In vitro Measurement of Electrolytes and Nutrients Transport through Intestinal Epithelium during Cholera Toxin Induced Secretion

Cholera toxin and other bacterial toxins can induce electrogenic chloride (Cl) secretion in the small intestine resulting in secretory diarrhoea, when the colonic water reabsorption capacity is overwhelmed. The mechanism underlying this phenomena is that, these toxins increase intracellular cGMP and/or cAMP level through activation of guanylyl and adenylyl cyclase leading to the phosphorylation of the apical chloride channel (CFTR) and electrogenic Cl secretion as revealed in vitro by an increase in short-circuit current reflecting an increase in electrolyte transport in the intestine. The aim of the study was to investigate the effects of D-(+) glucose on water and electrolyte movements across rat jejunum after challenging with cholera toxin and dbcAMP (a lipophilic analog of cAMP which readily crosses the basolateral membrane of small intestinal cells); and also to investigate whether the magnitude of response to D-(+) glucose was related to the extent of secretion induced by dbcAMP. The measurement of the ion transport across the unstripped rat jejunum was carried out using Ussing chambers. The response to D-(+) glucose was studied in both CT-treated and untreated tissue; the results showed no significant difference between Isc responses to D-(+) glucose in unstimulated and CT-stimulated rat jejunum (∆Isc = 45.3 ± 12.9 μA/cm versus 38.9 ± 13.9 μA/cm, n = 8), whereas, in the studies where tissues treated with dbcAMP instead of CT, results showed a small but significant difference in D-(+) glucose response affected by dbcAMP (∆Isc = 12.9 ± 4.7 μA/cm versus 24.0 ± 4.3 μA/cm, n = 8).