Hurley L S, Keen C L, Baly D L
Neurotoxicology. 1984 Spring;5(1):97-104.
Although manganese deficiency and manganese toxicity both have pathological consequences, the underlying biochemical lesions have not been well defined. Manganese is involved in carbohydrate metabolism; either deficiency or excess results in abnormal carbohydrate metabolism. Clinical studies have shown that patients with chronic manganism have hypoglycemia following a glucose load. One report has been published of a diabetic patient who responded to oral manganese with a consistent drop in blood glucose. Rats fed a manganese deficient diet respond to an oral glucose load with a diabetic type of glucose tolerance curve. Insulin release from the pancreas of manganese deficient animals in response to a glucose stimulus is lower than controls. Reduced insulin output occurs in both the first phase (release of stored hormone) and second phase (release of stored and newly synthesized hormone) of insulin output. Thus dietary manganese deficiency can result in abnormal insulin production producing impaired carbohydrate metabolism. Manganese toxicity also affects carbohydrate metabolism. Rats given intraperitoneal injections of high levels of manganese show a rapid hyperglycemia and hypoinsulinemia, followed by a reactionary hypoglycemia. The changes in blood glucose and blood insulin levels correlated with changes in liver and pancreatic manganese concentrations, suggesting that some of the effects of manganese on carbohydrate metabolism may be due to a direct effect on insulin release and gluconeogenesis.
尽管锰缺乏和锰中毒都会产生病理后果，但其潜在的生化损伤尚未得到明确界定。锰参与碳水化合物代谢；缺乏或过量都会导致碳水化合物代谢异常。临床研究表明，慢性锰中毒患者在摄入葡萄糖后会出现低血糖。有一份报告称，一名糖尿病患者口服锰后血糖持续下降。喂食缺锰饮食的大鼠对口服葡萄糖负荷的反应呈现出糖尿病类型的糖耐量曲线。缺锰动物胰腺对葡萄糖刺激的胰岛素释放低于对照组。胰岛素分泌的第一阶段（储存激素的释放）和第二阶段（储存和新合成激素的释放）的胰岛素输出均减少。因此，饮食中锰缺乏可导致胰岛素产生异常，进而损害碳水化合物代谢。锰中毒也会影响碳水化合物代谢。腹腔注射高剂量锰的大鼠会迅速出现高血糖和低胰岛素血症，随后出现反应性低血糖。血糖和血胰岛素水平的变化与肝脏和胰腺中锰浓度的变化相关，这表明锰对碳水化合物代谢的一些影响可能是由于对胰岛素释放和糖异生的直接作用。
