Kimura Y, Murase M, Nagata Y
Saga Research Institute, Otsuka Pharmaceutical Co., Ltd., Japan.
J Nutr Sci Vitaminol (Tokyo). 1996 Oct;42(5):407-22. doi: 10.3177/jnsv.42.407.
It is widely known that hypomagnesemia is one of the symptoms observed in diabetic patients. This study was performed to assess the effect of chronic magnesium (Mg) deficiency on glucose metabolism in rats. Male Sprague-Dawley rats (at the age of four weeks) were given a Mg-deficient diet or a control diet for two to eight weeks. The rats were orally administered sucrose solution (2 g/kg BW) every two weeks, and blood was drawn from a tail vein before and 15 min after sucrose loading to determine the concentrations of blood glucose and plasma insulin. At the same time, other rats in a non-fasted condition were sacrificed by decapitation (rats sacrificed at eight weeks were rats used for sucrose loading). The epididymal fat pads were immediately removed and adipocytes were isolated. The amount of glucose transporter 4 (GLUT4) in the plasma membranes and low-density microsomal membranes prepared from the adipocytes was measured by immunoblotting to estimate the influence of chronic Mg deficiency on glucose metabolism at the cellular level. In addition, plasma biochemical parameters and muscle mineral contents were also evaluated. The glucose concentration in fasted blood was significantly lower in Mg-deficient rats than in control rats throughout the experiment period. The feeding of a Mg-deficient diet also attenuated the response of blood glucose and plasma insulin: the glucose level in blood tended to be lower in Mg-deficient rats at 15 min after oral sucrose administration, and the difference was significant at two and eight weeks. The plasma insulin level in Mg-deficient rats was also lower, reaching a significant difference at two weeks. When animals were sacrificed in a non-fasted condition at 2-week intervals, the plasma glucose level was also significantly decreased in Mg-deficient rats as compared to control rats throughout the experiment period. The plasma insulin level in non-fasted Mg-deficient rats was also significantly decreased at two and six weeks. The Mg-deficient diet increased plasma triglyceride, but the difference was significant only at four weeks, and plasma cholesterol remained unchanged. The plasma Mg level was markedly lower in Mg-deficient rats throughout the experiment period. In Mg-deficient rats, the Mg content in muscle was significantly reduced at two and eight weeks, whereas the calcium and sodium contents were significantly increased throughout the experiment period. In Mg-deficient rats, the degree of translocation of GLUT4 to plasma membranes in the adipocytes stimulated by insulin was reduced only at eight weeks. In conclusion, since fasted and non-fasted blood glucose levels and the response of blood glucose to sucrose loading were decreased in Mg-deficient rats, it is suggested that Mg deficiency induces changes in the glucose metabolism via impaired glucose absorption in the intestine or an altered glucose uptake in the liver and/or peripheral tissues.
众所周知，低镁血症是糖尿病患者出现的症状之一。本研究旨在评估慢性镁（Mg）缺乏对大鼠葡萄糖代谢的影响。将雄性斯普拉格-道利大鼠（4周龄）给予缺镁饮食或对照饮食2至8周。每两周给大鼠口服蔗糖溶液（2 g/kg体重），在蔗糖负荷前及负荷后15分钟从尾静脉取血，以测定血糖和血浆胰岛素浓度。同时，将处于非禁食状态的其他大鼠断头处死（8周时处死的大鼠用于蔗糖负荷实验）。立即取出附睾脂肪垫并分离脂肪细胞。通过免疫印迹法测定从脂肪细胞制备的质膜和低密度微粒体膜中葡萄糖转运蛋白4（GLUT4）的含量，以评估慢性镁缺乏在细胞水平对葡萄糖代谢的影响。此外，还评估了血浆生化参数和肌肉矿物质含量。在整个实验期间，缺镁大鼠空腹血糖浓度显著低于对照大鼠。给予缺镁饮食也减弱了血糖和血浆胰岛素的反应：口服蔗糖后15分钟，缺镁大鼠的血糖水平往往较低，在2周和8周时差异显著。缺镁大鼠的血浆胰岛素水平也较低，在2周时达到显著差异。当每隔2周在非禁食状态下处死动物时，在整个实验期间，缺镁大鼠的血浆葡萄糖水平与对照大鼠相比也显著降低。非禁食缺镁大鼠的血浆胰岛素水平在2周和6周时也显著降低。缺镁饮食增加了血浆甘油三酯，但仅在4周时差异显著，血浆胆固醇保持不变。在整个实验期间，缺镁大鼠的血浆镁水平明显较低。在缺镁大鼠中，肌肉中的镁含量在2周和8周时显著降低，而钙和钠含量在整个实验期间显著增加。在缺镁大鼠中，仅在8周时胰岛素刺激的脂肪细胞中GLUT4向质膜的转位程度降低。总之，由于缺镁大鼠的空腹和非空腹血糖水平以及血糖对蔗糖负荷的反应降低，提示镁缺乏通过肠道葡萄糖吸收受损或肝脏和/或外周组织葡萄糖摄取改变诱导葡萄糖代谢变化。
