Islet Insulin Release and Net Calcium Retention In Vitro in Vitamin D–Deficient Rats

Abstract

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 greater than 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.(ABSTRACT TRUNCATED AT 250 WORDS)

Expression of 25-hydroxyvitamin D3-1α-hydroxylase in pancreatic islets

“…Vitamin D deficient rats secrete insufficient insulin in response to a glucose challenge. Insulin secretion and ␤ cell function is restored following correction of Vitamin D levels [1,2]. Recent data from two studies in Scandinavia have suggested a link between Vitamin D supplementation during pregnancy and protection of the offspring from type 1 diabetes [3,4].…”