Editor,—In cystic fibrosis intestine there is an increase in the rate of sodium coupled glucose absorption,1 which exacerbates the characteristic luminal dehydration of this disease resulting from the failure of chloride secretion. The mechanism for the sodium dependent uptake of sugars from the small intestine is now well established, but early studies of its cation dependency revealed that replacement of external sodium with potassium had a greater inhibitory effect than replacement with urea or Tris.2 This was explained as competition between sodium and potassium for a common binding site on the glucose transporter and it …