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

Abstract

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 ${{\text{SCFA}}} \mathord{\left/ {\vphantom {{{\text{SCFA}}} {{\text{HCO}}^{{\text{ - }}}_{{\text{3}}} }}} \right. \kern-\nulldelimiterspace} {{\text{HCO}}^{{\text{ - }}}_{{\text{3}}} }$ exchange. To provide factual evidence for the operation of ${{\text{SCFA}}} \mathord{\left/ {\vphantom {{{\text{SCFA}}} {{\text{HCO}}^{{\text{ - }}}_{{\text{3}}} }}} \right. \kern-\nulldelimiterspace} {{\text{HCO}}^{{\text{ - }}}_{{\text{3}}} }$ 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 ${\text{CO}}_{{\text{2}}} {\left( {{\text{HCO}}^{{\text{ - }}}_{{\text{3}}} {\text{ + CO}}_{{\text{2}}} } \right)}$ secretion (J_tCO2(sm)), and the short-circuit current (I_sc) with the mucosal side bathed with a Cl⁻ and ${\text{HCO}}^{{\text{ - }}}_{{\text{3}}}$-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 ${{\text{HCO}}^{{\text{ - }}}_{{\text{3}}} } \mathord{\left/ {\vphantom {{{\text{HCO}}^{{\text{ - }}}_{{\text{3}}} } {{\text{CO}}_{{\text{2}}} }}} \right. \kern-\nulldelimiterspace} {{\text{CO}}_{{\text{2}}} }$-containing solution than with a ${{\text{HCO}}^{{\text{ - }}}_{{\text{3}}} } \mathord{\left/ {\vphantom {{{\text{HCO}}^{{\text{ - }}}_{{\text{3}}} } {{\text{CO}}_{{\text{2}}} }}} \right. \kern-\nulldelimiterspace} {{\text{CO}}_{{\text{2}}} }$-free solution. The addition of propionate to the mucosal side caused an increase in J_OH(sm) and J_tCO2(sm), the magnitude of these increases both being much greater with the serosal side bathed with the ${{\text{HCO}}^{{\text{ - }}}_{{\text{3}}} } \mathord{\left/ {\vphantom {{{\text{HCO}}^{{\text{ - }}}_{{\text{3}}} } {{\text{CO}}_{{\text{2}}} }}} \right. \kern-\nulldelimiterspace} {{\text{CO}}_{{\text{2}}} }$-containing solution than with the ${{\text{HCO}}^{{\text{ - }}}_{{\text{3}}} } \mathord{\left/ {\vphantom {{{\text{HCO}}^{{\text{ - }}}_{{\text{3}}} } {{\text{CO}}_{{\text{2}}} }}} \right. \kern-\nulldelimiterspace} {{\text{CO}}_{{\text{2}}} }$-free solution. Acetazolamide, a carbonic anhydrase inhibitor, largely suppressed ${\text{HCO}}^{{\text{ - }}}_{{\text{3}}}$-dependent components of J_prop(ms), propionate-induced J_OH(sm), and propionate-induced J_tCO2(sm). Acetazolamide, however, did not affect I_sc. The ${\text{HCO}}^{{\text{ - }}}_{{\text{3}}}$-dependent component of J_prop(ms) was not inhibited by either lactate or α-cyano-4-hydroxycinnamate, a typical substrate and an inhibitor of the monocarboxylate transporter (MCT1), respectively. It is concluded that an electroneutral, carbonic anhydrase-dependent ${{\text{SCFA}}} \mathord{\left/ {\vphantom {{{\text{SCFA}}} {{\text{HCO}}^{{\text{ - }}}_{{\text{3}}} }}} \right. \kern-\nulldelimiterspace} {{\text{HCO}}^{{\text{ - }}}_{{\text{3}}} }$ exchange mechanism was involved in SCFA absorption. The apical membrane protein for this pathway is not MCT1 and remains to be determined.