胰抑制素在分离的大鼠肝细胞中的糖原分解作用是由一种不依赖环磷酸腺苷的钙依赖性机制介导的。
Glycogenolytic effect of pancreastatin in isolated rat hepatocytes is mediated by a cyclic-AMP-independent Ca(2+)-dependent mechanism.
作者信息
Sánchez V, Lucas M, Calvo J R, Goberna R
机构信息
Department of Medical Biochemistry and Molecular Biology, Medical School, University of Sevilla, Spain.
出版信息
Biochem J. 1992 Jun 15;284 ( Pt 3)(Pt 3):659-62. doi: 10.1042/bj2840659.
Abstract
We have studied the effect of pig pancreastatin on glucose and lactate production in freshly isolated rat hepatocytes. Pancreastatin stimulated the rate of glucose output, whereas, in contrast with glucagon, it failed to modify the rate of lactate production. The effective concentration of pancreastatin was in the range 0.1-100 nM, with half-maximal rate close to 1 nM. The ability of pancreastatin to increase glucose output was abolished by chelation of the calcium in the medium. By itself, pancreastatin did not increase cyclic AMP (cAMP) levels and had no influence on cAMP levels in glucagon-stimulated hepatocytes. Our results point out a possible role of pancreastatin in glycogenolysis. This appears to be mediated by a cAMP-independent Ca(2+)-dependent mechanism.
摘要
我们研究了猪胰抑制素对新鲜分离的大鼠肝细胞中葡萄糖和乳酸生成的影响。胰抑制素刺激了葡萄糖输出速率，然而，与胰高血糖素相反，它未能改变乳酸生成速率。胰抑制素的有效浓度范围为0.1 - 100 nM，半数最大速率接近1 nM。通过螯合培养基中的钙，胰抑制素增加葡萄糖输出的能力被消除。胰抑制素本身不会增加环磷酸腺苷（cAMP）水平，并且对胰高血糖素刺激的肝细胞中的cAMP水平没有影响。我们的结果指出了胰抑制素在糖原分解中可能发挥的作用。这似乎是由一种不依赖cAMP的、依赖Ca(2+)的机制介导的。
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