Glucose-stimulated sodium transport by the human intestine during experimental cholera

Net sodium absorption from oral rehydration solution is increased by both glucose-sodium cotransport and solvent drag. The aim of this study was to measure the relative importance of glucose-sodium cotransport and solvent drag in the stimulation of net sodium absorption by oral rehydration solution.

Total intestinal perfusion was used in normal subjects with and without intrajejunal cholera toxin using three test solutions containing 100 mmol/L sodium and either 100 mmol/L mannitol (control), 100 mmol/L glucose, or no additional solute (hypotonic solution). The increase in sodium absorption greater than control with hypotonic solution represented sodium absorption stimulated by solvent drag; the further increase in sodium absorption induced by glucose, greater than that noted with the hypotonic solution, represented sodium absorption stimulated by cotransport.

Without cholera toxin, solvent drag and cotransport promoted sodium absorption at rates of 62 and 33 mmol/h, respectively. With cholera toxin, solvent drag and cotransport promoted sodium absorption at rates of 44 and 71 mmol/h, respectively.

Net sodium absorption caused by cotransport increased more than twofold after exposure of the intestine to cholera toxin (P < 0.003). This could be mediated by increased cotransport, a change in the stoichiometry of cotransport, or an increase in chloride permeability.