Vitamin D and pancreatic islet function. II. Dynamics of insulin release and cationic fluxes.
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.
Billaudel
B
B
Laboratoire de Physiologie Animale (Endocrinologie), Université de Bordeaux, Talence, France.
Labriji-Mestaghanmi
H
H
Sutter
B C
BC
Malaisse
W J
WJ
D000818:Animals; D002118:Calcium / Q000493:pharmacokinetics / Q000494:pharmacology; D002412:Cations / Q000493:pharmacokinetics*; D005947:Glucose / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D012413:Rubidium / Q000493:pharmacokinetics / Q000494:pharmacology; D014807:Vitamin D / Q000494:pharmacology*
D002412:Cations; D007328:Insulin; D014807:Vitamin D; D005947:Glucose; D012413:Rubidium; D002118:Calcium