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糖尿病、钒和胰岛素对Wistar大鼠糖原合酶激活的影响。

Effects of diabetes, vanadium, and insulin on glycogen synthase activation in Wistar rats.

作者信息

Semiz Sabina, Orvig Chris, McNeill John H

机构信息

Faculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, Canada.

出版信息

Mol Cell Biochem. 2002 Feb;231(1-2):23-35. doi: 10.1023/a:1014437019586.

Abstract

In vivo effects of insulin and vanadium treatment on glycogen synthase (GS), glycogen synthase kinase-3 (GSK-3) and protein phosphatase-1 (PP1) activity were determined in Wistar rats with streptozotocin (STZ)-induced diabetes. The skeletal muscle was freeze-clamped before or following an insulin injection (5 U/kg i.v.). Diabetes, vanadium, and insulin in vivo treatment did not affect muscle GSK-3beta activity as compared to controls. Following insulin stimulation in 4-week STZ-diabetic rats muscle GS fractional activity (GSFA) was increased 3 fold (p < 0.05), while in 7-week diabetic rats it remained unchanged, suggesting development of insulin resistance in longer term diabetes. Muscle PP1 activity was increased in diabetic rats and returned to normal after vanadium treatment, while muscle GSFA remained unchanged. Therefore, it is possible that PP1 is involved in the regulation of some other cellular events of vanadium (other than regulation of glycogen synthesis). The lack of effect of vanadium treatment in stimulating glycogen synthesis in skeletal muscle suggests the involvement of other metabolic pathways in the observed glucoregulatory effect of vanadium.

摘要

在链脲佐菌素(STZ)诱导的糖尿病Wistar大鼠中,测定了胰岛素和钒治疗对糖原合酶(GS)、糖原合酶激酶-3(GSK-3)和蛋白磷酸酶-1(PP1)活性的体内效应。在胰岛素注射(5 U/kg静脉注射)之前或之后,将骨骼肌进行冷冻钳夹。与对照组相比,糖尿病、钒和胰岛素的体内治疗均未影响肌肉GSK-3β活性。在4周龄的STZ糖尿病大鼠中,胰岛素刺激后肌肉GS分数活性(GSFA)增加了3倍(p<0.05),而在7周龄的糖尿病大鼠中,该活性保持不变,这表明长期糖尿病会出现胰岛素抵抗。糖尿病大鼠的肌肉PP1活性增加,钒治疗后恢复正常,而肌肉GSFA保持不变。因此,PP1有可能参与了钒的某些其他细胞事件的调节(而非糖原合成的调节)。钒治疗对刺激骨骼肌糖原合成缺乏作用,这表明在观察到的钒的血糖调节作用中涉及其他代谢途径。

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