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
3D model (JSmol)
|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).
Butyrates are important as food for cells lining the mammalian colon (colonocytes). Without butyrates for energy, colon cells undergo autophagy (self digestion) and die. Short-chain fatty acids (SCFAs), 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 SCFAs benefit the colonocytes (cells of the colon) by increasing energy production and cell proliferation, and may protect against colon cancer.
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. In fact, butyrate is responsible for about 70% of energy from the colonocytes, being a critical SCFA in the colon homeostasis. Butyrate possesses both preventive and therapeutic potential to counteract inflammation-mediated ulcerative colitis (UC) and colorectal cancer. The reason why butyrate is an energy source for normal colonocytes and induces apoptosis in colon cancer cells, is due to the Warburg effect in cancer cells, which leads to butyrate not being properly metabolized. This phenomenon leads to the accumulation of butyrate in the nucleus, acting as a histone deacetylase (HDAC) inhibitor. 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 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 upregulation 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). Butyrate inhibits angiogenesis by inactivating Sp1 transcription factor activity and downregulating vascular endothelial growth factor gene expression.
- 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 . PMID 21531334.
- 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.
- Zeng, Huawei (2014-02-15). "Mechanisms linking dietary fiber, gut microbiota and colon cancer prevention". World Journal of Gastrointestinal Oncology. 6 (2). doi:10.4251/wjgo.v6.i2.41.
- Encarnação, J. C.; Abrantes, A. M.; Pires, A. S.; Botelho, M. F. (2015-09-01). "Revisit dietary fiber on colorectal cancer: butyrate and its role on prevention and treatment". Cancer and Metastasis Reviews. 34 (3): 465–478. doi:10.1007/s10555-015-9578-9. ISSN 0167-7659.
- 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. PMC . PMID 22517765.
- 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. PMID 18655767.