Hypoglycemia activates compensatory mechanism of glucose metabolism of brain

Acta Biol Hung. 2001;52(1):35-45. doi: 10.1556/ABiol.52.2001.1.5.


The effect of plasma glucose concentration on the cerebral uptake of [18F]-fluorodeoxy-D-glucose (FDG) was studied in a broad concentration range in a rabbit brain model using dynamic FDG PET measurements. Hypoglycemic and hyperglycemic conditions were maintained by manipulating plasma glucose applying i.v. glucose or insulin load. FDG utilization (K) and cerebral glucose metabolic rate (CGMR) were evaluated in a plasma glucose concentration range between 0.5 mM and 26 mM from the kinetic constant k1, k2, k3 obtained by the Sokoloff model of FDG accumulation. A decreasing set of standard FDG uptake values found with increasing blood glucose concentration was explained by competition between the plasma glucose and the radiopharmacon FDG. A similar trend was observed for the forward kinetic constants k1, and k3 in the entire concentration range studied. The same decreasing tendency of k2 was of a smaller magnitude and was reverted at the lowest glucose concentrations where a pronounced decrease of this backward transport rate constant was detected. Our kinetic data indicate a modulation of the kinetics of carbohydrate metabolism by the blood glucose concentration and report on a special mechanism compensating for the low glucose supply under conditions of extremely low blood glucose level.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood Glucose / analysis
  • Brain / metabolism
  • Brain / physiology*
  • Fluorodeoxyglucose F18 / pharmacokinetics
  • Glucose / metabolism*
  • Hypoglycemia / metabolism*
  • Models, Animal
  • Rabbits
  • Radiopharmaceuticals / pharmacokinetics
  • Tomography, Emission-Computed


  • Blood Glucose
  • Radiopharmaceuticals
  • Fluorodeoxyglucose F18
  • Glucose