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胰岛素和双(麦芽醇)氧钒(IV)对糖尿病大鼠骨骼肌和肝脏中蛋白激酶B活性的体内作用。

In vivo effects of insulin and bis(maltolato)oxovanadium (IV) on PKB activity in the skeletal muscle and liver of diabetic rats.

作者信息

Marzban L, Bhanot S, McNeill J H

机构信息

Division of Pharmacology and Toxicology, Faculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, Canada.

出版信息

Mol Cell Biochem. 2001 Jul;223(1-2):147-57. doi: 10.1023/a:1017943200785.

Abstract

In this study, the in vivo effects of insulin and chronic treatment with bis(maltolato)oxovanadium (IV) (BMOV) on protein kinase B (PKB) activity were examined in the liver and skeletal muscle from two animal models of diabetes, the STZ-diabetic Wistar rat and the fatty Zucker rat. Animals were treated with BMOV in the drinking water (0.75-1 mg/ml) for 3 (or 8) weeks and sacrificed with or without insulin injection. Insulin (5 U/kg, i.v.) increased PKBalpha activity more than 10-fold and PKBbeta activity more than 3-fold in both animal models. Despite the development of insulin resistance, insulin-induced activation of PKBalpha was not impaired in the STZ-diabetic rats up to 9 weeks of diabetes, excluding a role for PKBalpha in the development of insulin resistance in type 1 diabetes. Insulin-induced PKBalpha activity was markedly reduced in the skeletal muscle of fatty Zucker rats as compared to lean littermates (fatty: 7-fold vs. lean: 14-fold). In contrast, a significant increase in insulin-stimulated PKBalpha activity was observed in the liver of fatty Zucker rats (fatty: 15.7-fold vs. lean: 7.6-fold). Chronic treatment with BMOV normalized plasma glucose levels in STZ-diabetic rats and decreased plasma insulin levels in fatty Zucker rats but did not have any effect on basal or insulin-induced PKBalpha and PKBbeta activities. In conclusion (i) in STZ-diabetic rats PKB activity was normal up to 9 weeks of diabetes; (ii) in fatty Zucker rats insulin-induced activation of PKBalpha (but not PKBbeta) was markedly altered in both tissues; (iii) changes in PKBalpha activity were tissue specific; (iv) the glucoregulatory effects of BMOV were independent of PKB activity.

摘要

在本研究中,我们检测了胰岛素以及用双(麦芽醇)氧钒(IV)(BMOV)进行长期治疗对两种糖尿病动物模型(链脲佐菌素诱导糖尿病的Wistar大鼠和肥胖Zucker大鼠)肝脏和骨骼肌中蛋白激酶B(PKB)活性的体内影响。动物饮用含BMOV(0.75 - 1 mg/ml)的水3(或8)周,在注射或未注射胰岛素的情况下处死。在两种动物模型中,胰岛素(5 U/kg,静脉注射)使PKBα活性增加超过10倍,使PKBβ活性增加超过3倍。尽管出现了胰岛素抵抗,但在长达9周糖尿病病程的链脲佐菌素诱导糖尿病大鼠中,胰岛素诱导的PKBα激活并未受损,排除了PKBα在1型糖尿病胰岛素抵抗发生中的作用。与瘦的同窝仔相比,肥胖Zucker大鼠骨骼肌中胰岛素诱导的PKBα活性明显降低(肥胖组:7倍 vs. 瘦组:14倍)。相反,在肥胖Zucker大鼠肝脏中观察到胰岛素刺激的PKBα活性显著增加(肥胖组:15.7倍 vs. 瘦组:7.6倍)。用BMOV长期治疗可使链脲佐菌素诱导糖尿病大鼠的血糖水平正常化,并降低肥胖Zucker大鼠的血浆胰岛素水平,但对基础或胰岛素诱导的PKBα和PKBβ活性没有任何影响。总之,(i)在链脲佐菌素诱导糖尿病大鼠中,糖尿病长达9周时PKB活性正常;(ii)在肥胖Zucker大鼠中,胰岛素诱导的PKBα(而非PKBβ)激活在两种组织中均有明显改变;(iii)PKBα活性的变化具有组织特异性;(iv)BMOV的血糖调节作用独立于PKB活性。

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