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573 DEFECTIVE ENTEROCYTE GLUCOSE TRANSPORT IN ACUTE VIRAL ENTERITIS

We measured glucose transport in piglets with acute (40 h), experimentally induced transmissible gastroenteritis (TGE), an invasive viral enteritis closely resembling human rotavirus enteritis. Marker perfusion studies, in vivo, showed rising net glucose absorption as perfusate glucose increased in controls; in TGE, net glucose flux was reduced and didn't respond to increasing perfusate glucose. Net 3-0-methyl glucose flux was similarly reduced in TGE tissue compared with controls in Ussing chambers.In brush border membrane (BBM) vesicles, isolated from control piglet jejunum, we found sodium gradient-driven, active D-glucose uptake and Na+ dependent, glucose inhibitable, high affinity phlorizin binding. In BBM vesicles from TGE pigs we found little or no active glucose uptake and no specific phlorizin binding. We conclude that loss or dysfunction of the BBM Na-dependent glucose carrier contributes to defective glucose absorption in this viral enteritis.