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Hepatic PPARγ and LXRα independently regulate lipid accumulation in the livers of genetically obese mice

机译:肝PPARγ和LXRα独立调节遗传性肥胖小鼠肝脏中脂质的积累

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The nuclear hormone receptors liver X receptor α (LXRα) and peroxisome proliferator-activated receptor γ (PPARγ) play key roles in the development of fatty liver. To determine the link between hepatic PPARγ and LXRα signaling and the development of fatty liver, a LXRα-specific ligand, T0901317, was administered to normal OB/OB and genetically obese (ob/ob) mice lacking hepatic PPARγ (Pparγ ΔH). In ob/ob-PparγΔH and OB/OB-PparγΔH mice, as well as ob/ob- PparγWT and OB/OB-PparγWT mice, the liver weights and hepatic triglyceride levels were markedly increased in response to T0901317 treatment. These results suggest that hepatic PPARγ and LXRα signals independently contribute to the development of fatty liver.
机译:核激素受体肝X受体α(LXRα)和过氧化物酶体增殖物激活受体γ(PPARγ)在脂肪肝的发展中起关键作用。为了确定肝PPARγ和LXRα信号与脂肪肝的发展之间的联系,向正常OB / OB和缺乏肝PPARγ(PparγΔH)的遗传肥胖(ob / ob)小鼠施用LXRα特异性配体T0901317。在ob /ob-PparγΔH和OB /OB-PparγΔH小鼠以及ob /ob-PparγWT和OB /OB-PparγWT小鼠中,响应于T0901317处理,肝脏重量和肝甘油三酯水平显着增加。这些结果表明,肝PPARγ和LXRα信号独立地促进脂肪肝的发展。

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