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Effect of mitoquinone (Mito-Q) on neuropathic endpoints in an obese and type 2 diabetic rat model.
Free Radical Research ( IF 3.6 ) Pub Date : 2020-04-24 , DOI: 10.1080/10715762.2020.1754409
Brian Fink 1 , Lawrence Coppey 2 , Eric Davidson 2 , Hanna Shevalye 2 , Alexander Obrosov 2 , Pratik Rajesh Chheda 3 , Robert Kerns 3 , William Sivitz 1, 2, 4 , Mark Yorek 1, 2, 4, 5
Affiliation  

This study sought to determine whether the addition of mitoquinone (Mito-Q) in the diet is an effective treatment for peripheral neuropathy in animal models of diet-induced obesity (pre-diabetes) and type 2 diabetes. Unlike other anti-oxidative stress compounds investigated as a treatment for peripheral neuropathy, Mito-Q specifically targets mitochondria. Although mito-Q has been shown to reduce oxidative stress generated by mitochondria there have been no studies performed of the effect of Mito-Q on peripheral neuropathy induced by diet-induced obesity or type 2 diabetes. Diet-induced obese (12 weeks after high fat diet) or type 2 diabetic rats (12 weeks of high fat diet and 4 weeks after the onset of hyperglycemia) were treated via the diet with Mito-Q (0.93 g/kg diet) for 12 weeks. Afterwards, glucose utilization, vascular reactivity of epineurial arterioles to acetylcholine and peripheral neuropathy related endpoints were examined. The addition of Mito-Q to the diets of obese and diabetic rats improved motor and/or sensory nerve conduction velocity, cornea and intraepidermal nerve fibre density, cornea sensitivity and thermal nociception. Surprisingly, treating obese and diabetic rats with Mito-Q did not improve glucose utilization or vascular reactivity by epineurial arterioles to acetylcholine. These studies imply that mitochondrial dysfunction contributes to peripheral neuropathy in animal models of pre-diabetes and late-stage type 2 diabetes. However, improvement in peripheral neuropathy following treatment with Mito-Q was not associated with improvement in glucose utilization or vascular reactivity of epineurial arterioles to acetylcholine.



中文翻译:

米托醌(Mito-Q)对肥胖和2型糖尿病大鼠模型神经病理终点的影响。

这项研究试图确定在饮食诱发的肥胖症(糖尿病前期)和2型糖尿病动物模型中,饮食中添加米托醌(Mito-Q)是否是有效的治疗周围神经病变的方法。与研究用于治疗周围神经病变的其他抗氧化应激化合物不同,Mito-Q专门针对线粒体。尽管已经证明了mito-Q可以减轻线粒体产生的氧化应激,但尚未进行有关Mito-Q对饮食引起的肥胖症或2型糖尿病引起的周围神经病变的影响的研究。饮食引起的肥胖症(高脂饮食后12周)或2型糖尿病大鼠(高脂饮食12周和高血糖发作后4周)通过用Mito-Q(0.93 g / kg饮食)饮食12周。此后,检查了葡萄糖利用,肾上腺小动脉对乙酰胆碱的血管反应性和周围神经病的相关终点。在肥胖和糖尿病大鼠的饮食中添加Mito-Q可改善运动和/或感觉神经传导速度,角膜和表皮内神经纤维密度,角膜敏感性和热伤害感受。出人意料的是,用Mito-Q治疗肥胖和糖尿病大鼠并不能改善海马小动脉对乙酰胆碱的葡萄糖利用或血管反应性。这些研究暗示线粒体功能障碍在糖尿病前期和晚期2型糖尿病的动物模型中导致周围神经病变。然而,

更新日期:2020-06-30
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