The basic principle is that glucose (and other substrates, such as amino acids) are cotransported with sodium into enterocytes in the small intestine.
Unlike other mechanisms of sodium absorption, cotransport is intact in many forms of secretory diarrhea; thus, stimulation of sodium absorption by cotransport can be used to enhance sodium absorption, even in the presence of bacterial toxins.
The glucose-sodium cotransport leads to deposition of sodium in the basolateral space as a result of glucose absorption.
- Chloride must enter across the tight junction for sodium to remain on the basolateral side of the enterocyte.
- Otherwise, sodium diffuses back to the lumen through the tight junction in response to the electrical potential generated by cotransport, and no net sodium absorption would occur.
The duodenum and jejunum are the only areas of the gut in which sufficient chloride can permeate across tight junctions to allow cotransport to result in net sodium chloride (and water) absorption.
An alternative mechanism for glucose-stimulated sodium absorption is solvent drag.
- Removal of glucose from the luminal fluid by cotransport results in generation of an osmotic gradient between the lumen and the basolateral space.
- This generates a flux of water across the tight junctions, which entrains sodium and chloride ions by solvent drag.
- This mechanism also can only occur in the proximal small intestine because paracellular permeability is restricted in the ileum and glucose is not absorbed in the colon.
- In healthy humans, this alternative mechanism accounts for roughly two thirds of the total amount of glucose-stimulated sodium absorption. The situation may be different if paracellular permeability for water or electrolytes is altered by disease