法国路易·巴斯德大学的研究人员最近开发出一种药物，能诱导脂肪燃烧来达到减肥目的，使用这种药物的实验鼠即使大吃大喝也不会胖。
据英国《每日邮报》报道，这种药物还没有正式名称，只是暂名为“SRT1720”，其作用与红酒中所含的对人体有益的成分白藜芦醇相似，它们均能使一些哺乳动物体内的“SIRT1”蛋白质活跃起来，而这种蛋白质对调节体内能量供应起关键作用。如果“SIRT1”蛋白质比较活跃，那么即使食物充足，它也能让大脑认为需要燃烧储备的脂肪来补充能量，从而促进新陈代谢。
目前，这种药物已在实验鼠身上进行了测试，结果在“SRT1720”使用量较大的情况下，实验鼠连续10周食用高脂肪食物后体重也没有增加，不过“SRT1720”使用量较小时效果不明显。
研究人员还发现，实验鼠在大量摄入“SRT1720”后，其运动能力和耐心都有所增强，同时没有出现副作用。这一研究已发表在11月5日美国《细胞—代谢》（Cell Metabolism）杂志上。
研究人员说，希望能很快用“SRT1720”进行人体试验，并预计这种减肥药有望在5年内上市。（生物谷Bioon.com）
生物谷推荐原始出处：
Cell Metabolism，Volume 8, Issue 5, 347-358, 5 November 2008，Jér?me N. Feige, Peter J. Elliott and Johan Auwerx
Specific SIRT1 Activation Mimics Low Energy Levels and Protects against Diet-Induced Metabolic Disorders by Enhancing Fat Oxidation
Jérôme N. Feige1,Marie Lagouge1,Carles Canto1,Axelle Strehle1,Sander M. Houten2,Jill C. Milne3,Philip D. Lambert3,Chikage Mataki1,Peter J. Elliott3andJohan Auwerx1,4,5,
1 Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/Université Louis Pasteur, 67404, Illkirch, France
2 Academic Medical Center, University of Amsterdam, 1100DE Amsterdam, The Netherlands
3 Sirtris Pharmaceuticals Inc., 200 Technology Square, Cambridge, MA 02139, USA
4 Institut Clinique de la Souris, 67404, Illkirch, France
5 Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne (EPFL), CH-1015, Lausanne, Switzerland
The NAD+-dependent deacetylase SIRT1 controls metabolic processes in response to low nutrient availability. We report the metabolic phenotype of mice treated with SRT1720, a specific and potent synthetic activator of SIRT1 that is devoid of direct action on AMPK. SRT1720 administration robustly enhances endurance running performance and strongly protects from diet-induced obesity and insulin resistance by enhancing oxidative metabolism in skeletal muscle, liver, and brown adipose tissue. These metabolic effects of SRT1720 are mediated by the induction of a genetic network controlling fatty acid oxidation through a multifaceted mechanism that involves the direct deacetylation of PGC-1, FOXO1, and p53 and the indirect stimulation of AMPK signaling through a global metabolic adaptation mimicking low energy levels. Combined with our previous work on resveratrol, the current study further validates SIRT1 as a target for the treatment of metabolic disorders and characterizes the mechanisms underlying the therapeutic potential of SIRT1 activation.
