Vitamin D and pancreatic islet function. II. Dynamics of insulin release and cationic fluxes

J Endocrinol Invest. 1988 Sep;11(8):585-93. doi: 10.1007/BF03350186.


Pancreatic islets were prepared from control and vitamin D-deprived rats 2 or 5 weeks after weaning and, in the latter case, after 3 or 6 days treatment with exogenous vitamin D3 (60 nmol per day). The islets were prelabelled with both 86Rb and 45Ca and placed in a perfusion chamber. Vitamin D deprivation or administration failed to affect 86Rb outflow whether prior or after stimulation of the islets by a rise in either extracellular D-glucose or Ca2+ concentration. However, vitamin D deprivation decreased and vitamin D administration enhanced the basal 45Ca fractional outflow rate, as well as the magnitude of changes in both 45Ca and insulin release evoked by the rise in either D-glucose or extracellular Ca2+. It is proposed that the alteration in 45Ca fluxes and insulin release attributable to changes in the supply of vitamin D are, to a large extent, independent of the changes in nutrient catabolism conceivably associated with vitamin D deprivation and administration.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium / pharmacokinetics
  • Calcium / pharmacology
  • Cations / pharmacokinetics*
  • Glucose / pharmacology
  • Insulin / metabolism*
  • Insulin Secretion
  • Islets of Langerhans / drug effects
  • Islets of Langerhans / physiology*
  • Rats
  • Rubidium / pharmacokinetics
  • Rubidium / pharmacology
  • Vitamin D / pharmacology*


  • Cations
  • Insulin
  • Vitamin D
  • Glucose
  • Rubidium
  • Calcium