Effect of phlorizin on hepatic glucose output

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Abstract
Using phlorizin as an experimental tool, an investigation of the mechanisms responsible for the maintenance of plasma glucose levels was undertaken. Infusion of phlorizin has been shown to produce a prompt glucosuria and increase in hepatic glucose output (HGO), but without discernable hypoglycemia. This raises the question as to the nature of the stimulus for the increased HGO. The effect of phlorizin on net HGO was studied in anesthetized dogs with indwelling catheters in the portal and hepatic veins. Infusion of phlorizin into normal dogs produced a prompt glucosuria and a concomitant increase in HGO, without significant changes in the plasma glucose concentration in the portal vein. In functionally nephrectomized dogs, phlorizin did not change HGO nor circulating glucose levels. In dogs with intact kidneys, when glucosuria was prevented by urine recirculation into the inferior vena cava, the infusion of phlorizin again failed to alter HGO or circulating glucose levels. The data indicate that the phlorizin-induced increase in HGO is dependent on loss of glucose from the body. The enhancement of HGO could not be ascribed to a direct stimulation of the liver, kidney, or endocrine glands, or to an impairment of glucose utilization. Possible mechanisms to explain this effect of phlorizin are discussed.

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