CELLULAR MECHANISMS OF INSULIN RELEASE - THE EFFECTS OF VITAMIN-D DEFICIENCY AND REPLETION ON RAT INSULIN-SECRETION
CELLULAR MECHANISMS OF INSULIN RELEASE - THE EFFECTS OF VITAMIN-D DEFICIENCY AND REPLETION ON RAT INSULIN-SECRETION
复制标题
DOI：
10.1210/endo-113-4-1511
复制
发表时间：
1983-01-01
期刊：
影响因子：
4.8
通讯作者：
DELUCA, HF
中科院分区：
文献类型：
--
作者：
CHERTOW, BS;SIVITZ, WI;DELUCA, HF
为了确定维生素d缺乏（D-def）大鼠的灌注大鼠胰岛的胰岛素释放受损是维生素d缺乏的结果还是与食物摄入减少有关，我们比较了维生素d缺乏大鼠胰岛的胰岛素释放与配对喂养（pf）正常大鼠胰岛的胰岛素释放，并测量了1,25(OH)2D3处理对食物摄入和D-def大鼠胰岛胰岛素分泌的影响。与正常对照组相比，维生素D-def和正常大鼠胰岛的胰岛素释放明显减少，但彼此之间没有差异。1,25(OH)2D3灌胃后，大鼠胰岛灌流时食量增加，胰岛素分泌改善。当用125 (OH)2D3治疗的D-def大鼠与未治疗的D-def大鼠配对喂食，阻止它们增加对125 (OH)2D3的食物摄入量时，治疗大鼠的胰岛胰岛素释放量与未治疗的D-def大鼠无显著差异。为了分离维生素D缺乏和低钙血症的影响，我们将一组维生素D低钙大鼠与一组维生素D低钙大鼠进行了比较。正常钙血症并没有逆转胰岛素释放的缺陷。在细胞钙摄取的研究中，pf和D-def胰岛对钙的摄取都比正常胰岛少，但pf和D-def胰岛对钙的摄取没有差异。维生素D缺乏与双相胰岛素释放的明显损害有关，食物摄入量的减少可能至少部分解释了这种损害。
To determine whether impaired insulin release from perfused rat islets of vitamin D-deficient (D-def) rats is a result of vitamin D-deficiency specifically or an associated decrease in food intake, insulin release from islets of vitamin D-def rats was compared with insulin release from islets of pair fed (pf) normal rats, and measured the effects of 1,25(OH)2D3 treatment on food intake and insulin secretion from islets of D-def rats were measured. 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 perfusion 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 Ca uptake, both pf and D-def rat islets took up less Ca than normal islets but Ca uptake was not different between pf and D-def rat islets. Vitamin D deficiency is associated with marked impairment of biphasic insulin release and the decrease in food intake may account for this impairment at least in part.