Tewari P C, Tandon S K
Industrial Toxicology Research Centre, Lucknow, India.
Toxicol Ind Health. 1988 Mar;4(1):39-47. doi: 10.1177/074823378800400104.
Cadmium causes hyperglycemia, activation of hepatic and renal gluconeogenic enzymes such as glucose-6-phosphatase and fructose-1,6-diphosphatase, increases hepatic and renal zinc, renal copper and decreases hepatic and renal iron levels in rats. Glibenclamide, a hypoglycemic agent, significantly reversed most of the Cd effects, enhanced fecal excretion of Cd and potentiated urinary and fecal elimination of Cd by calcium trisodium diethylenetriaminepentaacetate (CaNa3DTPA), a commonly used metal chelator. However, the restoration of Cd-induced alterations in carbohydrate metabolism was not related to elimination of Cd from the tissues.
镉会导致大鼠出现高血糖，激活肝脏和肾脏中的糖异生酶，如葡萄糖-6-磷酸酶和果糖-1,6-二磷酸酶，使肝脏和肾脏中的锌含量增加，肾脏中的铜含量增加，并降低肝脏和肾脏中的铁含量。降糖药格列本脲可显著逆转镉的大部分影响，增加镉的粪便排泄，并增强常用金属螯合剂三钠二乙烯三胺五乙酸钙（CaNa3DTPA）对镉的尿排泄和粪便排泄作用。然而，镉诱导的碳水化合物代谢改变的恢复与组织中镉的清除无关。
