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1 Department of Molecular Genetics, Biochemistry, and Microbiology and 2 Department of Environmental Health, College of Medicine, University of Cincinnati, Cincinnati, Ohio 45267
The
expression of NHE2 and NHE3 on intestinal-brush border membranes
suggests that both Na+/H+ exchangers serve
absorptive functions. Studies with knockout mice showed that the loss
of NHE3, but not NHE2, causes diarrhea, demonstrating that NHE3 is the
major absorptive exchanger and indicating that any remaining absorptive
capacity contributed by NHE2 is not sufficient to compensate fully for
the loss of NHE3. To test the hypothesis that NHE2 provides partial
compensation for the diarrheal state of NHE3-deficient mice, we crossed
doubly heterozygous mice carrying null mutations in the Nhe2
and Nhe3 genes and analyzed the phenotypes of their
offspring. The additional loss of NHE2 in NHE3-deficient mice caused no
apparent reduction in viability, no further impairment of systemic
acid-base status or increase in aldosterone levels, and no apparent
worsening of the diarrheal state. These in vivo phenotypic correlates
of the absorptive defect suggest that the NaCl, HCO
sodium absorption; diarrhea; Slc9a2; Slc9a3
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