Cleland P J, Appleby G J, Rattigan S, Clark M G
Department of Biochemistry, University of Tasmania, Hobart, Australia.
J Biol Chem. 1989 Oct 25;264(30):17704-11.
Contraction-induced translocation of protein kinase C (Richter E.A., Cleland, P.J.F., Rattigan, S., and Clark, M.G. (1987) FEBS Lett. 217, 232-236) implies a role for this enzyme in muscle contraction or the associated metabolic adjustments. In the present study, this role is further examined particularly in relation to changes in glucose transport. Electrical stimulation of the sciatic nerve of the anesthetized rat in vivo led to a time-dependent translocation of protein kinase C and a 2-fold increase in the concentrations of both diacylglycerol and phosphatidic acid. Maximum values for the latter were reached at 2 min and preceded the maximum translocation of protein kinase C (10 min). Stimulation of muscles in vitro increased the rate of glucose transport, but this required 20 min to reach maximum. There was no reversal of translocation or decrease in the concentrations of diacylglycerol and phosphatidic acid even after 30 min of rest following a 5-min period of stimulation in vivo. Translocation was not influenced by variations in applied load at maximal fiber recruitment but was dependent on the frequency of nontetanic stimuli, reaching a maximum at 4 Hz. The relationship between protein kinase C and glucose transport was also explored by varying the number of tetanic stimuli. Whereas only one train of stimuli (200 ms, 100 Hz) was required for maximal effects on protein kinase C, diacylglycerol, and phosphatidic acid, more than 35 trains of stimuli were required to activate glucose transport. It is concluded that the production of diacylglycerol and the translocation of protein kinase C may be causally related. However, if the translocated protein kinase C is involved in the activation of glucose transport during muscle contractions, an accumulated exposure to Ca2+, resulting from multiple contractions, would appear to be necessary.
收缩诱导的蛋白激酶C易位（里希特·E.A.、克莱兰、P.J.F.、拉蒂根、S.以及克拉克·M.G.（1987年）《欧洲生物化学学会联合会快报》217，232 - 236）表明该酶在肌肉收缩或相关代谢调节中起作用。在本研究中，进一步研究了这一作用，特别是与葡萄糖转运变化的关系。对麻醉大鼠的坐骨神经进行体内电刺激导致蛋白激酶C随时间易位，二酰基甘油和磷脂酸的浓度增加了两倍。后者的最大值在2分钟时达到，先于蛋白激酶C的最大易位（10分钟）。体外刺激肌肉增加了葡萄糖转运速率，但这需要20分钟才能达到最大值。在体内刺激5分钟后即使休息30分钟，易位也没有逆转，二酰基甘油和磷脂酸的浓度也没有降低。在最大纤维募集时，易位不受施加负荷变化的影响，但取决于非强直刺激的频率，在4赫兹时达到最大值。还通过改变强直刺激的次数来探索蛋白激酶C与葡萄糖转运之间的关系。虽然对蛋白激酶C、二酰基甘油和磷脂酸产生最大影响仅需要一列刺激（200毫秒，100赫兹），但激活葡萄糖转运则需要超过35列刺激。得出的结论是，二酰基甘油的产生与蛋白激酶C的易位可能存在因果关系。然而，如果易位的蛋白激酶C参与肌肉收缩期间葡萄糖转运的激活，那么多次收缩导致的Ca2 +积累暴露似乎是必要的。
