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

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• 作者：Satoshi Hirako^a ; Yoshihiro Wakayama^b ; ^c ; Hyounju Kim^d ; Yuzuru Iizuka^d ; Akiyo Matsumoto^d ; Nobuhiro Wada^e ; Ai Kimura^f ; Mai Okabe^g ; Junichi Sakagami^b ; Mamiko Suzuki^h ; Fumiko Takenoyaⁱ ; Seiji Shioda^f ; ^{shioda@hoshi.ac.jp" class="auth_mail" title="E-mail the corresponding author}
• 关键词：AQP7 ; AQP9 ; Obesity ; Lipid metabolism ; Hepatic lipids
• 刊名：Obesity Research & Clinical Practice
• 出版年：2016
• 出版时间：November-December 2016
• 年：2016
• 卷：10
• 期：6
• 页码：710-718
• 全文大小：1059 K

文摘

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.