Baly D L, Curry D L, Keen C L, Hurley L S
J Nutr. 1984 Aug;114(8):1438-46. doi: 10.1093/jn/114.8.1438.
The effects of manganese (Mn) deficiency on carbohydrate metabolism in the Sprague-Dawley rat were investigated. Oral glucose tolerance tests were performed on offspring from Mn-sufficient female rats fed 45 micrograms Mn per gram diet (C-C), offspring from Mn-deficient female rats fed 1 microgram Mn per gram diet (D1-D1) and rats not exposed to Mn deficiency in utero but fed D1 diet from weaning to maturity (D1). Mn-deficient rats, D1 and D1-D1, had significantly lower concentrations of Mn in liver, kidney, heart and pancreas than controls. D1-D1 rats responded with a diabetic type of glucose tolerance curve when given oral glucose. Insulin levels of D1-D1 rats were not commensurate with their high glucose levels. Measurements made by using an isolated perfused-pancreas preparation indicate that insulin output due to release of stored hormone was 76% of control levels in D1-D1 rats. This suggests either lower insulin stores or impaired release of insulin in D1-D1 rats. Second phase insulin release was also significantly lower in D1-D1 rats than in controls. Pancreatic insulin content was 63% of control levels in D1-D1 rats, further supporting the idea of lower insulin stores in Mn-deficient rats. No differences in plasma glucose levels were observed between D1 rats and controls after an oral-glucose load. These findings indicate that dietary Mn deficiency can result in impaired insulin secretion producing impaired carbohydrate metabolism; however, the timing of the deficiency may be a critical factor in the expression of this abnormality.
研究了锰(Mn)缺乏对斯普拉格-道利大鼠碳水化合物代谢的影响。对饮食中每克含45微克锰的锰充足雌性大鼠的后代(C-C)、饮食中每克含1微克锰的锰缺乏雌性大鼠的后代(D1-D1)以及子宫内未接触锰缺乏但从断奶到成熟饲喂D1饮食的大鼠进行了口服葡萄糖耐量试验。锰缺乏的大鼠(D1和D1-D1)肝脏、肾脏、心脏和胰腺中的锰浓度明显低于对照组。给予口服葡萄糖后,D1-D1大鼠呈现出糖尿病类型的葡萄糖耐量曲线。D1-D1大鼠的胰岛素水平与其高血糖水平不相称。使用离体灌注胰腺制剂进行的测量表明,在D1-D1大鼠中,由于储存激素释放而产生的胰岛素输出量是对照组水平的76%。这表明D1-D1大鼠的胰岛素储存量较低或胰岛素释放受损。D1-D1大鼠的第二阶段胰岛素释放也明显低于对照组。D1-D1大鼠的胰腺胰岛素含量为对照组水平的63%,进一步支持了锰缺乏大鼠胰岛素储存量较低的观点。口服葡萄糖负荷后,D1大鼠和对照组之间的血浆葡萄糖水平未观察到差异。这些发现表明,饮食中锰缺乏可导致胰岛素分泌受损,进而导致碳水化合物代谢受损;然而,缺乏的时间可能是这种异常表现的关键因素。