美國(guó)科學(xué)家近日研究發(fā)現(xiàn),，吃過(guò)高脂肪食物后,，肝臟制造的一種蛋白質(zhì)會(huì)發(fā)送信號(hào)提示脂肪已被攝入,。這項(xiàng)發(fā)現(xiàn)可能會(huì)幫助找到治療肥胖及相關(guān)疾病的新療法。相關(guān)論文發(fā)表在12月的《細(xì)胞—代謝》（Cell Metabolism）上,。
研究人員發(fā)現(xiàn)小鼠的肝臟制造了一種稱為adropin的蛋白質(zhì)，攝入高脂肪食物后adropin含量升高,，禁食時(shí)則降低,。這一蛋白質(zhì)似乎起到了調(diào)節(jié)其他代謝基因活性的作用，尤其是參與了用碳水化合物制造脂類的基因,。對(duì)肥胖動(dòng)物體內(nèi)該種蛋白質(zhì)的研究顯示,，adropin也與胰島素反應(yīng)和防止如非酒精性脂肪肝病這種肝臟脂肪積聚有關(guān)。
路易斯安那州立大學(xué)的Andrew Butler表示：“值得注意的是,，該因子尤其受飲食中脂肪含量的影響，這使得它成為最早發(fā)現(xiàn)的類似因子之一。”研究人員11月26日曾在《細(xì)胞》上發(fā)表了一篇相關(guān)論文，論述了在高脂肪飲食后,，一種由內(nèi)臟制造的磷脂含量升高,，并給大腦發(fā)出信號(hào)，告訴大腦應(yīng)當(dāng)少吃,。
進(jìn)一步的研究結(jié)果表明,，利用adropin的療法可能能對(duì)抗肥胖及脂肪肝,、2型糖尿病等相關(guān)代謝失調(diào)。
研究人員發(fā)現(xiàn),，動(dòng)物食用高脂肪食物3個(gè)月,，或者由于遺傳變異不能正常制造adropin就會(huì)變得肥胖。不過(guò),，若讓肥胖動(dòng)物產(chǎn)生過(guò)量adropin或注入adropin的話,，動(dòng)物肝臟脂肪就會(huì)較少，而且能更好地響應(yīng)胰島素,。最終，小鼠吃得更少且體重下降,，不過(guò)Butler說(shuō),，其他代謝功能提升并不由體重降低決定。
Butler表示仍然有許多問(wèn)題需要解決,。比如,，缺少adropin的小鼠是否會(huì)變得肥胖并出現(xiàn)與肥胖和胰島素抗性相關(guān)的一系列疾病——代謝綜合癥。另外,，adropin的作用機(jī)理也尚不清楚,。研究人員說(shuō)：“總的來(lái)說(shuō)，adropin這種分泌蛋白在維持能量平衡和脂肪代謝中都起了一定的作用,。以adropin為基礎(chǔ),，或許能夠開(kāi)發(fā)出新療法，治療與肥胖有關(guān)的代謝失調(diào),。”（生物谷Bioon.com）
生物谷推薦原始出處：
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.
