title: Evaluation of the effect of glucose ingestion and kinetic model configurations of FDG in the normal liver.
abstract: The liver plays an important role in glucose homeostasis. PET studies with 2-[F-18]fluoro-2-deoxy-D-glucose (FDG) of the liver (e.g., in neoplasms) require an understanding of the effects of dietary conditions on hepatic FDG uptake.
  
  
  METHODS
  Twenty studies were performed on 10 normal volunteers (ages 24 +/- 4) after fasting 4 to 19 hr and again after oral consumption of 100 g of dextrose to investigate tracer kinetic model configurations of FDG in the normal liver and to evaluate the impact of oral glucose on liver in normal subjects. Dynamic PET images were acquired for about 1 hr using a Siemens/CTI 931 tomograph.
  
  
  RESULTS
  A three-compartment model with an input function delay time parameter was the statistically preferred model configuration. The model estimated transport rate constant from plasma to liver, K1, increased significantly (p < 0.05) from 0.864 +/- 0.136 ml/min/g in fasting studies to 1.058 +/- 0.269 ml/min/g in postglucose studies. Glucose loading also significantly increased (p < 0.01) the rate constant for FDG phosphorylation, k3, from 0.005 +/- 0.003 min-1 in fasting studies to 0.013 +/- 0.007 min-1 in postglucose administration and, consequently, significantly increased both the phosphorylation fraction (k3/(k2 + k3)) and the influx constant (K1k3/(k2 + k3)). No significant differences in the liver-to-plasma transport rate constant, k2, dephosphorylation constant, k4, or distribution volume of FDG (K1/(k2 + k3)) were observed.
  
  
  CONCLUSIONS
  Dynamic FDG-PET studies can be used to evaluate kinetics of liver glucose metabolism. The results indicate that dietary conditions have a significant effect on hepatic FDG kinetics. Because of the higher net FDG uptake by normal liver after glucose loading, fasting conditions are preferred for FDG liver tumor studies to increase the tumor-to-background contrast.
authors.affiliation: Department of Molecular and Medical Pharmacology, School of Medicine, University of California, Los Angeles.
authors.forename: Y
authors.initials: Y
authors.lastname: Choi
authors.forename: R A
authors.initials: RA
authors.lastname: Hawkins
authors.forename: S C
authors.initials: SC
authors.lastname: Huang
authors.forename: R C
authors.initials: RC
authors.lastname: Brunken
authors.forename: C K
authors.initials: CK
authors.lastname: Hoh
authors.forename: C
authors.initials: C
authors.lastname: Messa
authors.forename: E U
authors.initials: EU
authors.lastname: Nitzsche
authors.forename: M E
authors.initials: ME
authors.lastname: Phelps
authors.forename: H R
authors.initials: HR
authors.lastname: Schelbert
mesh_terms: D000284:Administration, Oral; D000293:Adolescent; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D003847:Deoxyglucose / Q000031:analogs & derivatives* / Q000493:pharmacokinetics; D019788:Fluorodeoxyglucose F18; D005947:Glucose / Q000008:administration & dosage / Q000494:pharmacology*; D006801:Humans; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D008954:Models, Biological
chemical_list: D001786:Blood Glucose; D019788:Fluorodeoxyglucose F18; D003847:Deoxyglucose; D005947:Glucose