Hughes B P, Barritt G J
Horm Metab Res. 1984 Oct;16(10):516-20. doi: 10.1055/s-2007-1014838.
Exposure of isolated hepatocytes to glucagon for 45 min caused a 2.5-fold increase in the time (Ca2+ retention time) for which mitochondria subsequently isolated from the cells retained a load of exogenous Ca2+ before its spontaneous release. Half maximal effect of glucagon was observed at a concentration of 0.6 nM. An increase in the Ca2+ retention time was observed after 30 but not 15 min exposure of cells to the hormone. Incubation of hepatocytes with dexamethasone, epinephrine, vasopressin, dibutyryl cyclic AMP or 8-bromo cyclic GMP also induced an increase in mitochondrial Ca2+ retention time. The effect of glucagon was associated with an increase in cellular cyclic AMP and was inhibited by puromycin, cycloheximide and cordycepin, but not by actinomycin D or chloramphenicol. Puromycin caused only a small inhibition of the stimulation by glucagon of mitochondrial pyruvate carboxylation. It is concluded that the effects of glucagon on mitochondrial Ca2+ retention require nuclear DNA-directed protein synthesis and differ, in this respect, from the rapid-onset effects of the hormone on other mitochondrial properties, including pyruvate carboxylation.
将分离的肝细胞暴露于胰高血糖素45分钟，会使随后从细胞中分离出的线粒体在其自发释放外源Ca2+之前保留Ca2+负荷的时间（Ca2+保留时间）增加2.5倍。在浓度为0.6 nM时观察到胰高血糖素的半数最大效应。细胞暴露于该激素30分钟后观察到Ca2+保留时间增加，但15分钟后未观察到。用 dexamethasone、肾上腺素、血管加压素、二丁酰环磷酸腺苷或8-溴环磷酸鸟苷孵育肝细胞也会导致线粒体Ca2+保留时间增加。胰高血糖素的作用与细胞内环磷酸腺苷的增加有关，并被嘌呤霉素、放线菌酮和冬虫夏草素抑制，但不被放线菌素D或氯霉素抑制。嘌呤霉素仅对胰高血糖素刺激线粒体丙酮酸羧化有轻微抑制作用。结论是，胰高血糖素对线粒体Ca2+保留的作用需要核DNA指导的蛋白质合成，在这方面，与该激素对其他线粒体特性（包括丙酮酸羧化）的快速起效作用不同。
