Locke R M, Rial E, Scott I D, Nicholls D G
Eur J Biochem. 1982 Dec 15;129(2):373-80. doi: 10.1111/j.1432-1033.1982.tb07060.x.
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 upon respiration, membrane potential and membrane proton conductance is monitored continuously. Fatty acids increase the proton conductance with no detectable threshold concentration, allowing the generated acyl carnitine 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 upon 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. It is concluded that fatty acids are the most plausible acute regulators of the proton conductance. The relation to the brown-fat-specific 32000-Mr protein is discussed.
研究了仓鼠棕色脂肪线粒体质子传导途径在非寒战产热过程中急性调节的可能机制。将分离的线粒体在接近非产热状态的条件下孵育，并持续监测脂肪酸或酰基衍生物的稳定输注对呼吸、膜电位和膜质子传导的影响。脂肪酸可增加质子传导，且无明显的阈值浓度，使生成的酰基肉碱能够快速氧化。去极化程度和呼吸增加程度是输注速率的函数。一旦输注终止，传导性降低，线粒体重新极化，呼吸恢复到初始速率。在高浓度的这些衍生物积累后，输注酰基辅酶A和酰基肉碱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传导性增加。酰基辅酶A对氯离子通透性的影响并非棕色脂肪线粒体所特有。注入大鼠肝脏线粒体孵育液中的脂肪酸会导致传导性小幅增加，与酰基辅酶A或酰基肉碱的情况相当。得出的结论是，脂肪酸是质子传导最合理的急性调节因子。文中还讨论了与棕色脂肪特异性32000-Mr蛋白的关系。
