Wititsuwannakul D, Kim K H
J Biol Chem. 1977 Nov 10;252(21):7812-7.
Palmityl-CoA inhibits free liver glycogen synthase; the concentration required for half-maximum inhibition is 3 to 4 micrometer. Almost complete inhibition was observed at 50 micrometer. Palmityl-CoA inhibition is associated with dissociation of the tetrameric enzyme into monomers, and binding of palmityl-CoA to the monomers. Glycogen-bound enzyme is also inhibited by palmityl-CoA, resulting in dissociation of the enzyme into monomers and concomitant release of the enzyme from the primer glycogen. Palmityl-CoA inhibition of the enzyme is partially reversed by the glycogen synthase activator, glucose-6-P, whereas sodium lauryl sulfate-inhibited enzyme is not reactivated by glucose-6-P. Sodium lauryl sulfate inhibition results in the dissociation of the tetramer into the monomers. Bovine serum albumin and cyclodextrin can prevent palmityl-CoA inhibition only when they are added prior to palmityl-CoA addition. The possible physiological role of palmityl-CoA in glucose homeostasis is discussed.
棕榈酰辅酶A抑制游离肝糖原合酶;半最大抑制所需浓度为3至4微摩尔。在50微摩尔时观察到几乎完全抑制。棕榈酰辅酶A抑制与四聚体酶解离成单体以及棕榈酰辅酶A与单体结合有关。与糖原结合的酶也受到棕榈酰辅酶A的抑制,导致酶解离成单体并同时从引物糖原中释放出来。糖原合酶激活剂葡萄糖-6-磷酸可部分逆转棕榈酰辅酶A对该酶的抑制作用,而十二烷基硫酸钠抑制的酶不能被葡萄糖-6-磷酸重新激活。十二烷基硫酸钠抑制导致四聚体解离成单体。牛血清白蛋白和环糊精只有在棕榈酰辅酶A添加之前添加才能防止其抑制作用。文中讨论了棕榈酰辅酶A在葡萄糖稳态中的可能生理作用。