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• W164893129 abstract "This study investigates the molecular function of NHE3 in H+-dipeptide transport regulation in the native intestine. Luminal application of the dipeptide Gly-Sar resulted in a strong increase in murine small intestinal fluid absorption in vivo, Isc response in chambered jejunal mucosa, and a decrease in pHi in BCECF-loaded enterocytes in isolated jejunal villi. Genetic ablation of PEPT1 abolished Gly-Sar-induced fluid absorption, Isc response, and enterocyte acidification. Genetic ablation, pharmacological or second-messenger-mediated inhibition of NHE3 also reduced Gly-Sar-induced fluid absorption in vivo and Isc response in vitro, but enhanced enterocyte acidification. Genetic ablation of Slc26a6 also enhanced enterocyte acidification, but did not alter either Gly-Sar induced fluid absorption or Isc response. The transmembrane proton gradient was irrelevant for sustained H+/dipeptide transport rates, but the luminal Na+ concentration, enterocyte Na+/K+ ATPase activity, and luminal membrane potential were essential determinants. PEPT1 is the only H+/dipeptide uptake pathway, and NHE3 function is essential for sustained H+/dipeptide uptake rates in the native intestine. We speculate that NHE3 is the major Na+-uptake pathway into enterocytes during dipeptide-induced volume increase, and therefore essential to the maintenance of membrane potential negativity." @default.
• W164893129 created "2016-06-24" @default.
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• W164893129 date "2009-04-01" @default.
• W164893129 modified "2023-09-26" @default.
• W164893129 title "Dual role of the Na+/H+ exchanger isoform 3 for PEPT1‐mediated H+/dipeptide cotransport in native murine intestine" @default.
• W164893129 doi "https://doi.org/10.1096/fasebj.23.1_supplement.796.42" @default.
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