Glucose enhances rotavirus enterotoxin-induced intestinal chloride secretion.

We examined the effects of NSP4 and glucose on sodium and chloride transport in mouse small intestines and Caco-2 cells. Mouse small intestines and Caco-2 cells were incubated with NSP4114-135 in the presence/absence of glucose. Absorption and secretion of sodium and chloride, fluid movement, peak amplitude of intracellular calcium fluorescence, and expression of Ano1 and sodium-glucose cotransporter 1 were assessed. NHE3 activity increased, and chloride secretory activity decreased with age. Net chloride secretion increased, and net sodium absorption decreased in the intestines of 3-week-old mice compared to 8-week-old mice with NSP4. Glucose increased NSP4-stimulated chloride secretion. Glucose increased NSP4-stimulated increase in short-circuit current measurements (I sc) and net chloride secretion. Ano1 cells with siRNA knockdown showed a significant difference in I sc in the presence of NSP4 and glucose without a significant difference in peak calcium fluorescence intracellular when compared to non-silencing (N.S.) cells. The failure of glucose to stimulate significant sodium absorption was likely due to the inhibition of sodium-hydrogen exchange and sodium-glucose cotransport by NSP4. Since glucose enhances intestinal chloride secretion and fails to increase sodium absorption in the presence of NSP4, glucose-based oral rehydration solutions may not be ideal for the management of rotaviral diarrhea. PMID: 28488023 [PubMed - as supplied by publisher]
Source: Pflugers Archiv : European Journal of Physiology - Category: Physiology Authors: Tags: Pflugers Arch Source Type: research