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甘油通道 AQP7 和 AQP9 在脂肪组织和肝脏中的代谢作用。

Metabolic impact of the glycerol channels AQP7 and AQP9 in adipose tissue and liver.

机构信息

The Danish Diabetes Academy, Odense, Denmark Department of Biomedicine, Aarhus University, Wilhelm Meyers Allé 3, DK-8000 Aarhus, Denmark.

出版信息

J Mol Endocrinol. 2014 Mar 14;52(2):R165-78. doi: 10.1530/JME-13-0268. Print 2014 Apr.

DOI:10.1530/JME-13-0268
PMID:24463099
Abstract

Obesity and secondary development of type 2 diabetes (T2D) are major health care problems throughout the developed world. Accumulating evidence suggest that glycerol metabolism contributes to the pathophysiology of obesity and T2D. Glycerol is a small molecule that serves as an important intermediate between carbohydrate and lipid metabolism. It is stored primarily in adipose tissue as the backbone of triglyceride (TG) and during states of metabolic stress, such as fasting and diabetes, it is released for metabolism in other tissues. In the liver, glycerol serves as a gluconeogenic precursor and it is used for the esterification of free fatty acid into TGs. Aquaporin 7 (AQP7) in adipose tissue and AQP9 in the liver are transmembrane proteins that belong to the subset of AQPs called aquaglyceroporins. AQP7 facilitates the efflux of glycerol from adipose tissue and AQP7 deficiency has been linked to TG accumulation in adipose tissue and adult onset obesity. On the other hand, AQP9 expressed in liver facilitates the hepatic uptake of glycerol and thereby the availability of glycerol for de novo synthesis of glucose and TG that both are involved in the pathophysiology of diabetes. The aim of this review was to summarize the current knowledge on the role of the two glycerol channels in controlling glycerol metabolism in adipose tissue and liver.

摘要

肥胖和 2 型糖尿病(T2D)的继发发展是整个发达世界的主要医疗保健问题。越来越多的证据表明,甘油代谢有助于肥胖和 T2D 的病理生理学。甘油是一种小分子,作为碳水化合物和脂质代谢之间的重要中间产物。它主要储存在脂肪组织中,作为甘油三酯(TG)的骨干,在代谢应激状态下,如禁食和糖尿病,它会被释放到其他组织中进行代谢。在肝脏中,甘油用作糖异生前体,用于将游离脂肪酸酯化形成 TG。脂肪组织中的水通道蛋白 7(AQP7)和肝脏中的水通道蛋白 9(AQP9)是跨膜蛋白,属于水通道蛋白的一个亚类,称为水通道甘油蛋白。AQP7 促进甘油从脂肪组织中流出,AQP7 缺乏与脂肪组织中 TG 的积累和成年肥胖有关。另一方面,在肝脏中表达的 AQP9 促进甘油在肝脏中的摄取,从而为葡萄糖和 TG 的从头合成提供甘油,这两者都参与了糖尿病的病理生理学。本综述的目的是总结目前关于这两种甘油通道在控制脂肪组织和肝脏中甘油代谢的作用的知识。

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