胰高血糖素处理以及处女鼠和泌乳期大鼠饥饿对离体肝线粒体中辛酰-L-肉碱和辛酸氧化速率的影响。

The effect of glucagon treatment and starvation of virgin and lactating rats on the rates of oxidation of octanoyl-L-carnitine and octanoate by isolated liver mitochondria.

作者信息

Zammit V A

出版信息

Biochem J. 1980 Aug 15;190(2):293-300. doi: 10.1042/bj1900293.

DOI:10.1042/bj1900293

PMID:7470052

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1162093/

Abstract

Oxygen-consumption rates owing to oxidation of octanoate or octanoylcarnitine by isolated mitochondria from livers of fed, starved and glucagon-treated virgin or 12-day-lactating animals were measured under State-3 and State-4 conditions, in the presence or absence of l-malate and inhibitors of tricarboxylic acid-cycle activity (malonate and fluorocitrate). 2. Mitochondria from fed lactating animals had a slightly lower rate of octanoylcarnitine oxidation than did those of fed virgin animals, whereas the rates of octanoate oxidation were unaffected. 3. Starvation of virgin animals for 24h or 48h resulted in a large (70-100%) increase in mitochondrial octanoylcarnitine oxidation; rates of octanoate oxidation were either unaffected (24 and 48h starvation in the absence of malonate and fluorocitrate) or diminished by 30% (48h starvation in the presence of inhibitors). In lactating animals, 24h starvation resulted in a smaller increase in the rate of octanoylcarnitine oxidation than that obtained for mitochondria from virgin rats. 4. Glucagon treatment (by intra-abdominal injection) of fed virgin and lactating rats increased the rate of mitochondrial oxidation of both octanoylcarnitine and octanoate. Injection of glucagon into 48h-starved virgin rats did not increase further the already elevated rate of octanoylcarnitine oxidation, but reversed the inhibition of octanoate beta-oxidation observed for these mitochondria in the presence of malonate and fluorocitrate. 5. It is suggested that glucagon activates octanoylcarnitine oxidation by increasing the activity of the carnitine/acylcarnitine transport system [Parvin & Pande (1979) J. Biol. Chem.254, 5423-5429] and that the increase in octanoate oxidation by mitochondria from glucagon-treated animals is caused by the increased rate of ATP synthesis in these mitochondria. 6. The results are discussed in relation to the increased capacity of the liver to oxidize long-chain fatty acids and carnitine esters of medium-chain fatty acids under conditions characterized by increased ketogenesis.

摘要

在有或没有L-苹果酸以及三羧酸循环活性抑制剂（丙二酸和氟柠檬酸）存在的情况下，于状态3和状态4条件下，测定了来自喂食、饥饿以及用胰高血糖素处理的未生育或泌乳12天动物肝脏的分离线粒体对辛酸或辛酰肉碱的氧化耗氧率。2. 喂食的泌乳动物的线粒体对辛酰肉碱的氧化率略低于喂食的未生育动物的线粒体，而辛酸氧化率不受影响。3. 未生育动物饥饿24小时或48小时导致线粒体对辛酰肉碱的氧化大幅增加（70 - 100%）；辛酸氧化率要么不受影响（在没有丙二酸和氟柠檬酸的情况下饥饿24小时和48小时），要么降低30%（在有抑制剂存在的情况下饥饿48小时）。在泌乳动物中，饥饿24小时导致辛酰肉碱氧化率的增加幅度小于未生育大鼠线粒体的增加幅度。4. 用胰高血糖素（通过腹腔注射）处理喂食的未生育和泌乳大鼠，增加了线粒体对辛酰肉碱和辛酸的氧化率。向饥饿48小时的未生育大鼠注射胰高血糖素并没有进一步提高已经升高的辛酰肉碱氧化率，但逆转了在丙二酸和氟柠檬酸存在下这些线粒体对辛酸β氧化的抑制作用。5. 有人提出，胰高血糖素通过增加肉碱/酰基肉碱转运系统的活性来激活辛酰肉碱氧化[帕尔文和潘德（1979年）《生物化学杂志》254，5423 - 5429]，并且胰高血糖素处理动物的线粒体对辛酸氧化的增加是由这些线粒体中ATP合成速率的增加引起的。6. 结合在酮生成增加的条件下肝脏氧化长链脂肪酸和中链脂肪酸的肉碱酯的能力增强这一情况，对结果进行了讨论。