Propionate absorption associated with bicarbonate secretion in vitro in the mouse cecum

Short-chain fatty acids (SCFAs) produced by the microbial fermentation of undigested polysaccharide are rapidly absorbed in the large intestine. One proposed mechanism for this SCFA absorption is SCFA/HCO3- exchange. To provide factual evidence for the operation of SCFA/HCO3- exchange, we mounted an isolated mouse cecum in the Ussing chamber and measured the rates of propionate absorption (J(prop(ms))), alkaline secretion (J(OH(sm))) and total CO2 (HCO3- + CO2) secretion (J(tCO2(sm))), and the short-circuit current (I-sc) with the mucosal side bathed with a Cl- and HCO3- free solution. In the presence of propionate only on the mucosal but not in the serosal solution, J(prop( ms)) was larger when the serosal side was bathed with a containing solution than with a HCO3-/CO2-free solution. The addition of propionate to the mucosal side caused an increase in JOH( sm) and JtCO2( sm), the magnitude of these increases both being much greater with the serosal side bathed with the HCO3-/CO2--containing solution than with the HCO3-/CO2-free solution. Acetazolamide, a carbonic anhydrase inhibitor, largely suppressed HCO3--dependent components of J(prop(ms)), propionate- induced J(OH( sm)), and propionate- induced J(tCO2( sm)). Acetazolamide, however, did not affect Isc. The HCO3- dependent component of Jprop( ms) was not inhibited by either lactate or alpha-cyano-4-hydroxycinnamate,a typical substrate and an inhibitor of the monocarboxylate transporter (MCT1), respectively. It is concluded that an electroneutral, carbonic anhydrase-dependent SCFA HCO3- exchange mechanism was involved in SCFA absorption. The apical membrane protein for this pathway is not MCT1 and remains to be determined.