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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Defective glycerol metabolism in aquaporin 9 (AQP9) knockout mice
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Defective glycerol metabolism in aquaporin 9 (AQP9) knockout mice

机译：水通道蛋白9（AQP9）基因敲除小鼠中的甘油代谢不良

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摘要

Aquaporin-9 (AQP9) is an aquaglyceroporin membrane channel shown biophysicaily to conduct water, glycerol, and other small solutes. Because the physiological role/s of AQP9 remain undefined and the expression sites of AQP9 remain incomplete and conflicting, we generated AQP9 knockout mice. In the absence of physiological stress, knockout mice did not display any visible behavioral or severe physical abnormalities. Immunohistochemical analyses using multiple antibodies revealed AQP9 specific labeling in hepatocytes, epididymis, vas deferens, and in epidermis of wild type mice, but a complete absence of labeling in AQP9~(-/-) mice. In brain, no detectable labeling was observed. Compared with control mice, plasma levels of glycerol and triglycerides were markedly increased in AQP9~(-/-) mice, whereas glucose, urea, free fatty acids, alkaline phosphatase, and cholesterol were not significantly different. Oral administration of glycerol to fasted mice resulted in an acute rise in blood glucose levels in both AQP9~(-/-) and AQP9~(+/-) mice, revealing no defect in utilization of exogenous glycerol as a gluconeogenic substrate and indicating a high gluconeogenic capacity in nonhepatic organs. Obese Lepr~(db)/Lepr~(db) AQP9~(-/-) and obese Lepr~(db)/Lepr~(db) AQP9~(+/-) mice showed similar body weight, whereas the glycerol levels in obese Lepr~(db)/Lepr~(db) AQP9~(-/-) mice were dramatically increased. Consistent with a role of AQP9 in hepatic uptake of glycerol, blood glucose levels were significantly reduced in Lepr~(db)/Lepr~(db) AQP9~(-/-) mice compared with Lepr~(db)l Lepr~(db) AQP9~(+/-) in response to 3 h of fasting. Thus, AQP9 is important for hepatic glycerol metabolism and may play a role in glycerol and glucose metabolism in diabetes mellitus.
机译：Aquaporin-9（AQP9）是一种水生甘油膜膜通道，具有生物物理性，可传导水，甘油和其他小溶质。由于AQP9的生理作用仍然不确定，并且AQP9的表达位点仍然不完整且相互矛盾，因此我们产生了AQP9敲除小鼠。在没有生理压力的情况下，基因敲除小鼠没有表现出任何可见的行为或严重的身体异常。使用多种抗体的免疫组织化学分析显示，野生型小鼠的肝细胞，附睾，输精管和表皮中存在AQP9特异性标记，但在AQP9〜（-/-）小鼠中完全没有标记。在大脑中，未观察到可检测的标记。与对照组相比，AQP9〜（-/-）小鼠血浆甘油和甘油三酯水平明显升高，而葡萄糖，尿素，游离脂肪酸，碱性磷酸酶和胆固醇水平无明显差异。禁食小鼠口服甘油会导致AQP9〜（-/-）和AQP9〜（+/-）小鼠的血糖水平急剧上升，表明利用外源甘油作为糖异生底物没有缺陷，这表明非肝器官的糖异生能力高。肥胖的Lepr〜（db）/ Lepr〜（db）AQP9〜（-/-）和肥胖的Lepr〜（db）/ Lepr〜（db）AQP9〜（+/-）小鼠显示相似的体重，而甘油的含量肥胖的Lepr〜（db）/ Lepr〜（db）AQP9〜（-/-）小鼠明显增加。与AQP9在肝脏摄取甘油中的作用一致，与Lepr〜（db）l Lepr〜（db）相比，Lepr〜（db）/ Lepr〜（db）AQP9〜（-/-）小鼠的血糖水平显着降低）AQP9〜（+/-）对禁食3 h的反应。因此，AQP9对肝甘油代谢很重要，并且可能在糖尿病患者的甘油和葡萄糖代谢中发挥作用。

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