Identification of adropin as a secreted factor linking dietary macronutrient intake with energy homeostasis and lipid metabolism.
Identification of adropin as a secreted factor linking dietary macronutrient intake with energy homeostasis and lipid metabolism.
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DOI：
10.1016/j.cmet.2008.10.011
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发表时间：
2008-12
期刊：
影响因子：
29
通讯作者：
Butler AA
中科院分区：
文献类型：
--
作者：
Kumar KG;Trevaskis JL;Lam DD;Sutton GM;Koza RA;Chouljenko VN;Kousoulas KG;Rogers PM;Kesterson RA;Thearle M;Ferrante AW Jr;Mynatt RL;Burris TP;Dong JZ;Halem HA;Culler MD;Heisler LK;Stephens JM;Butler AA
肥胖和营养平衡的联系机制尚未完全阐明。在这里，我们描述了一种分泌蛋白，adropin，由一个基因编码，能量稳态相关（Enho），在肝脏和大脑中表达。肝脏Enho表达受营养调节：与对照组相比，喂食高脂饮食（HFD）的瘦C57 BL/6 J小鼠表现出快速增加，而禁食降低表达。然而，肝脏Enho表达随着与3个月HFD相关的饮食诱导的肥胖（DIO）或遗传诱导的肥胖而下降，表明与肥胖状态下的代谢紊乱相关。在DIO小鼠中，转基因过表达或全身adropin治疗可减轻脂肪肝和胰岛素抵抗，与对肥胖或食物摄入的影响无关。Adropin调节肝脏脂肪生成基因和脂肪组织过氧化物酶体增殖物激活受体γ（脂肪生成的主要调节因子）的表达。因此，Adropin可能是一种控制葡萄糖和脂质稳态的因子，可防止与肥胖相关的脂肪肝和高胰岛素血症。
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.
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