*Geek Box: Short-Chain Fatty Acids

*Geek Box: Short-Chain Fatty Acids

SCFA are fatty acids of between 1 – 6 carbons in length, that are produced through fermentation of fibres, proteins and peptides, in the colon. There are three primary SCFAs: butyrate, propionate, and acetate. Butyrate is the primary fuel source for intestinal cells in the colon [‘colonocytes’],  and is used preferentially over other colonocyte fuel sources like the amino acid, glutamine. Butyrate is associated the suppression of pathogenic bacteria, anti-inflammatory effects, and improve peristalsis [movement of food through the GI tract]. Propionate is absorbed directly to the liver via the hepatic portal vein, while acetate is also absorbed to the liver but enters circulation and is metabolised by peripheral tissues, e.g., skeletal muscle.

SCFA’s are very efficiently absorbed, and only 5-10% of these fatty acids are excreted in faeces. As you can see from the different metabolic fates of these three SCFA, they each influence different processes. Acetate is used for the creation of new fat [lipogenesis], and is also used for cholesterol synthesis. Conversely, propionate may inhibit cholesterol synthesis and decrease free fatty acid concentrations. The majority of butyrate, however, between 70-90% is taken up by colonocytes. Thus, for the so-called ‘extra-intestinal’ effects on cardio-metabolic processes, it may be that the ratio of propionate to acetate is an important determinant.

It is important to stress that at this stage, much of the research is in animal models and in vitro studies, and well-conducted human studies are scarce, albeit continuing to accumulate. Nevertheless, the increase in SCFA levels, and the populations of bacteria which produce SCFA, are a consistent observation in populations with low prevalence of gastrointestinal diseases. The mechanistic and human data is suggestive of a number of explanations for these associations, but there is still a way to go in establishing effects of different fibre types on SCFAs, the precise metabolic fate and activity of SCFAs in humans, and the potential therapeutic application of targeting the production of SCFAs for specific conditions.