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Clock gene expression in the liver and adipose tissues of non-obese type 2 diabetic Goto-Kakizaki rats.

机译:非肥胖2型糖尿病五岛崎崎大鼠肝脏和脂肪组织中Clock基因的表达。

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摘要

Recent studies have revealed a close relationship between the pathophysiology of metabolic syndrome, which is characterized by obesity and hyperglycemia, and the functioning of internal molecular clocks. In this study, we show that the rhythmic mRNA expression of clock genes (Clock, Bmal1, Cry1, and Dbp) is not attenuated in the liver and visceral adipose tissues of Goto-Kakizaki rats, a model of nonobese, type 2 diabetes, as compared to control Wistar rats. Our results suggest that molecular clock impairment in peripheral tissues of obese diabetic animals may be either caused by obesity-related factor(s), but not hyperglycemia, or be a cause, but not a consequence, of hyperglycemia.
机译:最近的研究表明,以肥胖和高血糖为特征的代谢综合征的病理生理学与内部分子钟的功能之间存在着密切的关系。在这项研究中,我们显示了在非肥胖,2型糖尿病的模型Goto-Kakizaki大鼠的肝脏和内脏脂肪组织中,时钟基因(Clock,Bmal1,Cry1和Dbp)的节律性mRNA表达没有减弱。与对照组Wistar大鼠相比。我们的研究结果表明,肥胖糖尿病动物外周组织中的分子时钟损害可能是由肥胖相关因素引起的,而不是由高血糖引起的,也可能是高血糖的原因而不是后果。

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