Mechanism of colonic permeation of inulin: Is rat colon more permeable than small intestine?

Abstract

Background/Aims: Colonic epithelium is considered to be relatively tight. The colonic “pore” diameter is 6 Å; therefore, colonic epithelium has generally been considered to be impermeable to hydrophilic probes with a cross-sectional diameter of >6 Å. This study examined whether rat colon is permeable to inulin, a large hydrophilic macromolecule having a molecular weight of 5000 g/mol and a cross-sectional diameter of 15 Å (hydration diameter, 20 Å). Methods: The colonic permeation of inulin (10 μmol/L) in vivo was investigated by perfusion of rat colonic segments. Results: There was significant colonic permeation of inulin, but tissue retention of inulin was low. The net colonic flux of inulin was strongly dependent on net water flux, showing a strong solvent drag effect. Addition of 16,16-dimethyl prostaglandin E 2 decreased water flux with a corresponding decrease in inulin flux; this process seemed to be mediated by 5′-cyclic adenosine monophosphate because both the phosphodiesterase inhibitor aminophylline and dibutyryl adenosine 5′-cyclic adenosine monophosphate decreased water and inulin flux in a parallel manner. Chenodeoxycholic and taurocholic acids decreased net mucosal-to-serosal water flux but increased inulin flux. The net colonic permeation rate of inulin was higher than the small intestinal permeation rate. Conclusions: Rat colon is permeable to inulin. The higher net colonic permeability may be caused by differences in mucosal surface, permselectivity, solvent drag effect, and differences in net water fluxes of the colon and small intestine.