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首页> 外文期刊>Life sciences >Improvement of metabolic parameters and vascular function by metformin in obese non-diabetic rats.
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Improvement of metabolic parameters and vascular function by metformin in obese non-diabetic rats.

机译：二甲双胍可改善肥胖非糖尿病大鼠的代谢参数和血管功能。

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Metformin is an insulin sensitizing agent with beneficial effects in diabetic patients on glycemic levels and in the cardiovascular system. We examined whether the metabolic changes and the vascular dysfunction in monosodium glutamate-induced obese non-diabetic (MSG) rats might be improved by metformin.16 week-old MSG rats were treated with metformin for 15 days and compared with age-matched untreated MSG and non-obese non-diabetic rats (control). Blood pressure, insulin sensitivity, vascular reactivity and prostanoid release in the perfused mesenteric arteriolar bed as well as nitric oxide production and reactive oxygen species generation in isolated mesenteric arteries were analyzed.18-week-old MSG rats displayed higher Lee index, fat accumulation, dyslipidemia, insulin resistance and hyperinsulinemia. Metformin treatment improved these alterations. The norepinephrine-induced response, increased in the mesenteric arteriolar bed from MSG rats, was corrected by metformin. Indomethacin corrected the enhanced contractile response in MSG rats but did not affect metformin effects. The sensitivity to acetylcholine, reduced in MSG rats, was also corrected by metformin. Indomethacin corrected the reduced sensitivity to acetylcholine in MSG rats but did not affect metformin effects. The sensitivity to sodium nitroprusside was increased in preparations from metformin-treated rats. Metformin treatment restored both the reduced PGI2/TXA2 ratio and the increased reactive oxygen species generation in preparations from MSG rats.Metformin improved the vascular function in MSG rats through reduction in reactive oxygen species generation, modulation of membrane hyperpolarization, correction of the unbalanced prostanoids release and increase in the sensitivity of the smooth muscle to nitric oxide.
机译：二甲双胍是一种胰岛素增敏剂，对糖尿病患者的血糖水平和心血管系统具有有益作用。我们研究了二甲双胍是否可以改善味精钠诱导的肥胖非糖尿病（MSG）大鼠的代谢变化和血管功能障碍.16周龄MSG大鼠用二甲双胍治疗15天，并与年龄匹配的未治疗MSG进行比较和非肥胖非糖尿病大鼠（对照组）。分析了18周龄MSG大鼠的肠系膜动脉灌注后的血压，胰岛素敏感性，血管反应性和前列腺素释放，以及肠系膜动脉中一氧化氮的产生和活性氧的产生。血脂异常，胰岛素抵抗和高胰岛素血症。二甲双胍治疗改善了这些改变。用二甲双胍纠正了味精大鼠肠系膜小动脉床中去甲肾上腺素引起的反应。消炎痛纠正了味精大鼠中增强的收缩反应，但不影响二甲双胍的作用。在二甲双胍中也纠正了味精大鼠中对乙酰胆碱的敏感性降低。消炎痛可纠正MSG大鼠对乙酰胆碱的敏感性降低，但不影响二甲双胍的作用。二甲双胍治疗大鼠的制剂对硝普钠的敏感性增加。二甲双胍治疗可恢复MSG大鼠制剂中降低的PGI2 / TXA2比值和增加的活性氧物种生成.Metformin通过减少活性氧物种生成，调节膜超极化，纠正不平衡的前列腺素释放来改善MSG大鼠的血管功能。并增加了平滑肌对一氧化氮的敏感性。

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