|This article needs additional citations for verification. (December 2009)|
|Jmol-3D images||Image 1|
|Molar mass||87.098 g mol-1|
|Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa)|
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. 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 colonocyte 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. 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).
- 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.
- 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.
- Mary A. Zimmerman, Nagendra Singh, Pamela M. Martin, Muthusamy Thangaraju, Vadivel Ganapathy, Jennifer L. Waller, Huidong Shi, Keith D. Robertson, David H. Munn, and Kebin Liu. 2012. Butyrate suppresses colonic inflammation through HDAC1-dependent Fas Upregulation and Fas-mediated apoptosis of T cells. Am J Physiol Gastrointest Liver Physiol 302: G1405-G1415