Strieleman P J, Schalinske K L, Shrago E
J Biol Chem. 1985 Nov 5;260(25):13402-5.
The effect of fatty acids, palmitoyl-CoA, and N',N-dicyclohexylcarbodiimide on the ion conductance of the reconstituted brown adipose tissue mitochondria uncoupling protein was investigated. 1, 5, and 10 microM palmitic acid induced a specific, GDP inhibited, increase in proton conductance in proteoliposomes containing the uncoupling protein but not in proteoliposomes prepared with purified protein extracts of liver mitochondria. 10 microM oleic acid, like palmitic acid, increased proton conductance in proteoliposomes prepared with the uncoupling protein. Palmitoyl-CoA and caprylic acid had no effect on increasing proton conductance. Similar to the observation in mitochondria, there was no effect of palmitic acid on Cl-conductance, but unlike mitochondria its activation by palmitoyl-CoA or inhibition by N',N-dicyclohexylcarbodiimide was lost. The results, obtained in an isolated system, provide support for the contention that long chain fatty acids act as an acute physiological activator of the uncoupling protein.
研究了脂肪酸、棕榈酰辅酶A和N'，N-二环己基碳二亚胺对重组棕色脂肪组织线粒体解偶联蛋白离子电导的影响。1、5和10微摩尔的棕榈酸在含有解偶联蛋白的蛋白脂质体中诱导了一种特异性的、受GDP抑制的质子电导增加，但在用肝线粒体纯化蛋白提取物制备的蛋白脂质体中未观察到这种现象。10微摩尔的油酸与棕榈酸一样，增加了用解偶联蛋白制备的蛋白脂质体中的质子电导。棕榈酰辅酶A和辛酸对增加质子电导没有作用。与在线粒体中的观察结果相似，棕榈酸对氯离子电导没有影响，但与线粒体不同的是，其被棕榈酰辅酶A激活或被N'，N-二环己基碳二亚胺抑制的作用消失了。在分离系统中获得的结果支持了长链脂肪酸作为解偶联蛋白的急性生理激活剂的观点。
