as butanoic acid). The formula of the butyrate ion is C₄H₇O₂⁻. The name is used as part of the name of esters and salts of butyric acid, a short chain fatty acid. Examples include

• Cellulose acetate butyrate, an aircraft dope
• Methyl butyrate
• Ethyl butyrate
• Butyl butyrate
• Pentyl butyrate
• Sodium butyrate, a HDAC inhibitor used in psychiatry

Butyrates are important as food for cells lining the mammalian colon (colonocytes). Without butyrates for energy, colon cells undergo autophagy (self digestion) and die.^[1] Short-chain fatty acids, which include butyrate, are produced by beneficial colonic bacteria (probiotics) that feed on, or ferment prebiotics, which are plant products that contain adequate amounts of dietary fiber. These short-chain fatty acids benefit the colonocytes (cells of the colon) by increasing energy production and cell proliferation, and may protect against colon cancer.^[2]

Butyrate is a major metabolite in colonic lumen arising from bacterial fermentation of dietary fiber and has been shown to be a critical mediator of the colonic inflammatory response. Butyrate possesses both preventive and therapeutic potential to counteract inflammation-mediated ulcerative colitis (UC) and colorectal cancer. One mechanism underlying butyrate function in suppression of colonic inflammation is inhibition of the IFN-γ/STAT1 signaling pathways at least partially through acting as a histone deacetylase (HDAC) inhibitor. While transient IFN-γ signaling is generally associated with normal host immune response, chronic IFN-γ signaling is often associated with chronic inflammation. It has been shown that Butyrate inhibits activity of HDAC1 that is bound to the Fas gene promoter in T cells, resulting in hyperacetylation of the Fas promoter and up-regulation of Fas receptor on the T cell surface. It is thus suggested that Butyrate enhances apoptosis of T cells in the colonic tissue and thereby eliminates the source of inflammation (IFN-γ production).^[3] Butyrate inhibits angiogenesis by inactivating Sp1 transcription factor activity and down regulating vascular endothelial growth factor gene expression.^[4]

See also

• Butyric acid

References

1. Donohoe, Dallas R.; Garge, Nikhil; Zhang, Xinxin; Sun, Wei; O'Connell, Thomas M.; Bunger, Maureen K.; Bultman, Scott J. (2011). "The Microbiome and Butyrate Regulate Energy Metabolism and Autophagy in the Mammalian Colon". Cell Metabolism 13 (5): 517–26. doi:10.1016/j.cmet.2011.02.018. PMC 3099420. PMID 21531334.
2. Lupton, Joanne R. (February 1, 2004). Microbial Degradation Products Influence Colon Cancer Risk: the Butyrate Controversy. vol. 134 no. 2: J. Nutr. pp. 479–482.
3. Zimmerman, M. A.; Singh, N.; Martin, P. M.; Thangaraju, M.; Ganapathy, V.; Waller, J. L.; Shi, H.; Robertson, K. D.; Munn, D. H.; Liu, K. (19 April 2012). "Butyrate suppresses colonic inflammation through HDAC1-dependent Fas upregulation and Fas-mediated apoptosis of T cells". AJP: Gastrointestinal and Liver Physiology 302 (12): G1405–G1415. doi:10.1152/ajpgi.00543.2011.
4. Prasanna Kumar, S.; Thippeswamy, G.; Sheela, M.L.; Prabhakar, B.T.; Salimath, B.P. (October 2008). "Butyrate-induced phosphatase regulates VEGF and angiogenesis via Sp1". Archives of Biochemistry and Biophysics 478 (1): 85–95. doi:10.1016/j.abb.2008.07.004.