Balaban R S, Blum J J
Am J Physiol. 1982 Mar;242(3):C172-7. doi: 10.1152/ajpcell.1982.242.3.C172.
Hepatocytes isolated from fasted male rats were incubated with a mixture of glucose, ribose, mannose, glycerol, and acetate and then treated with vasopressin (ADH), glucagon, or vasoactive intestinal polypeptide (VIP). Each of these hormones causes a rapid transient increase in the fluorescence signal arising from NADH and a sustained increase in the rate of metabolic oxygen consumption (QO2). The NADH transient was largest in response to glucagon, followed by ADH and VIP, respectively. For each hormone the responses were prevented by addition of a calcium-chelating agent. These results show that a transient, Ca2+-dependent redox shift in NADH and stimulation of QO2, perhaps resulting from an increase in the rate of delivery of reducing equivalents to the mitochondrion, occur early in the sequence of events by which several hormones that increase gluconeogenesis act.
从禁食的雄性大鼠中分离出的肝细胞，用葡萄糖、核糖、甘露糖、甘油和乙酸盐的混合物进行孵育，然后用血管加压素（抗利尿激素）、胰高血糖素或血管活性肠肽（VIP）进行处理。这些激素中的每一种都会使由NADH产生的荧光信号迅速短暂增加，并使代谢氧消耗率（QO2）持续增加。NADH的短暂变化对胰高血糖素的反应最大，其次分别是对血管加压素和血管活性肠肽的反应。对于每种激素，添加钙螯合剂可阻止其反应。这些结果表明，在几种促进糖异生的激素发挥作用的事件序列早期，会发生NADH中短暂的、Ca2+依赖性的氧化还原变化以及QO2的刺激，这可能是由于还原当量向线粒体的输送速率增加所致。
