Intestinal D-galactose transport in an endotoxemia model in the rabbit

Lipopolysaccharide ( LPS) is an endotoxin causing sepsis. Studies from our laboratory revealed impaired intestinal absorption of L- leucine and D- fructose in LPS- treated rabbits. The aim of this study was to examine intestinal D- galactose transport following intravenous administration of LPS in the rabbit and to identify the cellular mechanisms driving this process. Endotoxin treatment diminished the buildup of D- galactose in intestinal tissue, the mucosal to serosal transepithelial flux of the sugar and its uptake by brush border membrane vesicles ( BBMVs). Intracellular signaling pathways associated with protein kinase C ( PKC), protein kinase A ( PKA), p38 mitogen- activated protein kinase ( p38MAPK), Jun N- terminal kinase ( JNK), MAPK/ extracellular signalregulated kinases 1 and 2 ( MEK1/ 2) and proteasome were found to be involved in this reduction in sugar uptake. Na+/ glucose cotransporter 1 ( SGLT1) protein levels in BBMVs were lower for LPS- treated animals than control animals. These findings indicate that LPS inhibits the intestinal absorption of D- galactose via a complex cellular mechanism that could involve posttranscriptional regulation of the SGLT1 transporter.