睡眠剥夺与二甲双胍治疗小鼠胰、肝功能的关系

S. Periasamy, S. Chien, Chen Hsu, D. Hsu, Ming‐Yie Liu
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引用次数: 0

摘要

二甲双胍已被广泛用作治疗高血糖和糖尿病的药物。睡眠是一个重要的恢复过程,是器官正常运作所必需的。睡眠不足会导致多器官损伤,包括可能导致高血糖和糖尿病的胰腺和肝脏损伤。我们研究了二甲双胍在逆转睡眠剥夺引起的小鼠高血糖和胰腺和肝脏功能障碍中的作用。然而,与对照组相比,睡眠剥夺降低了参与GLUT2- PPARγ - pampk糖酵解途径的蛋白质水平。睡眠剥夺加上二甲双胍降低了血糖和GPT水平以及胰腺炎症。然而,这种组合增加了参与GLUT2- PPARγ - pampk糖酵解途径的蛋白水平。此外,单用二甲双胍可增加AMYL水平,并导致胰岛萎缩、边缘不规则和胰腺腺泡细胞紊乱。二甲双胍可减轻睡眠不足小鼠的高血糖,减少胰腺和肝脏炎症;然而,它可能导致胰腺功能障碍。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Association between Sleep Deprivation and Metformin Treatment on Pancreatic and Liver Function in Mice
Metformin has been widely used as a therapeutic drug for hyperglycemia and diabetes. Sleep is a vital and restorative process that is necessary for the proper functioning of organs. Sleep deprivation can induce multi-organ injury, including damage to the pancreas and liver that may result in hyperglycemia and diabetes. We studied the role of metformin in reversing sleep deprivation-induced hyperglycemia and pancreatic and liver dysfunction in mice. Mice were kept in However, compared with control, sleep deprivation decreased the levels of proteins involved in the GLUT2- PPARγ -pAMPK glycolytic pathway. Sleep deprivation plus metformin decreased blood glucose and GPT levels and pancreatic inflammation. However, the combination increased the levels of proteins involved in the GLUT2- PPARγ -pAMPK glycolytic pathway. In addition, metformin alone increased the levels of AMYL, as well as resulted in islet atrophy, edge irregularities, and disordered pancreatic acinar cells. Metformin attenuates hyperglycemia and reduces pancreatic and liver inflammation in sleep-deprived mice; however, it may cause pancreatic dysfunction.
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