美国科学家近日研究发现，吃过高脂肪食物后，肝脏制造的一种蛋白质会发送信号提示脂肪已被摄入。这项发现可能会帮助找到治疗肥胖及相关疾病的新疗法。相关论文发表在12月的《细胞—代谢》（Cell Metabolism）上。
研究人员发现小鼠的肝脏制造了一种称为adropin的蛋白质，摄入高脂肪食物后adropin含量升高，禁食时则降低。这一蛋白质似乎起到了调节其他代谢基因活性的作用，尤其是参与了用碳水化合物制造脂类的基因。对肥胖动物体内该种蛋白质的研究显示，adropin也与胰岛素反应和防止如非酒精性脂肪肝病这种肝脏脂肪积聚有关。
路易斯安那州立大学的Andrew Butler表示：“值得注意的是，该因子尤其受饮食中脂肪含量的影响，这使得它成为最早发现的类似因子之一。”研究人员11月26日曾在《细胞》上发表了一篇相关论文，论述了在高脂肪饮食后，一种由内脏制造的磷脂含量升高，并给大脑发出信号，告诉大脑应当少吃。
进一步的研究结果表明，利用adropin的疗法可能能对抗肥胖及脂肪肝、2型糖尿病等相关代谢失调。
研究人员发现，动物食用高脂肪食物3个月，或者由于遗传变异不能正常制造adropin就会变得肥胖。不过，若让肥胖动物产生过量adropin或注入adropin的话，动物肝脏脂肪就会较少，而且能更好地响应胰岛素。最终，小鼠吃得更少且体重下降，不过Butler说，其他代谢功能提升并不由体重降低决定。
Butler表示仍然有许多问题需要解决。比如，缺少adropin的小鼠是否会变得肥胖并出现与肥胖和胰岛素抗性相关的一系列疾病——代谢综合症。另外，adropin的作用机理也尚不清楚。研究人员说：“总的来说，adropin这种分泌蛋白在维持能量平衡和脂肪代谢中都起了一定的作用。以adropin为基础，或许能够开发出新疗法，治疗与肥胖有关的代谢失调。”（生物谷Bioon.com）
生物谷推荐原始出处：
Cell Metabolism，doi:10.1016/j.cmet.2008.10.011，K. Ganesh Kumar， Andrew A. Butler
Identification of Adropin as a Secreted Factor Linking Dietary Macronutrient Intake with Energy Homeostasis and Lipid Metabolism
K. Ganesh Kumar1,11,James L. Trevaskis1,11,Daniel D. Lam2,Gregory M. Sutton1,Robert A. Koza3,Vladimir N. Chouljenko4,Konstantin G. Kousoulas4,Pamela M. Rogers5,Robert A. Kesterson6,Marie Thearle7,Anthony W. Ferrante7,Randall L. Mynatt8,Thomas P. Burris5,Jesse Z. Dong9,Heather A. Halem9,Michael D. Culler9,Lora K. Heisler2,Jacqueline M. Stephens10andAndrew A. Butler1,8,,
1 Neuropeptides Laboratory, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA
2 Department of Pharmacology, University of Cambridge, Cambridge CB2 1PD, UK
3 Genomics Core Facility, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA
4 Division of Biotechnology and Molecular Medicine, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70802, USA
5 Nuclear Receptor Biology Laboratory, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA
6 Department of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA
7 Naomi Berrie Diabetes Center, Columbia University Medical Center, New York, NY 10032, USA
8 Clinical Nutrition Research Unit, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA
9 Biomeasure Incorporated, IPSEN, Milford, MA 01757, USA
10 Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70802, USA
11 These authors contributed equally to this work
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.
