Prolyl Hydroxylase Domain Protein 2 Plays a Critical Role in Diet-Induced Obesity and Glucose Intolerance
Prolyl Hydroxylase Domain Protein 2 Plays a Critical Role in Diet-Induced Obesity and Glucose Intolerance
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DOI：
10.1161/circulationaha.113.001742
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发表时间：
2013-05-28
期刊：
影响因子：
37.8
通讯作者：
Sunagawa, Kenji
中科院分区：
文献类型：
--
作者：
Matsuura, Hirohide;Ichiki, Toshihiro;Sunagawa, Kenji
背景-最近的研究表明，氧敏感通路由转录因子缺氧诱导因子和脯氨酰羟化酶结构域蛋白（PHDs）组成，在葡萄糖代谢中起着关键作用。然而，脂肪细胞PHD在肥胖发展中的作用尚未阐明。我们研究了脂肪细胞中主要的氧传感器PHD 2的缺失是否影响饮食诱导的肥胖和相关的代谢abnormals.Methods和Results-To删除脂肪细胞中的PHD 2，PHD 2-floxed小鼠与aP 2-Cre转基因小鼠杂交（Phd 2（f/f）/aP 2-Cre）。Phd 2（f/f）/aP 2-Cre小鼠对高脂饮食诱导的肥胖有抵抗力（36.7 +/- 1.7 vs 44.3 +/- 2.0 g; P
Background-Recent studies suggest that the oxygen-sensing pathway consisting of transcription factor hypoxia-inducible factor and prolyl hydroxylase domain proteins (PHDs) plays a critical role in glucose metabolism. However, the role of adipocyte PHD in the development of obesity has not been clarified. We examined whether deletion of PHD2, the main oxygen sensor, in adipocytes affects diet-induced obesity and associated metabolic abnormalities.Methods and Results-To delete PHD2 in adipocyte, PHD2-floxed mice were crossed with aP2-Cre transgenic mice (Phd2(f/f)/aP2-Cre). Phd2(f/f)/aP2-Cre mice were resistant to high-fat diet-induced obesity (36.7 +/- 1.7 versus 44.3 +/- 2.0 g in control; P