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Butyrate or butanoate is the traditional name for the conjugate base of butyric acid also known as butanoic acid. The name is used as part of the name of esters and salts of butyric acid. As a short chain fatty acid , butyric acid is fully ionized near neutral pH. In nature, the cation associated with butyrate is unknown or unimportant to the metabolizing enzymes. Butyrates are important as food for cells lining the mammalian colon colonocytes. Without butyrates for energy, colon cells undergo autophagy self digestion and die. These SCFAs benefit the colonocytes cells of the colon by increasing energy production and may protect against colon cancer by inhibiting cell proliferation. 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. 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. 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. Butyrate is extremely essential to host immune homeostasis. Although the role and importance of butyrate in the gut is not fully understood, many researchers argue that a depletion of butyrate-producing bacteria in patients with several vasculitic conditions is essential to the pathogenesis of these disorders. A depletion of butyrate in the gut is typically caused by an absence or depletion of butyrate-producing-bacteria BPB. This depletion in BPB leads to microbial dysbiosis. This dysbiosis is characterized by an overall low biodiversity and a depletion of key butyrate-producing members. Butyrate is an essential microbial metabolite with a vital role as a modulator of proper immune function in the host. Butyrate has shown to promote the differentiation of regulatory T cells. In particular, circulating butyrate prompts the generation of extrathymic regulatory T cells. The low-levels of butyrate in human subjects could favor reduced regulatory T cell-mediated control, thus promoting a powerful immuno-pathological T-cell response. The absence or depletion of these BPB in the gut could therefore be a possible aide in the overly-active inflammatory response. Butyrate in the gut also protects the integrity of the intestinal epithelial barrier. Decreased butyrate levels therefore lead to a damaged or dysfunctional intestinal epithelial barrier. In a research study conducted by Furusawa et al, microbe-derived butyrate was found to be essential in inducing the differentiation of colonic regulatory T cells in mice. This is of great importance and possibly relevant to the pathogenesis and vasculitis associated with many inflammatory diseases because regulatory T cells have a central role in the suppression of inflammatory and allergic responses. The anti-inflammatory capacity of butyrate has been extensively analyzed and supported by many studies. It has been found that microorganism-produced butyrate expedites the production of regulatory T cells. An increase in regulatory T cell numbers was observed upon a butyrate provision. Due to the importance of butyrate as an inflammatory regulator and immune system contributor, butyrate depletions could be a key factor influencing the pathogenesis of many vasculitic conditions. Because of this, it is essential to harvest healthy levels of butyrate in the gut. Butyrate provisions or fecal microbiota transplants to restore BPB and symbiosis in the gut could be effective in replenishing butyrate levels. A fecal microbiota transplant, also known as fecal bacteriotherapy, is the process of restoring bacteria commonly found in the digestive tract with an infusion of feces from a donor. While the description of this may disgust some, fecal bacteriotherapy may quickly and efficiently restore symbiosis in imbalanced microbiomes. In this treatment option, a healthy individual would donate their stool to be transplanted into an individual with dysbiosis. Another less-invasive treatment option that may be effective in decreasing inflammation in individuals with vasculitic conditions is the administration of butyrate. This could be as easy as buying oral butyrate supplements online. Another way to administer butyrate into the gut—which may be more effective though also more invasive—is by the administration of butyrate enemas. Butyrate—both oral supplements and enemas—has been shown to be very effective in terminating symptoms of inflammation with minimal-to-no side-effects. In a study where patients with ulcerative colitis were treated with butyrate enemas, inflammation decreased significantly, and bleeding ceased completely after butyrate provision. Salts of butyrates are also well known. One example is sodium butyrate , a colorless, water-soluble salt. It is a histone deacetylase inhibitor HDAC used in psychiatry. From Wikipedia, the free encyclopedia. CAS Number. Interactive image. PubChem CID. Chemical formula. Cell Metabolism. February World Journal of Gastrointestinal Oncology. Cancer and Metastasis Reviews. American Journal of Physiology. Gastrointestinal and Liver Physiology. October Archives of Biochemistry and Biophysics. Journal of Allergy and Clinical Immunology. April Autoimmunity Reviews. Mucosal Immunology. Bibcode : Natur. Scientific Reports. Epigenetics in Psychiatry. Categories : Butyrates Carboxylate anions. Namespaces Article Talk. Views Read Edit View history. Help Learn to edit Community portal Recent changes Upload file. Download as PDF Printable version. IUPAC name butanoate.