辅酶A失调、代谢灵活性丧失与糖尿病
Deregulated coenzyme A, loss of metabolic flexibility and diabetes.
作者信息
Jackowski Suzanne, Leonardi Roberta
机构信息
*Department of Infectious Diseases, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, U.S.A.
†Department of Biochemistry, School of Medicine, West Virginia University, One Medical Center Drive, Morgantown, WV 26506, U.S.A.
出版信息
Biochem Soc Trans. 2014 Aug;42(4):1118-22. doi: 10.1042/BST20140156.
Abstract
CoA (coenzyme A) is an essential cofactor that is emerging as a global regulator of energy metabolism. Tissue CoA levels are tightly regulated and vary in response to different conditions including nutritional state and diabetes. Recent studies reveal the ability of this cofactor to control the output of key metabolic pathways. CoA regulation is important for the maintenance of metabolic flexibility and glucose homoeostasis.
摘要
辅酶A是一种必需的辅因子，正成为能量代谢的全局调节因子。组织中的辅酶A水平受到严格调控，并会根据包括营养状态和糖尿病在内的不同条件而变化。最近的研究揭示了这种辅因子控制关键代谢途径输出的能力。辅酶A的调节对于维持代谢灵活性和葡萄糖稳态很重要。
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本文引用的文献
1
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Diabetologia. 2014 Jul;57(7):1466-75. doi: 10.1007/s00125-014-3245-5. Epub 2014 Apr 30.
2
Malonyl-CoA: the regulator of fatty acid synthesis and oxidation.丙二酰辅酶 A：脂肪酸合成与氧化的调节物。
J Clin Invest. 2012 Jun;122(6):1958-9. doi: 10.1172/jci63967.
3
Germline deletion of pantothenate kinases 1 and 2 reveals the key roles for CoA in postnatal metabolism.胚系敲除泛酸激酶 1 和 2 揭示了 CoA 在出生后代谢中的关键作用。
PLoS One. 2012;7(7):e40871. doi: 10.1371/journal.pone.0040871. Epub 2012 Jul 17.
4
Enhancing liver mitochondrial fatty acid oxidation capacity in obese mice improves insulin sensitivity independently of hepatic steatosis.增强肥胖小鼠肝脏线粒体脂肪酸氧化能力可改善胰岛素敏感性，而不依赖于肝脂肪变性。
J Hepatol. 2012 Mar;56(3):632-9. doi: 10.1016/j.jhep.2011.10.008. Epub 2011 Oct 25.
5
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EMBO Mol Med. 2011 Dec;3(12):755-66. doi: 10.1002/emmm.201100180. Epub 2011 Oct 14.
6
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8
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Hepatology. 2011 Mar;53(3):821-32. doi: 10.1002/hep.24140. Epub 2011 Feb 11.
9
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Biochem Biophys Res Commun. 2011 Feb 4;405(1):64-7. doi: 10.1016/j.bbrc.2010.12.126. Epub 2011 Jan 5.
10
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