Wang Y, Yu B
Endocrine Research Unit, Sun Yat-Sen University of Medical Sciences, Guangzhou, China.
Drugs Exp Clin Res. 1997;23(3-4):111-5.
Although it was proved that peroxovanadate-nicotinic acid (POV) can decrease hyperglycaemia and hyperlipaemia, its molecular biochemical mechanism of action is unclear. The present investigation aimed at studying the effect of POV on gene expression and enzymatic activity of hepatic phosphoenolpyruvate carboxykinase (PEPCK) and blood lipid metabolism in streptozotocin-diabetic rats in order to suggest the molecular biochemical mechanism of POV action in lowering hyperglycaemia and hyperlipaemia. The results showed that the gene expression and enzymatic activity of hepatic cytosolic PEPCK, which were increased in diabetic rats, were significantly reduced following POV treatment. Similarly, POV was shown to oppose significantly the hyperglycaemia and hyperlipaemia in these diabetic rats. These results suggested that a possible mechanism of POV action was to inhibit PEPCK gene expression as well as PEPCK activity which could explain the reduced gluconeogenesis and hyperglycaemia.
虽然已证明过氧钒酸盐-烟酸(POV)可降低高血糖和高血脂,但其分子生化作用机制尚不清楚。本研究旨在探讨POV对链脲佐菌素诱导的糖尿病大鼠肝脏磷酸烯醇式丙酮酸羧激酶(PEPCK)基因表达、酶活性及血脂代谢的影响,以揭示POV降低高血糖和高血脂的分子生化机制。结果显示,糖尿病大鼠肝脏胞质PEPCK基因表达及酶活性升高,POV治疗后显著降低。同样,POV可显著对抗这些糖尿病大鼠的高血糖和高血脂。这些结果提示,POV作用的可能机制是抑制PEPCK基因表达及PEPCK活性,这可能解释了糖异生减少和高血糖降低的原因。