Cellular mechanisms of insulin release: the effects of vitamin D deficiency and repletion on rat insulin secretion

Abstract

To determine whether impaired insulin release from perifused rat islets of vitamin D-deficient (D-def) rats is a result of vitamin D-deficiency specifically or an associated decrease in food intake, we: 1) compared insulin release from islets of vitamin D-def rats with insulin release from islets of pair fed (pf) normal rats, and 2) measured the effects of 1,25(OH)2D3 treatment on food intake and insulin secretion from islets of D-def rats. Both vitamin D-def and pf normal rat islets showed significantly diminished insulin release in comparison with normal controls but were not different from each other. When D-def rats were repleted with 1,25(OH)2D3, food intake increased and insulin secretion improved during perifusion of rat islets. When D-def rats treated with 1,25(OH)2D3 were prevented from increasing their food intake in response to 1,25(OH)2D3 by pair feeding to a group of untreated D-def rats, insulin release from islets of treated rats was not significantly different from untreated D-def rats. To separate the effects of vitamin D deficiency from hypocalcemia, a group of vitamin D-def hypocalcemic rats was compared with a group of D-def normocalcemic rats. Normocalcemia did not reverse the defect in insulin release. In studies of cellular calcium uptake, both pf and D-def rat islets took up less calcium than normal islets but calcium uptake was not different between pf and D-def rat islets. Our studies suggest that vitamin D deficiency is associated with marked impairment of biphasic insulin release and that the decrease in food intake may account for this impairment at least in part.