Some may think that GOS, FOS, inulin, or HMO simply pass the upper parts of the gastrointestinal tract without any effects until they reach more distal parts of the ileum and the colon where they are metabolized by certain (desired) bacteria, producing short chain fatty acids (SCFA) that then affect the host through several different mechanisms. Because all of these oligosaccharides are degraded to SCFA in the end, their effects may very well be the same—It is most likely not as simple as that (Fig. 2). The intact oligosaccharides may have direct effects that highly depend on their distinct structures; and GOS, FOS, or inulin are structurally very different from the oligosaccharides that naturally occur in human milk (Fig. 1). Many bacteria, for example, express lectins that bind to specific glycans on the host's epithelial cell surface. This initial adhesion is essential for the virulence of most pathogenic microorganisms. Some HMO structurally resemble epithelial cell surface glycans and block pathogen adhesion, which protects the breast-fed infant from certain infections and diarrhea (17). GOS, FOS, or inulin may not be able to mimic these protective effects because most of them do not resemble epithelial cell surface glycans.
http://www.nature.com/pr/journal/v64/n1/full/pr2008136a.htmlThere is also first in vitro evidence that HMO may alter intestinal epithelial gene expression and cell surface glycome composition (18), as well as cell differentiation, proliferation, and apoptosis—at least at very high concentrations (19). Although the underlying mechanisms, receptors and signaling pathways are currently unknown, it can be speculated that these effects are also mediated through epithelial cell surface lectins. Again, GOS, FOS, or inulin may not be recognized by these lectins or bind to other lectins that trigger a different cell response.