Low extracellular magnesium does not impair glucose-stimulated insulin secretion

There is an increasing amount of clinical evidence that hypomagnesemia (serum Mg2+ levels < 0.7 mmol/l) contributes to type 2 diabetes mellitus pathogenesis. Amongst other hypotheses, it has been suggested that Mg2+ deficiency affects insulin secretion. The aim of this study was, therefore, to investigate the acute effects of extracellular Mg2+ on glucose-stimulated insulin secretion in primary mouse islets of Langerhans and the rat insulinoma INS-1 cell line. Here we show that acute lowering of extracellular Mg2+ concentrations from 1.0 mM to 0.5 mM did not affect glucose-stimulated insulin secretion in islets or in insulin-secreting INS-1 cells. The expression of key genes in the insulin secretory pathway (e.g. Gck, Abcc8) was also unchanged in both experimental models. Knockdown of the most abundant Mg2+ channel Trpm7 by siRNAs in INS-1 cells resulted in a 3-fold increase in insulin secretion at stimulatory glucose conditions compared to mock-transfected cells. Our data suggest that insulin secretion is not affected by acute lowering of extracellular Mg2+ concentrations.

临床证据日益增多，表明低镁血症（血清Mg2+水平低于0.7 mmol/l）可能参与2型糖尿病的发病机制。在众多假设中，镁离子缺乏可能影响胰岛素分泌的观点已被提出。因此，本研究旨在探讨细胞外镁离子对原发性小鼠Langerhans胰岛和胰岛素瘤细胞系INS-1中葡萄糖刺激胰岛素分泌的急性效应。本研究结果表明，将细胞外镁离子浓度从1.0 mM降至0.5 mM的急性降低并未影响胰岛或胰岛素分泌细胞INS-1中的葡萄糖刺激胰岛素分泌。在胰岛素分泌途径中的关键基因（如Gck、Abcc8）的表达在两种实验模型中也未发生改变。通过siRNA敲低最丰富的镁离子通道Trpm7在INS-1细胞中，与对照转染细胞相比，在刺激性葡萄糖条件下胰岛素分泌量增加了3倍。我们的数据表明，急性降低细胞外镁离子浓度对胰岛素分泌没有影响。