In our previous studies, perifused islets from vitamin D-deficient (D-def) rats showed marked impairment of glucose-induced biphasic release, accounted for at least in part by a decrease in food intake. In studies reported here, we test whether D-def rat islets have an impaired response to 5.6 mM glucose or tolbutamide, (T), and if so, whether this impairment is related to a decrease in food intake or a defect in islet calcium metabolism. We isolated islets of normal rats, D-def rats, and rats pair fed (PF) to D-def rats. Biphasic insulin release from perifused islets and net 45Ca retention in lot-incubated islets were measured in response to 5.6 mM glucose, 0.37 mM T, or both.
Compared with secretion from normal islets, biphasic insulin release from islets of both D-def rats and PF rats was diminished by 50% in response to 5.6 mM glucose alone or 5.6 mM glucose plus T. Insulin secretion was not significantly different between islets of D-def rats and islets of PF rats. In contrast, net calcium retention in islets of D-def rats was decreased to 68% of retention in islets of PF rats. However, net calcium retention in islets of both PF and D-def rats increased in response to T.
The pair-feeding experiments suggest that the decrease in insulin release from islets of D-def rats is due to the decrease in food intake associated with the D-def state. On the other hand, the defect in calcium retention in islets of D-def rats raises the possibility that vitamin D may have a specific effect on islet calcium metabolism. In this case, the mechanism of impaired insulin release in islets of D-def rats would be different from that in islets of PF rats and would involve a defect in intracellular calcium handling.