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首页> 外文期刊>RSC Advances >Effect of dietary oxidized tyrosine products on insulin secretion via the oxidative stress-induced mitochondria damage in mice pancreas
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Effect of dietary oxidized tyrosine products on insulin secretion via the oxidative stress-induced mitochondria damage in mice pancreas

机译：日粮氧化酪氨酸产物对小鼠胰腺线粒体氧化应激的氧化应激作用

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Oxidized tyrosine products (OTPs) have been detected in commercial food and have been demonstrated to induce oxidative damage in vivo. The pancreas plays an important role in glucose metabolism, but its antioxidant capacity is low. The present study investigates the potential impact of dietary OTPs on the pancreatic function. Sprague Dawley (SD) rats (8 rats per group) were fed a diet containing OTPs for 24 weeks, and the blood glucose and plasma insulin levels were then measured. Elevated fasting blood glucose and decreased plasma insulin levels indicated dysfunction of the pancreatic islets. The rats fed the OTPs-containing diet also exhibited pancreatic oxidative stress, accompanied by inflammation. Furthermore, the expression of genes involved in the Nrf2/ARE pathway was down-regulated in the OTPs-treated groups. In addition, supplementation with lipoic acid (LA) significantly remitted the OTPs induced oxidative stress of the pancreas, and mitigated the effects of OTPs on the blood glucose and insulin synthesis. A gavage experiment was performed to explore whether dityrosine (Dityr), a major component of OTPs, was responsible for the injury induced by OTP. The OTPs, including Dityr, induced mitochondrial defects in cultured mice insulinoma MIN-6 cells and mice pancreas, as evidenced by less ATP production, loss of mitochondrial membrane potential, mitochondrial DNA (mtDNA) depletion, and alteration of the mRNA levels of genes involved in mitochondrial function. Moreover, the apoptosis of pancreatic islets and MIN-6 cells increased after exposure to OTPs/Dityr. The findings suggest that decreased insulin secretion triggered by OTPs may be mediated by oxidative stress and mitochondrial damage in pancreatic β cells.
机译：在商业食品中已检测到氧化酪氨酸产物（OTPs），并已证明在体内会引起氧化损伤。胰腺在葡萄糖代谢中起重要作用，但其抗氧化能力低。本研究调查了饮食中OTP对胰腺功能的潜在影响。给Sprague Dawley（SD）大鼠（每组8只大鼠）喂食含有OTP的饮食24周，然后测量血糖和血浆胰岛素水平。空腹血糖升高和血浆胰岛素水平降低表明胰岛功能异常。喂食含有OTPs的饮食的大鼠也表现出胰腺氧化应激，并伴有炎症。此外，在OTPs治疗组中，与Nrf2 / ARE途径有关的基因表达被下调。此外，补充硫辛酸（LA）可显着缓解OTP诱导的胰腺氧化应激，并减轻OTP对血糖和胰岛素合成的影响。进行了管饲实验，以探讨OTPs的主要成分二氢酪氨酸（Dityr）是否对OTP引起的损伤负责。包括Dityr在内的OTP诱导了培养的小鼠胰岛素瘤MIN-6细胞和小鼠胰腺中的线粒体缺陷，这可通过减少ATP产生，线粒体膜电位损失，线粒体DNA（mtDNA）耗竭以及所涉及基因的mRNA水平改变来证明线粒体功能而且，暴露于OTP / Dityr后，胰岛和MIN-6细胞的凋亡增加。这些发现表明，由OTP触发的胰岛素分泌减少可能是由胰腺β细胞的氧化应激和线粒体损伤所介导的。

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