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首页> 外文期刊>Cell metabolism >Identification of adropin as a secreted factor linking dietary macronutrient intake with energy homeostasis and lipid metabolism.
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Identification of adropin as a secreted factor linking dietary macronutrient intake with energy homeostasis and lipid metabolism.

机译：将adropin鉴定为将饮食中大量营养素摄入与能量稳态和脂质代谢联系起来的分泌因子。

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摘要

Obesity and nutrient homeostasis are linked by mechanisms that are not fully elucidated. Here we describe a secreted protein, adropin, encoded by a gene, Energy Homeostasis Associated (Enho), expressed in liver and brain. Liver Enho expression is regulated by nutrition: lean C57BL/6J mice fed high-fat diet (HFD) exhibited a rapid increase, while fasting reduced expression compared to controls. However, liver Enho expression declines with diet-induced obesity (DIO) associated with 3 months of HFD or with genetically induced obesity, suggesting an association with metabolic disorders in the obese state. In DIO mice, transgenic overexpression or systemic adropin treatment attenuated hepatosteatosis and insulin resistance independently of effects on adiposity or food intake. Adropin regulated expression of hepatic lipogenic genes and adipose tissue peroxisome proliferator-activated receptor gamma, a major regulator of lipogenesis. Adropin may therefore be a factor governing glucose and lipid homeostasis, which protects against hepatosteatosis and hyperinsulinemia associated with obesity.
机译：肥胖与营养稳态之间的关系还没有得到充分阐明。在这里，我们描述了一种在肝脏和大脑中表达的，由能量稳态相关基因（Enho）编码的分泌蛋白adropin。肝脏Enho的表达受营养的调节：与对照组相比，高脂饮食（HFD）喂养的瘦C57BL / 6J小鼠表现出快速的增加，而禁食的表达却下降。然而，肝Enho表达随饮食诱发肥胖（DIO）与HFD 3个月或遗传诱发肥胖而下降，提示与肥胖状态下的代谢异常有关。在DIO小鼠中，转基因过表达或全身性adropin处理可独立于对肥胖或食物摄入的影响而减弱肝脂肪变性和胰岛素抵抗。 Adropin调节肝脂肪形成基因和脂肪组织过氧化物酶体增殖物激活的受体γ（脂肪形成的主要调节剂）的表达。因此，Adropin可能是控制葡萄糖和脂质体内稳态的因素，可预防与肥胖相关的肝脂肪变性和高胰岛素血症。

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