Ozawa K, Yamada T, Honjo I
Ann Surg. 1974 Nov;180(5):716-9. doi: 10.1097/00000658-197411000-00002.
The subcutaneous administration of insulin did not induce a significant effect on oxidative phosphorylation of the mitochondria from normal rat liver. However, in rats subjected to ligation of a branch of portal vein, the phosphorylative activity of the mitochondria from the ligated lobe deprived of portal blood fell rapidly and at 12 hours decreased to approximately 50% of nomal liver mitochondria. After the insulin administration, the phosphorylative activity of the mitochondria from ligated lobe was rapidly stimulated within 30 minutes, reached the maximal level of normal liver mitochondria at 2 hours (p < 0.005) and then fell to subnormal levels. The respiratory control ratio, state 3 respiration and P/O ratio remarkably increased in parallel with an increase of phosphorylative activity. The contents of respiratory enzymes making up ATP remained unchanged. Considering the previous report that a factor, which is capable of stimulating oxidative phosphorylation of the liver mitochondria, is present in portal blood, it is suggested that insulin may play an important role in the mechanism by which the portal blood controls mitochondrial metabolism.
皮下注射胰岛素对正常大鼠肝脏线粒体的氧化磷酸化没有显著影响。然而，在门静脉分支结扎的大鼠中，结扎叶缺乏门静脉血供的线粒体的磷酸化活性迅速下降，12小时时降至正常肝脏线粒体的约50%。注射胰岛素后，结扎叶线粒体的磷酸化活性在30分钟内迅速受到刺激，2小时时达到正常肝脏线粒体的最大水平（p<0.005），然后降至低于正常的水平。呼吸控制率、状态3呼吸和P/O比值随着磷酸化活性的增加而显著平行增加。构成ATP的呼吸酶含量保持不变。鉴于之前的报告表明门静脉血中存在一种能够刺激肝脏线粒体氧化磷酸化的因子，提示胰岛素可能在门静脉血控制线粒体代谢的机制中起重要作用。
