Metformin reduces vascular production of vasoconstrictor prostanoids in fructose overloaded rats

A. M. Puyó, J. S. Borroni, S. Boudou, Y. Santander, A. Carranza, A. S. Donoso, H. A. Peredo
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引用次数: 9

Abstract

1 Metformin is a hypoglycaemic drug currently used to increase insulin sensitivity in the treatment of type 2 diabetes and metabolic syndrome. Its main mechanism of action is through activation of AMP-activated protein kinase, an enzyme that regulates cellular and whole organ metabolism.

2 The fructose-overloaded rat is an experimental model with features that resemble human metabolic syndrome. We have previously reported alterations in vascular prostanoids (PR) in this model.

3 The aim of this study was to analyse the effects of metformin treatment on blood pressure, metabolic parameters and PR production in aorta and mesenteric vascular bed (MVB) from fructose-overloaded animals. Four groups of male Sprague–Dawley rats were used: control, fructose overloaded (10% w/v fructose), metformin treated (50 mg kg−1 day−1) and fructose-overloaded treated with metformin.

4 Rats with fructose overload had significantly elevated systolic blood pressure, glycaemia, triglyceridaemia, cholesterolaemia and insulinaemia compared with controls. Except for insulinaemia, metformin limited all these increases in fructose-overloaded animals.

5 Fructose overload reduced prostacyclin levels in aorta and MVB, but prostaglandin E2 levels were only reduced in MVB. Metformin treatment reduced the levels of the vasoconstrictor prostaglandins, PGF2α and thromboxane, in both vascular preparations from fructose-overloaded rats. PGF2α levels were significantly reduced by metformin in controls.

6 In conclusion, one of the mechanisms by which metformin reduced blood pressure in this model is by decreasing vasoconstrictor prostaglandin production.

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二甲双胍减少果糖超载大鼠血管收缩剂前列腺素的生成
二甲双胍是一种降糖药物,目前用于增加2型糖尿病和代谢综合征治疗中的胰岛素敏感性。其主要作用机制是通过活化amp活化的蛋白激酶,一种调节细胞和整个器官代谢的酶。2果糖超载大鼠是一种具有类似人类代谢综合征特征的实验模型。我们之前报道过该模型中血管前列腺素(PR)的改变。本研究的目的是分析二甲双胍治疗对果糖超载动物的血压、代谢参数和主动脉和肠系膜血管床(MVB) PR产生的影响。采用四组雄性Sprague-Dawley大鼠:对照组、果糖超载(10% w/v果糖)、二甲双胍处理(50 mg kg−1 day−1)和二甲双胍处理果糖超载。与对照组相比,果糖过量的大鼠收缩压、血糖、甘油三酯血症、胆固醇血症和胰岛素血症显著升高。除了胰岛素血症外,二甲双胍限制了果糖超载动物的所有这些增加。5果糖超载降低了主动脉和MVB中的前列环素水平,但前列腺素E2水平仅在MVB中降低。二甲双胍治疗降低了果糖超载大鼠血管制剂中血管收缩剂前列腺素、PGF2α和血栓素的水平。二甲双胍显著降低对照组PGF2α水平。总之,二甲双胍在该模型中降低血压的机制之一是通过减少血管收缩剂前列腺素的产生。
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Issue Information Autonomic and Autacoid Pharmacology: Goodbye and thank you Attenuation of the anti-contractile effect of cooling in the rat aorta by perivascular adipose tissue Retraction: Dopamine receptor immunohistochemistry in the rat choroid plexus. Issue Information
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