Description
Tributyrin (C15H26O6), also known as butyrin or glyceryl tributyrate, is the triester of glycerin and butyric acid. It is prepared by esterifcation of glycerin with excess butyric acid. Glycerol tributyrate has a characteristic odor and a bitter taste.
Tributyrin is essentially a triacylglyceride (TAG), which is an ester derived from glycerol and 3 fatty acids. Tributyrin requires lipase to release the butyrate attached to the glycerol. Although 1 tributyrin contains 3 butyrate, not all 3 butyrate is guaranteed to be released. This is because lipase is regioselective. It can hydrolyse triacylglycerides at R1 and R3, only R2, or non-specifically. Lipase also has substrate specificity in that the enzyme can differentiate between acyl chains attached to the glycerol and preferentially cleaving certain types. Since tributyrin requires lipase to release its butyrate, there may be competition between tributyrin and other TAGs for lipase.
Chemical Properties
Glycerol tributyrate has a characteristic odor and bitter taste.
Chemical Properties
Tributyrin is a colorless, oily liquid
with a bitter taste. It is soluble in alcohol and ether and fairly insoluble in water.
Definition
ChEBI: A triglyceride obtained by formal acylation of the three hydroxy groups of glycerol by butyric acid.
Preparation
Prepared by esterifcation of glycerol with excess butyric acid.
Production Methods
Tributyrin is manufactured via esterification of glycerol
with butyric acid.
Taste threshold values
Taste characteristics at 30 ppm: bitter, waxy, fatty, cheese and butter nuances.
General Description
Tributyrin is a short-chain triacylglycerol that mainly occurs in butter. It shows potent anti-cancer property.
Biochem/physiol Actions
Taste at 30 ppm
Carcinogenicity
Administration of sodium
butyrate in drinking water potentiates 1,2-dimethylhydrazine-
induced colon cancer in rats . In mice, dietary
administration of 5% tributyrin for 48 weeks did not lead to
an increase in colonic tumor incidence or focal areas of
dysplasia as compared to controls . Therefore, it has
been suggested that the agent responsible for enhanced
tumorigenesis in the rat study was sodium, rather than
butyrate.
