Dietary fibres are fermented by bacteria in the colon to form short-chain fatty acids: acetate (C2), propionate (C3) and butyrate (C4). Fatty acids are taken up by colonocytes, and processed in the mitochondria using β-oxidation. This metabolism of — otherwise indigestible — carbohydrates via gut flora provides a major source of energy in humans.
Those of you interested in SCFA metabolism would do well to follow the work of Barbara Bakker [1-3]. In a recent paper with Karen van Eunen and friends, Babs created a mathematical model of β-ox in the rat liver. The model considers competition between acyl-CoAs with differing chain lengths for the same enzymes, which can lead to pathway saturation. I’ve created SBML versions of their model: have a play.
- van Eunen K, Simons SM, Gerding A, Bleeker A, den Besten G, Touw CM, Houten SM, Groen BK, Krab K, Reijngoud DJ, Bakker BM (2013) “Biochemical competition makes fatty-acid β-oxidation vulnerable to substrate overload” PLoS Computational Biology 9:e1003186.
- den Besten G, van Eunen K, Groen AK, Venema K, Reijngoud DJ, Bakker BM (2013) “The role of short-chain fatty acids in the interplay between diet, gut microbiota, and host energy metabolism” Journal of Lipid Research 54:2325-2340.
- den Besten G, Lange K, Havinga R, van Dijk TH, Gerding A, van Eunen K, Müller M, Groen AK, Hooiveld GJ, Bakker BM, Reijngoud DJ (2013) “Gut-derived short-chain fatty acids are vividly assimilated into host carbohydrates and lipids” American Journal of Physiology – Gastrointestinal and Liver Physiology 305:G900-910.