Targeted delivery of short-chain fatty acids to the human large bowel

Abstract

The cecum and colon are an integral, but somewhat neglected, part of the human digestive system. This digestion is affected not by human enzymes but by the microbiota that degrade undigested dietary components and body secretions that pass through the ileocecal valve. The main fermentative substrates are the indigestible polysaccharides that constitute the greater part of total dietary fiber, whereas the short-chain fatty acids (SCFAs) 2 acetate, propionate, and butyrate are important end products (1). Generally, SCFAs are formed in the order of acetate . propionate $ butyrate, the same as they are in ruminant and nonruminant obligate herbivores. The 2 SCFAs of greatest potential interest for their physiologic effects (propionate and butyrate) are formed in the lowest amounts, which is clearly important for health outcomes. The similarity of the fermentation and its products between (omnivorous) humans and herbivores is striking. In fact, the first comparison of SCFAs between species showed concentrations in the hind gut of the pig to be similar to those in the digestive fluid of herbivores. The pig is an omnivore, like humans, and a study in stoma patients confirmed high SCFA concentrations in effluent from those with sigmoid colostomy and lower in those with distal colostomy and in feces (2). This is consistent with SCFA uptake by the host and, by extension, his or her metabolism. A recent study in surgical patients showed this to be true when concentrations in the major blood vessels were measured, including the hepatic portal vein (3). Rectal infusion of butyrate failed to increase peripheral blood concentrations, consistent with metabolism by the viscera. This means that mixed venous SCFAs are not necessarily a precise measure of concentrations in the proximal large bowel and the hepatic portal vein.Although there is a body of knowledge of human large bowel SCFA production and metabolism, it is relatively underdeveloped. The obvious question is, why? Part of the reason lies in the technical difficulties of accessing the proximal large bowel (which is the site of production) and the hepatic portal vein (the main transport vessel). This has necessitated the use of model animal species. Another issue seems to lie in the history of the fiber hypothesis itself. The concept grew from early observations of the major differences in the disease risk profile and diets of African natives and Europeans living in the same location. On the basis of observation and not measurement, it appeared that the former ate more fiber than the latter, consistent with very low rates of diet-related diseases such as colorectal cancer in the natives, which explained their low risk of noncommunicable diseases quite conveniently. In this context, fiber was approximately equated to the plant's structural nonstarch polysaccharides (NSPs), which are the main components of the feed of production animals such as sheep. Consequently, the assumption has become entrenched that NSPs are the active elements of fiber. In fact, the ethnic comparison...

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