Butanoic acid/Butyric acid

Butyric acid, (from Greek βουτυρος = butter) IUPAC name n-Butanoic acid, or normal butyric acid, is a carboxylic acid with structural formula CH₃CH₂CH₂-COOH.

It is found in rancid butter, parmesan cheese, and vomit, and has an unpleasant odor and acrid taste, with a sweetish aftertaste. Butyric acid can be detected by mammals with good scent detection abilities.

Butyric acid is a fatty acid occurring in the form of esters in animal fats and plant oils. The glyceride of butyric acid makes up 3% to 4% of butter. When butter goes rancid, butyric acid is liberated from the glyceride by hydrolysis leading to the unpleasant odor.

It is an important member of the fatty acid sub-group called short chain fatty acids.

It is ordinarily prepared by the fermentation of sugar or starch, brought about by the addition of putrefying cheese, with calcium carbonate added to neutralize the acids formed in the process. The butyric fermentation of starch is aided by the direct addition of Bacillus subtilis.

The acid is an oily colorless liquid that solidifies at -8 °C; it boils at 164 °C. It is easily soluble in water, ethanol, and ether, and is thrown out of its aqueous solution by the addition of calcium chloride.

Highly-fermentable fibers like oat bran, pectin, and guar are transformed by colonic bacteria into short-chain fatty acids including butyrate.

Butyrate has diverse and, it seems, paradoxical effects on cellular proliferation, apoptosis and differentiation that may be either pro-neoplastic or anti-neoplastic, depending upon factors such as the level of exposure, availability of other metabolic substrate, and the intracellular milieu. Butyrate is thought by some to be protective against colon cancer. However, not all studies support a chemopreventive effect for butyrate, and the lack of agreement (particularly between in vivo and in vitro studies) on butyrate and colon cancer has been termed the "butyrate paradox." There are many reasons for this discrepant effect, including differences between the in vitro and in vivo environments, the timing of butyrate administration, the amount of butyrate administered, the source of butyrate (usually dietary fiber) as a potential confounder, and an interaction with dietary fat. Together, the studies suggest that the chemopreventive benefits of butyrate depend in part on amount, time of exposure with respect to the tumorigenic process, and the type of fat in the diet. Low carbohydrate diets like the Atkins diet are known to reduce the amount of butyrate produced in the colon.

Butyric acid has been associated with the ability to inhibit the function of histone deacetylase enzymes, thereby favouring an acetylated state of histones in the cell. Acetylated histones have a lower affinity for DNA than non-acetylated histones, due to the neutralisation of electrostatic charge interections. In general, it is thought that transcription factors will be unable to access regions where histones are tightly associated with DNA (ie non-acetylated, e.g., heterochromatin). Therefore, it is thought that butyric acid enhances the transcriptional activity at promoters, which are typically silenced/downregulated due to histone deacetylase activity.