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饮食诱导肥胖小鼠和ob/ob小鼠中甘油水通道蛋白表达与脂肪肝发生发展的关系。

The relationship between aquaglyceroporin expression and development of fatty liver in diet-induced obesity and ob/ob mice.

作者信息

Hirako Satoshi, Wakayama Yoshihiro, Kim Hyounju, Iizuka Yuzuru, Matsumoto Akiyo, Wada Nobuhiro, Kimura Ai, Okabe Mai, Sakagami Junichi, Suzuki Mamiko, Takenoya Fumiko, Shioda Seiji

机构信息

Department of Health and Nutrition, University of Human Arts and Sciences, Saitama, Japan.

Department of Anatomy, Showa University School of Medicine, Tokyo, Japan; Wakayama Clinic, Machida-shi, Tokyo, Japan.

出版信息

Obes Res Clin Pract. 2016 Nov-Dec;10(6):710-718. doi: 10.1016/j.orcp.2015.12.001. Epub 2015 Dec 30.

Abstract

Aquaporin (AQP) 7 and AQP9 are subcategorised as aquaglyceroporins which transport glycerin in addition to water. These AQPs may play a role in the homeostasis of energy metabolism. We examined the effect of AQP7, AQP9, and lipid metabolism-related gene expression in obese mice. In diet-induced obese (DIO) mice, excess lipid accumulated in the liver, which was hyperleptinemic and hyperinsulinemic. Hepatic AQP9 gene expression was significantly increased in both DIO and ob/ob mice compared to controls. The mRNA expression levels of fatty acid and triglyceride synthesis-related genes and fatty acid β oxidation-related genes in the liver were also higher in both mouse models, suggesting that triglyceride synthesis in this organ is promoted as a result of glycerol release from adipocytes. Adipose AQP7 and AQP9 gene expressions were increased in DIO mice, but there was no difference in ob/ob mice compared to wild-type mice. In summary, adipose AQP7 and AQP9 gene expressions are increased by diet-induced obesity, indicating that this is one of the mechanisms by which lipid accumulates in response to a high fat diet, not the genetic mutation of ob/ob mice. Hepatic AQP9 gene expression was increased in both obesity model mice. AQP7 and AQP9 therefore have the potential of defining molecules for the characterisation of obesity or fatty liver and may be a target molecules for the treatment of those disease.

摘要

水通道蛋白(AQP)7和AQP9被归类为水甘油通道蛋白,除了运输水之外还运输甘油。这些水通道蛋白可能在能量代谢的稳态中发挥作用。我们研究了肥胖小鼠中AQP7、AQP9以及脂质代谢相关基因表达的影响。在饮食诱导的肥胖(DIO)小鼠中,肝脏中积累了过量脂质,这些小鼠血瘦素水平和血胰岛素水平升高。与对照组相比,DIO小鼠和ob/ob小鼠肝脏中的AQP9基因表达均显著增加。在这两种小鼠模型中,肝脏中脂肪酸和甘油三酯合成相关基因以及脂肪酸β氧化相关基因的mRNA表达水平也更高,这表明由于脂肪细胞释放甘油,该器官中的甘油三酯合成得到促进。DIO小鼠脂肪组织中的AQP7和AQP9基因表达增加,但与野生型小鼠相比,ob/ob小鼠没有差异。总之,饮食诱导的肥胖会增加脂肪组织中AQP7和AQP9基因的表达,这表明这是高脂饮食导致脂质积累的机制之一,而非ob/ob小鼠的基因突变。两种肥胖模型小鼠肝脏中的AQP9基因表达均增加。因此,AQP7和AQP9有潜力成为定义肥胖或脂肪肝特征的分子,并且可能是治疗这些疾病的靶分子。

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