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Acetate, the most abundant SCFA in the foregut lumen, is absorbed immediately after ingestion, although the mechanism by which this absorption occurs is not fully understood. We investigated the distribution and function of candidate SCFA transporters in rat duodenum. The Na<jats:sup>+<\/jats:sup>-coupled monocarboxylate transporter-1 (SMCT1) was localized to the brush border, whereas the pH-dependent monocarboxylate transporter (MCT) 1 and MCT4 were localized to the duodenocyte basolateral membrane. In Ussing chambered duodenal mucosa, luminal acetate dose-dependently increased short-circuit current ( I<jats:sub>sc<\/jats:sub>) in the presence of serosal bumetanide and indomethacin by a luminal Na<jats:sup>+<\/jats:sup>-dependent, ouabain-sensitive mechanism. The I<jats:sub>sc<\/jats:sub> response was inhibited dose-dependently by the SMCT1 nonsubstrate inhibitor ibuprofen, consistent with net electrogenic absorption of acetate via SMCT1. Other SCFAs and lactate also increased I<jats:sub>sc<\/jats:sub>. Furthermore, duodenal loop perfusion of acetate increased portal venous acetate concentration, inhibited by coperfusion of ibuprofen or a MCT inhibitor. Luminal acetate perfusion increased duodenal HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> secretion via capsaicin-sensitive afferent nerve activation and cyclooxygenase activity, consistent with absorption-mediated HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> secretion. These results suggest that absorption of luminal SCFA via SMCT1 and MCTs increases duodenal HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> secretion. 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