MATERIALSAND MEtHODS

he liver is an importantcomponent in the regulationof plasmaglucose concentrations. After carbohydrateintake, increasing glucose concentrations in the plasma inactivates glycogen phosphorylase @ and activates glycogen syn thetase. This leads to hepatic glycogen synthesis. These direct actions ofglucose stimulating the synthesis and stor age of glycogen are reinforced by increased secretion of insulin. During fasting, the reaction steps are reversed and stored glycogen is metabolized. The blood glucose level is, therefore, bufferedby the liver. PET with 2-[F-18]fluoro-2-deoxy-D-glucose (FDG) has been demonstratedto be useful in the evaluation of malig nant tumors and other liver diseases (1—2).In order to interpret hepatic FDG studies meaningfully, however, one must understand normal hepatic FDG kinetics and the effect of dietary influences on these studies. The purposes of this study are: 1. To investigate differenttracer kinetic model configu rations of FDG (including two-compartment model, three-compartment model, three-compartment model with vascular volume parameter,and three-compart ment model with input function time delay parame ter) in the liver. 2. To determine the optimal tracer kinetic model. 3. To use the best model configuration to evaluate the impact of oral glucose loading on liver in normal subjects