糖尿病大鼠肌肉中磷脂酶A2活性增加。

Increased muscular phospholipase A2 activity in diabetic rats.

作者信息

Vettor R, Martini C, Calò L, Cantaro S, Macor C, De Palo C, Sicolo N, Scandellari C, Federspil G

机构信息

Institute of Semeiotica Medica-Patologia Medica 3, University of Padua, Italy.

出版信息

Diabete Metab. 1992 May-Jun;18(3):213-7.

PMID:1397475

Abstract

Anomalies in prostaglandin (PG) synthesis have been suggested in both experimental and human diabetes mellitus; increased levels of plasma and tissue eicosanoids has been recently reported by several investigators. One step in prostaglandin synthesis is the enzymatic hydrolysis of membrane phospholipids by Phospholipase A2 (PLA2). Nevertheless the alternative pathway involving Phospholipase C must be considered. An evaluation of PLA2 activity is therefore a useful method for studying prostaglandin synthesis in the peripheral target tissues of insulin activity. We studied PLA2 activity in normal and diabetic rat muscle. Streptozotocin-induced diabetic rats showed significantly higher muscular PLA2 activity when compared with controls (3.04 x 10(-2) +/- 0.50 x 10(-2) versus 1.34 x 10(-2) +/- 0.35 x 10(-2) arachidonic acid pMol.mg protein-1.min-1 (p less than 0.01). This effect was not observed in diabetic animals successfully treated with insulin (1.78 x 10(-2) +/- 0.5 x 10(-2) versus 1.34 x 10(-2) +/- 0.35 x 10(-2) arachidonic acid pMol.mg protein-1.min-1), and a significant correlation was found between blood glucose and muscular PLA2 activity (r = 0.42; p less than 0.05). Our results clearly show that in streptozotocin-induced diabetic rats muscular PLA2 activity is significantly higher. The relationship between blood glucose levels and muscular PLA2 activity and the decrease of PLA2 activity after insulin treatment suggest that these changes may be related to a defect in insulin effect.

摘要

实验性糖尿病和人类糖尿病均提示存在前列腺素（PG）合成异常；近期有几位研究者报告血浆和组织类花生酸水平升高。前列腺素合成的一个步骤是磷脂酶A2（PLA2）对膜磷脂进行酶促水解。然而，必须考虑涉及磷脂酶C的替代途径。因此，评估PLA2活性是研究胰岛素活性外周靶组织中前列腺素合成的一种有用方法。我们研究了正常和糖尿病大鼠肌肉中的PLA2活性。与对照组相比，链脲佐菌素诱导的糖尿病大鼠肌肉PLA2活性显著更高（花生四烯酸为3.04×10⁻²±0.50×10⁻²对1.34×10⁻²±0.35×10⁻² pMol·mg蛋白⁻¹·min⁻¹，p<0.01）。在用胰岛素成功治疗的糖尿病动物中未观察到这种效应（花生四烯酸为1.78×10⁻²±0.5×10⁻²对1.34×10⁻²±0.35×10⁻² pMol·mg蛋白⁻¹·min⁻¹），并且发现血糖与肌肉PLA2活性之间存在显著相关性（r = 0.42；p<0.05）。我们的结果清楚地表明，在链脲佐菌素诱导的糖尿病大鼠中，肌肉PLA2活性显著更高。血糖水平与肌肉PLA2活性之间的关系以及胰岛素治疗后PLA2活性的降低表明，这些变化可能与胰岛素效应缺陷有关。