Schofield P S, Kirk C J, Sugden M C
Biochem Int. 1984 Nov;9(5):611-20.
Vasopressin, angiotensin II and the catecholamines decreased ketogenesis from oleate but increased ketogenesis from butyrate in hepatocytes from fed rats. The hormones increase CO2 production from both oleate and butyrate. It is suggested that whereas the mitochondrial uptake of butyrate is linked to its rate of oxidation, that of oleate is independent of its intramitochondrial metabolism, and consequently the oxidation of oleate to CO2 occurs at the expense of ketogenesis. Effects of the hormones on ketogenesis from oleate or butyrate were not observed after pre-treatment of the hepatocytes with dibutyryl cyclic AMP for 1 hour. The insensitivity of ketogenesis to the hormones after this treatment (which mimics the effects of acute carbohydrate deprivation in vivo) questions the physiological significance of hormonal regulation of ketogenesis other than at the onset of starvation.
血管升压素、血管紧张素II和儿茶酚胺可减少喂食大鼠肝细胞中油酸生成酮体的过程,但会增加丁酸生成酮体的过程。这些激素会增加油酸和丁酸的二氧化碳生成量。有人提出,虽然丁酸的线粒体摄取与其氧化速率相关,但油酸的摄取与其线粒体内代谢无关,因此油酸氧化为二氧化碳是以酮体生成的减少为代价的。在用二丁酰环磷酸腺苷预处理肝细胞1小时后,未观察到这些激素对油酸或丁酸生成酮体的影响。这种处理(模拟体内急性碳水化合物缺乏的影响)后酮体生成对激素不敏感,这对饥饿开始以外的激素对酮体生成调节的生理意义提出了质疑。