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脂肪细胞中甘油代谢的改变与 n3-PUFA 缺乏大鼠的代谢综合征动物模型有关。

Glycerol metabolism alteration in adipocytes from n3-PUFA-depleted rats, an animal model for metabolic syndrome.

机构信息

Laboratory of Experimental Surgery L. Deloyers, Université Libre de Bruxelles, Brussels, Belgium.

出版信息

Horm Metab Res. 2012 Jan;44(1):28-32. doi: 10.1055/s-0031-1297942. Epub 2011 Dec 28.

Abstract

Aquaglyceroporin 7 (AQP7) is a glycerol transporter expressed in adipocytes. Its expression has been shown to be modulated in obesity. Metabolic syndrome is characterized by abdominal obesity, insulin resistance, dyslipidemia, and hypertension. An animal model displaying several features of metabolic syndrome was used to study the AQP7 expression at both mRNA and protein level and glycerol flux in adipocytes. Second generation n3-PUFA depleted female rats is a good animal model for metabolic syndrome as it displays characteristic features such as liver steatosis, visceral obesity, and insulin resistance. Our data show a reduced expression of AQP7 at the protein level in adipose tissue from n3-PUFA-depleted rats, without any changes at the mRNA levels. [U-(14)C]-Glycerol uptake was not modified in adipocytes from n3-PUFA-depleted animals.

摘要

水通道蛋白 7(AQP7)是一种在脂肪细胞中表达的甘油转运体。其表达已被证明在肥胖中受到调节。代谢综合征的特征是腹部肥胖、胰岛素抵抗、血脂异常和高血压。一种表现出代谢综合征多种特征的动物模型被用于研究脂肪细胞中 AQP7 的 mRNA 和蛋白水平表达以及甘油流量。第二代 n3-PUFA 耗尽雌性大鼠是代谢综合征的良好动物模型,因为它表现出肝脂肪变性、内脏肥胖和胰岛素抵抗等特征。我们的数据显示,n3-PUFA 耗尽大鼠脂肪组织中 AQP7 的蛋白水平表达降低,而 mRNA 水平没有变化。[U-(14)C]-甘油摄取在 n3-PUFA 耗尽动物的脂肪细胞中没有改变。

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