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无氧代谢、冬眠和夏眠中的代谢率降低及生化适应

Metabolic rate depression and biochemical adaptation in anaerobiosis, hibernation and estivation.

作者信息

Storey K B, Storey J M

机构信息

Institute of Biochemistry, Carleton University, Ottawa, Ontario, Canada.

出版信息

Q Rev Biol. 1990 Jun;65(2):145-74. doi: 10.1086/416717.

Abstract

For many animals, the best defense against harsh environmental conditions is an escape to a hypometabolic or dormant state. Facultative metabolic rate depression is the common adaptive strategy of anaerobiosis, hibernation, and estivation, as well as a number of other arrested states. By reducing metabolic rate by a factor ranging from 5 to 100 fold or more, animals gain a comparable extension of survival time that can support months or even years of dormancy. The present review focuses on the molecular control mechanisms that regulate and coordinate cellular metabolism for the transition into dormancy. These include reversible control over the activity state of enzymes via protein phosphorylation or dephosphorylation reactions, pathway regulation via the association or dissociation of particle-bound enzyme complexes, and fructose-2,6-bisphosphate regulation of the use of carbohydrate reserves for biosynthetic purposes. These mechanisms, their interactions, and the regulatory signals (e.g., second messenger molecules, pH) that coordinate them form a common molecular basis for metabolic depression in anoxia-tolerant vertebrates (goldfish, turtles) and invertebrates (marine molluscs), hibernation in small mammals, and estivation in land snails and terrestrial toads.

摘要

对于许多动物来说,抵御恶劣环境条件的最佳防御方式是进入低代谢或休眠状态。兼性代谢率降低是无氧呼吸、冬眠、夏眠以及许多其他静止状态的常见适应性策略。通过将代谢率降低5到100倍甚至更多,动物获得了相当的生存时间延长,这可以支持数月甚至数年的休眠。本综述重点关注调节和协调细胞代谢以进入休眠状态的分子控制机制。这些机制包括通过蛋白质磷酸化或去磷酸化反应对酶活性状态的可逆控制、通过颗粒结合酶复合物的缔合或解离进行的途径调节,以及果糖-2,6-二磷酸对用于生物合成目的的碳水化合物储备利用的调节。这些机制、它们之间的相互作用以及协调它们的调节信号(例如第二信使分子、pH值)构成了耐缺氧脊椎动物(金鱼、海龟)和无脊椎动物(海洋软体动物)代谢降低、小型哺乳动物冬眠以及陆地蜗牛和蟾蜍夏眠的共同分子基础。

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