Effect of phlorizin on hepatic bile production before and during glucose infusion.

During intravenous infusion of glucose, bile secretion is reduced (cholestasis), indicating that hepatocellular metabolism of glucose could have harmful effects on the liver. Phlorizin has been identified as a compound capable of impeding glucose uptake of liver cells. To examine whether phlorizin had any effect on glucose-associated cholestasis, three groups of experiments were performed on anaesthetized pigs. In group I phlorizin (100 mg/kg body wt) during normoglycaemia stimulated bicarbonate-dependent bile secretion by 56 +/- 4%. After phlorizin, hyperglycaemia decreased both bile acid- and bicarbonate-dependent bile secretion by 37 +/- 4%. But after the glucose load normalization of plasma glucose concentration increased the bicarbonate-dependent fraction by 38 +/- 4%. In group II phlorizin (100 mg/kg body wt, infused intravenously) during hyperglycaemia stimulated bicarbonate-dependent bile secretion by 35 +/- 5%. In group III bile secretion was continuously stimulated by infusion of Na-taurocholate. Hyperglycaemia reduced bicarbonate-dependent bile secretion by 33 +/- 4%, but after phlorizin both bile acid- and bicarbonate-dependent bile secretion increased on average by 121 +/- 8%. The osmotic effect of hyperglycaemia cannot be blocked by phlorizin, but judged by the effect on bile secretion, phlorizin may decrease the cholestatic effect induced by metabolism of glucose. Phlorizin could be an interesting compound for use in solutions for organ preservation.