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首页> 外文期刊>Cell metabolism >The differential role of Hif1beta/Arnt and the hypoxic response in adipose function, fibrosis, and inflammation.
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The differential role of Hif1beta/Arnt and the hypoxic response in adipose function, fibrosis, and inflammation.

机译：Hif1beta / Arnt和低氧反应在脂肪功能，纤维化和炎症中的差异作用。

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摘要

In obesity, adipocytes distant from vasculature become hypoxic and dysfunctional. This hypoxic response is mediated by hypoxia-inducible factors (Hif1alpha, Hif2alpha, and Hif3alpha) and their obligate partner, Hif1beta (Arnt). We show that mice lacking Hif1beta in fat (FH1betaKO) are lean, exhibit reduced adipocyte size, and are protected from age- and diet-induced glucose intolerance. There is also reduced Vegf and vascular permeability in FH1betaKO fat, but diet-induced inflammation and fibrosis is unchanged. Adipocytes from FH1betaKO mice have reduced glucose uptake due to decreased Glut1 and Glut4, which is mirrored in 3T3-L1 adipocytes with Hif1beta knockdown. Hif1beta knockdown cells also fail to respond appropriately to hypoxia with reduced cellular respiration and reduced mitochondrial gene expression. Some, but not all, of these effects are reproduced by Hif1alpha knockdown. Thus, Hif1beta/Arnt regulates glucose uptake, mitochondrial gene expression, and vascular permeability to control adipose mass and function, providing a target for obesity therapy.
机译：在肥胖症中，远离脉管系统的脂肪细胞变得缺氧和功能异常。这种缺氧反应是由缺氧诱导因子（Hif1alpha，Hif2alpha和Hif3alpha）及其专职伴侣Hif1beta（Arnt）介导的。我们显示，缺少脂肪中的Hif1beta的小鼠（FH1betaKO）苗条，脂肪细胞减少，并且免受年龄和饮食引起的葡萄糖耐量异常的影响。 FH1betaKO脂肪中的Vegf和血管通透性也降低，但饮食引起的炎症和纤维化没有改变。 FH1betaKO小鼠的脂肪细胞由于减少了Glut1和Glut4而降低了葡萄糖摄取，这在具有Hif1beta抑制作用的3T3-L1脂肪细胞中得到了反映。 Hif1beta组合式细胞还不能通过减少细胞呼吸和减少线粒体基因表达来适当应对缺氧。 Hif1alpha组合可复制其中一些（但不是全部）效果。因此，Hif1beta / Arnt调节葡萄糖摄取，线粒体基因表达和血管通透性，以控制脂肪的质量和功能，为肥胖症治疗提供了目标。

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