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首页> 美国卫生研究院文献>Frontiers in Endocrinology >Retinoic acid-related orphan receptors α and γ: key regulators of lipid/glucose metabolism inflammation and insulin sensitivity
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Retinoic acid-related orphan receptors α and γ: key regulators of lipid/glucose metabolism inflammation and insulin sensitivity

机译：维甲酸相关的孤儿受体α和γ：脂质/葡萄糖代谢炎症和胰岛素敏感性的关键调节剂

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Retinoic acid-related orphan receptors RORα and RORγ play a regulatory role in lipid/glucose homeostasis and various immune functions, and have been implicated in metabolic syndrome and several inflammatory diseases. RORα-deficient mice are protected against age- and diet-induced obesity, hepatosteatosis, and insulin resistance. The resistance to hepatosteatosis in RORα-deficient mice is related to the reduced expression of several genes regulating lipid synthesis, transport, and storage. Adipose tissue-associated inflammation, which plays a critical role in the development of insulin resistance, is considerably diminished in RORα-deficient mice as indicated by the reduced infiltration of M1 macrophages and decreased expression of many proinflammatory genes. Deficiency in RORγ also protects against diet-induced insulin resistance by a mechanism that appears different from that in RORα deficiency. Recent studies indicated that RORs provide an important link between the circadian clock machinery and its regulation of metabolic genes and metabolic syndrome. As ligand-dependent transcription factors, RORs may provide novel therapeutic targets in the management of obesity and associated metabolic diseases, including hepatosteatosis, adipose tissue-associated inflammation, and insulin resistance.
机译：维甲酸相关的孤儿受体RORα和RORγ在脂质/葡萄糖稳态和各种免疫功能中起调节作用，并与代谢综合征和几种炎症性疾病有关。缺乏RORα的小鼠可预防年龄和饮食引起的肥胖症，肝脂肪变性和胰岛素抵抗。 RORα缺陷型小鼠对肝脂肪变性的抵抗力与调节脂质合成，转运和储存的几种基因的表达降低有关。 M1巨噬细胞浸润减少和许多促炎基因表达降低表明，在胰岛素抵抗的发展中起关键作用的脂肪组织相关炎症在RORα缺陷型小鼠中已大大减少。 RORγ缺乏还通过一种不同于RORα缺乏的机制来防止饮食诱导的胰岛素抵抗。最近的研究表明，ROR在昼夜节律机制及其对代谢基因和代谢综合征的调节之间提供了重要的联系。作为依赖配体的转录因子，RORs可在肥胖症和相关代谢疾病（包括肝硬脂病，脂肪组织相关炎症和胰岛素抵抗）的治疗中提供新的治疗靶标。

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