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Apart from malabsorption and intestinal barrier dysfunction (via a ‘leak-flux’ mechanism), diarrhoea may reflect active ion secretion in the small intestine and/or colon. In recent years, our understanding about intestinal secretory mechanisms has increased enormously. Important new findings are (1) chloride, bicarbonate and potassium may be secreted simultaneously, but via independent transport processes and (2) movement of a specific ion across cell membranes may occur via several types of channels selective for that ion, but differing in their molecular structure and intrinsic biophysical properties. Additionally, Linley and coworkers now present evidence that (3) specific types of chloride and potassium channels involved in chloride and potassium secretion are differentially expressed in the apical membrane of enterocytes and goblet cells along the surface cell-crypt cell axis. Thus, we are now in a position to reconsider the ancient concept of exclusively secretory crypt cells and absorptive surface cells.1
In general, underlying active intestinal ion secretion is Na+/K+-ATPase-dependent primary transport, which results in low intracellular sodium and high intracellular potassium concentrations. The sodium gradient across the basolateral membrane facilitates basolateral chloride or bicarbonate uptake via sodium-coupled cotransport (secondary active transport), as a result of which these anions accumulate intracellularly above their electrochemical equilibrium. As a result of this gradient across the apical membrane, they are subsequently secreted into …
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