Inhibition of glycolysis in brain by a phospholipid effect on interconversion of fructose phosphates. A possible regulatory control on utilization of glucose 6-phosphate

J Biol Chem. 1976 Nov 25;251(22):7149-56.

Abstract

Glucose 6-phosphate accumulation in 10,000 X g supernatant of rat brain was enhanced up to 16-fold by the addition of phosphatidylcholine, other common phospholipids, or linoleate. This glucose 6-phosphate is of endogenous origin via UDP-glucose and glucose 1-phosphate but not glucose. The accumulation is the result of inhibition of glycolysis by an effect of phospholipid on the interconversion of fructose 6-phosphate and fructose 1,6-bisphosphate. Brain is therefore capable of gluconeogenesis from fructose 1,6-bisphosphate. A regulatory function for phospholipid which coordinates glycolysis and other major routes of utilization of glucose 6-phosphate in brain, e.g. inositol synthesis, is proposed.

MeSH terms

  • Animals
  • Brain / drug effects
  • Brain / metabolism*
  • Calcium / pharmacology
  • Deoxycholic Acid / pharmacology
  • Fructosephosphates / metabolism*
  • Glucosephosphates / metabolism*
  • Glycolysis / drug effects*
  • Hexosediphosphates / metabolism
  • Kinetics
  • Linoleic Acids / pharmacology
  • Phosphatidylcholines / pharmacology
  • Phospholipids / pharmacology*
  • Rats

Substances

  • Fructosephosphates
  • Glucosephosphates
  • Hexosediphosphates
  • Linoleic Acids
  • Phosphatidylcholines
  • Phospholipids
  • Deoxycholic Acid
  • Calcium