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首页> 外文期刊>Cell metabolism >Reciprocal regulation of hepatic and adipose lipogenesis by liver X receptors in obesity and insulin resistance
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Reciprocal regulation of hepatic and adipose lipogenesis by liver X receptors in obesity and insulin resistance

机译：肝X受体在肥胖和胰岛素抵抗中对肝脏和脂肪脂肪形成的相互调节

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Liver X receptors (LXRs) regulate lipogenesis and inflammation, but their contribution to the metabolic syndrome is unclear. We show that LXRs modulate key aspects of the metabolic syndrome in mice. LXRαβ-deficient-ob/ob (LOKO) mice remain obese but show reduced hepatic steatosis and improved insulin sensitivity compared to ob/ob mice. Impaired hepatic lipogenesis in LOKO mice is accompanied by reciprocal increases in adipose lipid storage, reflecting tissue-selective effects on the SREBP, PPARγ, and ChREBP lipogenic pathways. LXRs are essential for obesity-driven SREBP-1c and ChREBP activity in liver, but not fat. Furthermore, loss of LXRs in obesity promotes adipose PPARγ and ChREBP-β activity, leading to improved insulin sensitivity. LOKO mice also exhibit defects in β cell mass and proliferation despite improved insulin sensitivity. Our data suggest that sterol sensing by LXRs in obesity is critically linked with lipid and glucose homeostasis and provide insight into the complex relationships between LXR and insulin signaling.
机译：肝X受体（LXR）调节脂肪生成和炎症，但是它们对代谢综合征的贡献尚不清楚。我们表明，LXRs调节小鼠代谢综合征的关键方面。 LXRαβ缺陷型ob / ob（LOKO）小鼠仍然肥胖，但与ob / ob小鼠相比，肝脏脂肪变性降低，胰岛素敏感性提高。 LOKO小鼠的肝脏脂肪生成受损，同时伴随着脂肪脂质储存的相互增加，反映出组织对SREBP，PPARγ和ChREBP脂肪生成途径的选择性作用。 LXR对于肥胖驱动的肝脏SREBP-1c和ChREBP活性至关重要，但对于脂肪却不是。此外，肥胖中LXR的缺失会促进脂肪PPARγ和ChREBP-β的活性，从而改善胰岛素敏感性。尽管胰岛素敏感性提高，LOKO小鼠也表现出β细胞量和增殖缺陷。我们的数据表明，肥胖中LXR引起的固醇感与脂质和葡萄糖体内稳态密切相关，可深入了解LXR与胰岛素信号之间的复杂关系。

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