Caffeine releases a glucose-primed endoplasmic reticulum Ca2+ pool in the insulin secreting cell line INS-1

FEBS Lett. 1999 Mar 12;446(2-3):309-12. doi: 10.1016/s0014-5793(99)00220-3.


Caffeine mobilized an intracellular Ca2+ pool in intact fura-2-loaded INS-1 cells in suspension exposed to high (16 mM) [glucose], while a minor effect was observed with low (2 mM) [glucose]. Cells were kept in a medium containing diaxozide or no Ca2+ to prevent the influx of extracellular Ca2+. The caffeine-sensitive intracellular Ca2+ pool was within the endoplasmic reticulum since it was depleted by the inhibitor of the reticular Ca2+ pumps thapsigargin and the InsP3-dependent agonist carbachol. No effect of caffeine was observed in the parent glucose-insensitive RINmF5 cells. In microsomes from INS-1 but not RINmF5 cells, the type 2 ryanodine receptor was present as revealed by Western blotting. It was concluded that the endoplasmic reticulum of INS-1 cells possesses caffeine-sensitive type 2 ryanodine receptors Ca2+ channels.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Caffeine / metabolism*
  • Caffeine / pharmacology
  • Calcium / metabolism*
  • Carbachol / pharmacology
  • Cell Line
  • Diazoxide / pharmacology
  • Electrophysiology
  • Endoplasmic Reticulum / drug effects
  • Endoplasmic Reticulum / metabolism
  • Endoplasmic Reticulum / physiology*
  • Glucose / metabolism*
  • Glucose / pharmacology
  • Insulin*
  • Rabbits
  • Thapsigargin / pharmacology


  • Insulin
  • Caffeine
  • Thapsigargin
  • Carbachol
  • Glucose
  • Diazoxide
  • Calcium