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Melatonin attenuates smoking-induced hyperglycemia via preserving insulin secretion and hepatic glycogen synthesis in rats.
Journal of Pineal Research ( IF 10.3 ) Pub Date : 2018-03-25 , DOI: 10.1111/jpi.12475
Tianjia Li 1 , Leng Ni 1 , Zhewei Zhao 1 , Xinnong Liu 1 , Zhichao Lai 1 , Xiao Di 1 , Zhibo Xie 1 , Xitao Song 1 , Xuebin Wang 1 , Rui Zhang 1 , Changwei Liu 1
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Epidemiology survey indicated that cigarette smoking is a risk factor of diabetes. However, the precise mechanisms remain to be clarified. In this study, we found that smoking caused metabolic malfunctions on pancreas and liver in experimental animal model. These were indicated by hyperglycemia, increased serum hemoglobin A1c level and decreased insulin secretion, inhibition of liver glycogen synthase (LGS), and hepatic glycogen synthesis. Mechanistic studies revealed that all these alterations were caused by the inflammatory reaction and reactive oxygen species (ROS) induced by the smoking. Melatonin treatment significantly preserved the functions of both pancreas and liver by reducing β cell apoptosis, CD68-cell infiltration, ROS production, and caspase-3 expression. The siRNA-knockdown model identified that the protective effects of melatonin were mediated by melatonin receptor-2 (MT2). This study uncovered potentially underlying mechanisms related to the association between smoking and diabetes. In addition, it is, for first time, to report that melatonin effectively protects against smoking-induced glucose metabolic alterations and the signal transduction pathway of melatonin is mainly mediated by its MT2 receptor. These observations provide solid evidence for the clinically use of melatonin to reduce smoking-related diabetes, and the therapeutic regimens are absent currently.

中文翻译:

褪黑素通过保持大鼠的胰岛素分泌和肝糖原合成来减轻吸烟引起的高血糖症。

流行病学调查表明,吸烟是糖尿病的危险因素。但是,确切的机制仍有待阐明。在这项研究中,我们发现吸烟会在实验动物模型中引起胰腺和肝脏的代谢功能异常。高血糖,血清血红蛋白A1c水平升高,胰​​岛素分泌降低,肝糖原合酶(LGS)抑制和肝糖原合成表明了这些现象。机理研究表明,所有这些改变都是由吸烟引起的炎症反应和活性氧(ROS)引起的。褪黑素治疗可通过减少β细胞凋亡,CD68细胞浸润,ROS产生和caspase-3表达来显着保留胰腺和肝脏的功能。siRNA敲低模型确定褪黑激素的保护作用是由褪黑激素受体2(MT2)介导的。这项研究发现了潜在的潜在机制与吸烟和糖尿病之间的关联。另外,首次报道褪黑激素有效地保护了免受吸烟引起的葡萄糖代谢改变,并且褪黑激素的信号转导途径主要由其MT2受体介导。这些观察结果为褪黑激素在临床上减少吸烟相关的糖尿病提供了有力的证据,并且目前尚无治疗方案。报告说褪黑素有效地防止了吸烟引起的葡萄糖代谢改变,褪黑素的信号转导途径主要是由其MT2受体介导的。这些观察结果为褪黑激素在临床上减少吸烟相关的糖尿病提供了有力的证据,并且目前尚无治疗方案。报告说褪黑素有效地防止了吸烟引起的葡萄糖代谢改变,褪黑素的信号转导途径主要是由其MT2受体介导的。这些观察结果为褪黑激素在临床上减少吸烟相关的糖尿病提供了有力的证据,并且目前尚无治疗方案。
更新日期:2018-03-25
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