The stimulus-secretion coupling in glucose-induced insulin release xliv. A possible link between glucose metabolism and phosphate flush

Diabetologia. 1980 Nov;19(5):458-64. doi: 10.1007/BF00281826.

Abstract

Above a threshold of 3.0-4.2 mmol/l, D-glucose provoked a transient increase in 32P fractional outflow rate from rat pancreatic islets prelabelled with 32P-orthophosphate. Nutrients which stimulate insulin release in the absence of glucose, alpha-ketoisocaproate and L-leucine, also provoked a phosphate flush. No flush occurred in islets exposed to non-insulinotropic nutrients (L-glutamine and and L-lactate) or non-nutriet secretagogues (arginine, tolbutamide, theophylline). A late increase in 32P fractional outflow rate was observed in Ca2+ deprived islets stimulated with BaCl2 and theophylline. The occurrence of a phosphate flush did not appear to be attributable to changes in insulin release, cyclic AMP content, membrane polarisation, K+ conductance, or reduced pyridine nucleotide content. The 32P response to glucose was slightly decreased in the absence of extracellular Ca2+ or HCO3-, markedly impaired in the absence of K4, and virtually abolished in the presence of menadione (10 mumol/l). It is proposed that the occurrence of a phosphate flush is linked to the metabolism of nutrient secretagogues, possibly via an increase in O2 uptake and the production rate of NAD(P)H and ATP.

MeSH terms

  • Adenosine Triphosphate / biosynthesis
  • Animals
  • Female
  • Glucose / metabolism
  • Glucose / pharmacology*
  • Insulin / metabolism*
  • Insulin Secretion
  • Islets of Langerhans / drug effects*
  • Islets of Langerhans / metabolism
  • Keto Acids / pharmacology
  • Leucine / pharmacology
  • NADP / biosynthesis
  • Oxygen Consumption
  • Phosphates / metabolism*
  • Phosphorus Radioisotopes
  • Rats
  • Secretory Rate / drug effects

Substances

  • Insulin
  • Keto Acids
  • Phosphates
  • Phosphorus Radioisotopes
  • NADP
  • Adenosine Triphosphate
  • Leucine
  • Glucose