EFFECTS OF GLUCAGON AND N6O2'-DIBUTYRYLADENOSINE 3'-5'-CYCLIC MONOPHOSPHATE ON CALCIUM-TRANSPORT IN ISOLATED RAT-LIVER MITOCHONDRIA
EFFECTS OF GLUCAGON AND N6O2'-DIBUTYRYLADENOSINE 3'-5'-CYCLIC MONOPHOSPHATE ON CALCIUM-TRANSPORT IN ISOLATED RAT-LIVER MITOCHONDRIA
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DOI：
10.1042/bj1760295
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发表时间：
1978-01-01
影响因子：
4.1
通讯作者：
BARRITT, GJ
中科院分区：
文献类型：
--
作者：
HUGHES, BP;BARRITT, GJ
胰升糖素对灌胃大鼠的影响注射或用Mortimore方法灌流喂饲高血糖素的大鼠的肝脏，在随后从肝脏分离的线粒体保留给定负荷的外源性钙离子的时间内，分别增加了15倍和5倍。N6O2‘-二丁酰环AMP也能诱导胰高血糖素的这种作用，环己酰亚胺完全阻断这种作用，起效较慢(15-60分钟)，在琥珀酸存在下，ADP刺激的氧利用率和钙转运速率可增加约20%。经胰高血糖素灌流的大鼠肝脏线粒体的内源性钙、镁和磷的浓度分别比对照组增加了50%、无显著变化和40%。给喂养的大鼠注射胰岛素或肾上腺素[肾上腺素]后，游离肝脏线粒体保持钙离子的时间分别增加了10倍和8倍。肝脏胰岛素灌流对线粒体钙滞留时间无影响。用高血糖素灌流饥饿大鼠的肝脏，或给饥饿大鼠注射高血糖素或胰岛素，分别增加了约2.5倍和15倍，这是分离的线粒体保持钙离子的时间。讨论了可能导致观察到的钙离子保留时间变化的机制。
Glucagon administration to fed rats by i.p. injection, or the perfusion of livers from fed rats with glucagon by the method of Mortimore was associated with increases of 15- and 5-fold respectively, in the time for which a given load of exogenous Ca2+ is retained by mitochondria subsequently isolated from the liver. This effect of glucagon was also induced by N6O2''-dibutyryl cyclic AMP, completely blocked by cycloheximide, relatively slow in onset (15-60 min) and associated with a stimulation of about 20% in the rates of ADP-stimulated O2 utilization and Ca2+ transport measured in the presence of succinate. Perfusion of livers with glucagon resulted in the isolation of mitochondria which showed a 50% increase, no significant change and a 40% increase in the concentrations of endogenous Ca, Mg and Pi, respectively, when compared with mitochondria isolated from control perfused livers. The administration of insulin or adrenaline [epinephrine] to fed rats induced increases of 10- and 8-fold respectively, in the time for which Ca2+ is retained by isolated liver mitochondria. Perfusion of livers with insulin had no effect on mitochondrial Ca2+ retention time. The perfusion of livers from starved rats with glucagon, or the administration of either glucagon or insulin to starved rats, increased by about 2.5- and 15-fold respectively, the time for which isolated mitochondrial retain Ca2+. Mechanisms which may be responsible for the observed alterations in Ca2+-retention time are discussed.