日本研究人員在新一期美國《細(xì)胞—代謝》雜志網(wǎng)絡(luò)版上發(fā)表論文說，對于處在極度饑餓狀態(tài)的人來說,，醋酸在其維持能量供應(yīng)的過程中起著至關(guān)重要的作用。
在生命體內(nèi),，代謝產(chǎn)生的三磷酸腺苷（ATP）是身體運(yùn)動及維持體溫等生命活動的能量源泉,。在爆發(fā)式運(yùn)動中，葡萄糖是產(chǎn)生ATP的主要物質(zhì),，而在持久運(yùn)動時，脂肪酸和酮體是ATP的主要來源,。
東京大學(xué)尖端科學(xué)技術(shù)研究中心的研究人員注意到,，醋酸也參與產(chǎn)生ATP的代謝過程,。他們通過基因操作,，使實(shí)驗(yàn)鼠體內(nèi)能夠代謝葡萄糖和脂肪酸，但不能代謝醋酸,，然后比較這些實(shí)驗(yàn)鼠和正常實(shí)驗(yàn)鼠在喂給餌料和絕食48個小時的情況下,，身體狀態(tài)有何不同,。結(jié)果發(fā)現(xiàn),，在被迫長時間絕食的狀態(tài)下,，不能代謝醋酸的實(shí)驗(yàn)鼠體溫和耐力明顯降低,。
研究人員認(rèn)為,，實(shí)驗(yàn)證明，醋酸對極度饑餓的實(shí)驗(yàn)鼠維持生命活動所需能量十分重要,，由于醋酸是生命體內(nèi)基本物質(zhì)，而實(shí)驗(yàn)鼠身體構(gòu)造又與人體非常接近，因此可以推論醋酸對人體的作用也是一樣的,。對吸收和利用葡萄糖都極少的糖尿病患者來說,，醋酸或許可以作為一種不會提升血糖值的能量源,。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
