Inducible nitric oxide regulates intestinal glutamine assimilation during chronic XXXX .

@entity71792 @entity32 @entity95
UNASSIGNED: To facilitate assimilation of glutamine, different Na-dependent glutamine absorptive pathways are present in the @entity95 small intestine, specifically B0AT1 in villus and @entity71792 in crypt cell brush border membrane. Further, both are uniquely regulated in the chronically inflamed intestine. B0AT1 is inhibited secondary to reduced number of brush border membrane (BBM) co-transporters while @entity71792 is stimulated secondary to an increased affinity for glutamine. These unique changes are reversible by treatment with a broad spectrum immune modulator such as glucocorticoids. However, whether inducible nitric oxide (iNO), known to be elevated in the mucosa of the chronically inflamed intestine, may be responsible for these co-transporter alterations is not known. In the present study, treatment of chronically inflamed @entity95 with L-NIL, a selective inhibitor of iNO synthase, reversed the inhibition of B0AT1 in villus and the stimulation of @entity71792 in crypt cells. At the level of the co-transporter in the brush border membrane, inhibition of iNO production reversed the inhibition of villus B0AT1 by restoring the co-transporter numbers while the stimulation of crypt @entity71792 was reversed back to normal by restoring its affinity for glutamine. Western blot analyses of BBM proteins also confirmed the kinetic studies. Thus, L-NIL treatment restores the uniquely altered Na-glutamine co-transporters in the enterocytes of chronically inflamed intestine. All these data indicate that iNO functions as an upstream immune modulator directly regulating glutamine assimilation during chronic @entity32 .
