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Several studies in our laboratory have shown that microbial degradation of tryptophan by pig gastrointestinal bacteria results mainly in the two volatile indolic compounds indole and skatole, skatole via a transient accumulation of indole acetic acid (IAA). Analogously with indole and skatole, indole propionic acid is also an end product of tryptophan metabolism, and has recently been shown to be produced in small amounts in the hind gut of pigs [1]. While the conversion of tryptophane to indole and IAA is performed by a variety of bacteria, only very few bacteria species are capable of further degradation of IAA to skatole [2]. The production of skatole increases through the colon and reaches a maximum in the distal part of the large intestine. From the intestinal tract, a portion of the produced skatole is absorbed to the blood and transported via the portal vein to the liver, where more than half of the amount absorbed is degraded by cytochrome P450. It has been demonstrated that the liver extraction is relatively constant within the individual animal, but varies between animals, and between sexes, showing a lower elimination rate of skatole in male pigs than female pigs [3]. Skatole avoiding degradation in the liver is deposited in peripheral tissues and due to the lipophilic characteristics of skatole the majority accumulates in the adipose tissue. To summarize, the amount of skatole stored in adipose tissue depends on the concentration in the peripheral blood, which is influenced by the production in the large intestine and the degradation capacity of the liver. As the production of skatole is the incipient cause of tainted meat a limitation of the microbial fermentation of tryptophan in the large intestine would be an effective approach to solve the problem with boar odour caused by skatole.

Prevention of boar taint in pig production. Factors affecting the level of skatole