Vandorpe G, Bollen M, Van Herck E, Bouillon R, Stalmans W
Afdeling Biochemie, Faculteit Geneeskunde, Katholieke Universiteit Leuven, Belgium.
FEBS Lett. 1992 Sep 7;309(2):209-12. doi: 10.1016/0014-5793(92)81096-5.
Na3VO4 (6.5 mumol/100 g rat weight), co-injected with a trace amount of [14C]glucose, increased within 15 min the incorporation of radiolabel in diaphragmal glycogen. After 2 h the vanadate-induced increases were 12-fold in the diaphragm and 7-8-fold in heart and liver. In contrast, when added to isolated diaphragms for up to 1 h, vanadate (0.1-5 mM) had no effect on the synthesis of glycogen from 5 mM glucose. In search of a putative mediator of vanadate's action in vivo, insulin and the insulin-like growth factors (IGFs) were considered. Their plasma concentration was not affected by vanadate treatment. In isolated diaphragms, 1 mM vanadate did not potentiate insulin-induced glycogen synthesis, but it caused a several-fold increase in glycogen synthesis in the presence of concentrations of IGF-I which, alone, had no effect. A similar synergism occurred between vanadate and IGF-II. We propose that the glycogenic action of vanadate in vivo, at least in some tissues, involves a potentiation of the action of IGF-I.
将6.5微摩尔/100克大鼠体重的偏钒酸钠与微量的[14C]葡萄糖共同注射后,15分钟内膈膜糖原中放射性标记物的掺入量增加。2小时后,钒酸盐诱导的增加在膈膜中为12倍,在心脏和肝脏中为7至8倍。相比之下,当将钒酸盐(0.1至5毫摩尔)添加到分离的膈膜中长达1小时时,钒酸盐对由5毫摩尔葡萄糖合成糖原没有影响。为了寻找钒酸盐在体内作用的假定介质,考虑了胰岛素和胰岛素样生长因子(IGF)。它们的血浆浓度不受钒酸盐处理的影响。在分离的膈膜中,1毫摩尔钒酸盐不会增强胰岛素诱导的糖原合成,但在单独无作用的IGF-I浓度存在时,它会使糖原合成增加几倍。钒酸盐和IGF-II之间也出现了类似的协同作用。我们提出,钒酸盐在体内的糖原生成作用,至少在某些组织中,涉及增强IGF-I的作用。