Singhal R L, Merali Z, Kacew S, Sutherland D J
Science. 1974 Mar 15;183(4129):1094-6. doi: 10.1126/science.183.4129.1094.
Daily intraperitoneal injection of cadmium chloride (1 milligram per kilogram) for 45 days enhanced gluconeogenesis as evidenced by significant increases in the activities of liver and kidney cortex pyruvate carboxylase, phosphopyruvate carboxylase, hexosediphosphatase, and glucose-6-phosphatase, the quartet of key, rate-limiting enzymes involved in the biotransformation of noncarbohydrate precursors into glucose. Whereas cadmium treatment decreased the level of hepatic glycogen, the concentration of blood glucose and urea was significantly elevated by this heavy metal. Discontinuation of the heavy metal treatment for 28 days, in rats previously injected with cadmium for 45 days, failed to restore the observed biochemical alterations in hepatic and renal carbohydrate metabolism to control values. Evidence indicates that cadmium augments the glucose-synthesizing capacity of liver and kidney cortex and that various metabolic changes persist even after a 4-week period of withdrawal from exposure to the heavy metal.
连续45天每天腹腔注射氯化镉(1毫克/千克)增强了糖异生作用,这表现为肝脏和肾皮质丙酮酸羧化酶、磷酸丙酮酸羧化酶、己糖二磷酸酶和葡萄糖-6-磷酸酶的活性显著增加,这四种关键的限速酶参与了非碳水化合物前体向葡萄糖的生物转化。虽然镉处理降低了肝糖原水平,但这种重金属使血糖和尿素浓度显著升高。在先前注射镉45天的大鼠中,停止重金属处理28天未能将观察到的肝脏和肾脏碳水化合物代谢的生化改变恢复到对照值。有证据表明,镉增强了肝脏和肾皮质的葡萄糖合成能力,并且即使在停止接触这种重金属4周后,各种代谢变化仍然存在。