Kimura S, Suzaki T, Kobayashi S, Abe K, Ogata E
Biochem Biophys Res Commun. 1984 Feb 29;119(1):212-9. doi: 10.1016/0006-291x(84)91640-1.
The effects of glucagon on the respiratory function of mitochondria in situ were investigated in isolated perfused rat liver. Glucagon at the concentrations higher than 20 pM and cyclic AMP (75 microM) stimulated hepatic respiration, and shifted the redox state of pyridine nucleotide (NADH/NAD) in mitochondria in situ to a more reduced state as judged by organ fluorometry and beta-hydroxybutyrate/acetoacetate ratio. The organ spectrophotometric study revealed that glucagon and cyclic AMP induced the reduction of redox states of cytochromes a(a3), b and c+c1. Atractyloside (4 micrograms/ml) abolished the effects of glucagon on these parameters and gluconeogenesis from lactate. These observations suggest that glucagon increases the availability of substrates for mitochondrial respiration, and this alteration in mitochondrial function is crucial in enhancing gluconeogenesis.
在离体灌注大鼠肝脏中研究了胰高血糖素对原位线粒体呼吸功能的影响。浓度高于20 pM的胰高血糖素和环磷酸腺苷（75 microM）刺激肝脏呼吸，并通过器官荧光测定法和β-羟基丁酸酯/乙酰乙酸酯比率判断，使原位线粒体中吡啶核苷酸（NADH/NAD）的氧化还原状态转变为更还原的状态。器官分光光度研究表明，胰高血糖素和环磷酸腺苷诱导细胞色素a（a3）、b以及c + c1的氧化还原状态降低。苍术苷（4微克/毫升）消除了胰高血糖素对这些参数以及从乳酸生成葡萄糖的影响。这些观察结果表明，胰高血糖素增加了线粒体呼吸底物的可用性，并且线粒体功能的这种改变对于增强糖异生至关重要。
