日本研究人员在新一期美国《细胞—代谢》杂志网络版上发表论文说，对于处在极度饥饿状态的人来说，醋酸在其维持能量供应的过程中起着至关重要的作用。
在生命体内，代谢产生的三磷酸腺苷（ATP）是身体运动及维持体温等生命活动的能量源泉。在爆发式运动中，葡萄糖是产生ATP的主要物质，而在持久运动时，脂肪酸和酮体是ATP的主要来源。
东京大学尖端科学技术研究中心的研究人员注意到，醋酸也参与产生ATP的代谢过程。他们通过基因操作，使实验鼠体内能够代谢葡萄糖和脂肪酸，但不能代谢醋酸，然后比较这些实验鼠和正常实验鼠在喂给饵料和绝食48个小时的情况下，身体状态有何不同。结果发现，在被迫长时间绝食的状态下，不能代谢醋酸的实验鼠体温和耐力明显降低。
研究人员认为，实验证明，醋酸对极度饥饿的实验鼠维持生命活动所需能量十分重要，由于醋酸是生命体内基本物质，而实验鼠身体构造又与人体非常接近，因此可以推论醋酸对人体的作用也是一样的。对吸收和利用葡萄糖都极少的糖尿病患者来说，醋酸或许可以作为一种不会提升血糖值的能量源。（生物谷Bioon.com）
生物谷推荐原始出处：
Cell Metabolism, 4 February 2009,doi:10.1016/j.cmet.2008.12.008
Fasting-Induced Hypothermia and Reduced Energy Production in Mice Lacking Acetyl-CoA Synthetase 2
Iori Sakakibara1,2,Takahiro Fujino3,Makoto Ishii2,4,Toshiya Tanaka1,Tatsuo Shimosawa5,Shinji Miura6,Wei Zhang7,Yuka Tokutake8,Joji Yamamoto2,9,Mutsumi Awano10,Satoshi Iwasaki1,2,Toshiyuki Motoike2,11,Masashi Okamura1,9,Takeshi Inagaki1,Kiyoshi Kita10,Osamu Ezaki6,Makoto Naito13,Tomoyuki Kuwaki7,Shigeru Chohnan8,Tokuo T. Yamamoto14,Robert E. Hammer12,Tatsuhiko Kodama1,Masashi Yanagisawa2,11andJuro Sakai1,2,,
1 Laboratory for Systems Biology and Medicine, Research Center for Advanced Science and Technology, University of Tokyo, Tokyo 153-8904, Japan
2 ERATO, Japan Science and Technology Agency (JST), Tokyo 102-0075, Japan
3 Department of Bioscience, Integrated Center for Sciences, Ehime University Graduate School of Medicine, Ehime 791-0295, Japan
4 Department of Neurology, Weill Cornell Medical College of Cornell University, 525 East 68th Street, New York, NY 10021, USA
5 Department of Clinical Laboratory, Faculty of Medicine, University of Tokyo, Tokyo 113-8655, Japan
6 Nutritional Science Program, National Institute of Health and Nutrition, 1-23-1, Toyama, Shinjuku-ku, Tokyo 162-8636, Japan
7 Departments of Molecular & Integrative Physiology and Autonomic Physiology, Graduate School of Medicine, Chiba University, Chiba, 260-8670, Japan
8 Department of Bioresource Science, Ibaraki University College of Agriculture, 3-21-1 Chuo, Ami, Ibaraki 300-0393, Japan
9 Division of Nephrology, Endocrinology, and Vascular Medicine, Department of Medicine, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan
10 Department of Biomedical Chemistry, Graduate School of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan
11 Howard Hughes Medical Institute, Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA
12 Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA
13 Department of Cellular Function, Division of Cellular and Molecular Pathology, Niigata University Graduate School of Medical and Dental Sciences, Niigata 951-8510, Japan
14 Center for Advanced Genome Research, Institute of Development, Aging, and Cancer, Tohoku University, Sendai 981-8555, Japan
Acetate is activated to acetyl-CoA by acetyl-CoA synthetase 2 (AceCS2), a mitochondrial enzyme. Here, we report that the activation of acetate by AceCS2 has a specific and unique role in thermogenesis during fasting. In the skeletal muscle of fasted AceCS2/ mice, ATP levels were reduced by 50% compared to AceCS2+/+ mice. Fasted AceCS2/ mice were significantly hypothermic and had reduced exercise capacity. Furthermore, when fed a low-carbohydrate diet, 4-week-old weaned AceCS2/ mice also exhibited hypothermia accompanied by sustained hypoglycemia that led to a 50% mortality. Therefore, AceCS2 plays a significant role in acetate oxidation needed to generate ATP and heat. Furthermore, AceCS2/ mice exhibited increased oxygen consumption and reduced weight gain on a low-carbohydrate diet. Our findings demonstrate that activation of acetate by AceCS2 plays a pivotal role in thermogenesis, especially under low-glucose or ketogenic conditions, and is crucially required for survival.
