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Effect of Amorphophallus Konjac oligosaccharides on STZ-induced diabetes model of isolated islets.

机译:魔芋魔芋低聚糖对STZ诱导的胰岛糖尿病模型的影响。

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Three oligosaccharide fractions from the root of Amorphophallus Konjac, which was reported with hypoglycemic effects on diabetes subjects, were isolated and studied using the STZ-treated diabetes model. Among them, one fraction named as KOS-A, was found with nitric oxide (NO(*)) free radical regulation effect, while the other two were not. At concentrations less than 1.5 mM, KOS-A positively decreased STZ-induced NO(*) level of islets, but normal NO(*) release for non-STZ-treated islets was not affected within the range. At 15 mM, KOS-A played a contrary role and increased NO(*) level for islets both with and without STZ-treatment. Islets insulin secretion changed corresponding to NO(*) level in the assay. Increased insulin secretion appeared parallel to the decrease of NO(*), and normal insulin release was not affected by KOS-A less than 1.5 mM. Structure determination of KOS-A shows that it is a tetrasaccharide with Mw of 666 Da and reductive end of alpha-D-mannose. These results indicate that low dosage of KOS-A, with its function on attenuating STZ-induced NO(*) level, doesn't alter normal NO(*) and insulin secretion pathways of isolated islets. The NO(*) attenuation function of KOS-A on the diabetes model is mainly resulted from environmental free radical scavenging by the oligosaccharide. Present results also imply the mechanism of clinical Amorphophallus Konjac hypoglycemic function maybe related with free radical attenuation and lower risks of islets damage from NO(*) radical.
机译:分离并研究了来自魔芋魔芋根的三个低聚糖成分,这些糖成分对糖尿病患者具有降血糖作用,并使用STZ治疗的糖尿病模型进行了研究。其中,发现一个名为KOS-A的组分具有一氧化氮(NO(*))自由基调节作用,而其他两个组分则没有。在小于1.5 mM的浓度下,KOS-A会积极降低STZ诱导的胰岛的NO(*)水平,但未经过STZ处理的胰岛的正常NO(*)释放在该范围内不受影响。在15 mM时,无论是否进行STZ处理,KOS-A的作用都相反,并且胰岛的NO(*)水平升高。胰岛的胰岛素分泌量相应于测定中的NO(*)水平而变化。胰岛素分泌增加似乎与NO(*)减少平行,并且正常胰岛素释放不受小于1.5 mM的KOS-A影响。 KOS-A的结构测定表明它是四糖,Mw为666Da,还原端为α-D-甘露糖。这些结果表明,低剂量的KOS-A具有减弱STZ诱导的NO(*)水平的功能,不会改变正常的NO(*)和孤立胰岛的胰岛素分泌途径。 KOS-A对糖尿病模型的NO(*)衰减功能主要是由于寡糖清除环境自由基所致。目前的结果还暗示临床魔芋魔芋降血糖功能的机制可能与自由基衰减和降低NO(*)自由基对胰岛造成损害的风险有关。

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