FATTY-ACIDS AS ACUTE REGULATORS OF THE PROTON CONDUCTANCE OF HAMSTER BROWN-FAT MITOCHONDRIA
FATTY-ACIDS AS ACUTE REGULATORS OF THE PROTON CONDUCTANCE OF HAMSTER BROWN-FAT MITOCHONDRIA
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DOI：
10.1111/j.1432-1033.1982.tb07060.x
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发表时间：
1982-01-01
期刊：
影响因子：
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通讯作者：
NICHOLLS, DG
中科院分区：
文献类型：
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作者：
LOCKE, RM;RIAL, E;NICHOLLS, DG
可能的机制评估了仓鼠棕色脂肪线粒体质子传导途径的急性调节，这是活跃的非寒战产热。分离的线粒体在接近非产热状态的条件下孵育，持续监测脂肪酸或酰基衍生物对呼吸、膜电位和膜质子电导的影响。脂肪酸增加质子电导，没有可检测的阈值浓度，允许生成的酰基肉碱被迅速氧化。去极化和呼吸增加的程度是输注速率的函数。立即停止输注，电导降低，线粒体复极，呼吸恢复到初始速率。在积累了高浓度的酰基辅酶a和酰基肉碱后，输注这些衍生物仅引起轻微的去极化或呼吸增加。任何降低脂肪酸转化为酰基辅酶a速率的因素都会增强电导的增加。酰基辅酶a对氯离子渗透性的影响不是棕色脂肪线粒体所特有的。注入大鼠肝脏线粒体孵育的脂肪酸产生了少量的电导增加，与酰基辅酶a或酰基肉碱相当。脂肪酸是质子电导最合理的急性调节器。讨论了与棕色脂肪特异性32,000-MW蛋白的关系。
Possible mechanisms are evaluated for the acute regulation of the hamster brown-fat mitochondrial proton-conductance pathway which is active during non-shivering thermogenesis. Isolated mitochondria are incubated under conditions designed to approximate to the non-thermogenic state, and the effect of the steady infusion of fatty acids or acyl derivatives on respiration, membrane potential and membrane proton conductance is monitored continuously. Fatty acids increase the proton conductance with no detectable threshold concentration, allowing the generated acylcarnitine to be rapidly oxidized. The extent of depolarization and of respiratory increase is a function of the rate of infusion. Immediately infusion is terminated the conductance decreases, the mitochondria repolarize and respiration returns to the initial rate. Infusion of acyl-CoA and acylcarnitine cause only a slight depolarization or respiratory increase after high concentrations of these derivatives have accumulated. Any factor which decreases the rate of conversion of fatty acid to acyl-CoA potentiates the conductance increase. An effect of acyl-CoA on chloride permeability is not specific to brown-fat mitochondria. Fatty acids infused into rat liver mitochondrial incubations produced a small conductance increase, comparable to that of acyl-CoA or acylcarnitine. Fatty acids are the most plausible acute regulators of the proton conductance. The relation to the brown-fat-specific 32,000-MW protein is discussed.