Yamamoto T, Iwai M, Kimura S, Shimazu T
Department of Medical Biochemistry, Ehime University School of Medicine, Japan.
Eur J Biochem. 1995 Dec 1;234(2):466-71. doi: 10.1111/j.1432-1033.1995.466_b.x.
The regulatory mechanism of ketone-body output by the hepatic sympathetic nerves was studied in rat liver perfused in situ. Enrichment of the perfusion medium with 1 mM octanoate increased the basal ketone-body output from the liver up to 1.5 mumol.min-1.g liver-1. Under these conditions, electrical stimulation of the hepatic nerves (20 V, 20 Hz, 2 ms) decreased the output of both acetoacetate and beta-hydroxybutyrate, and was accompanied by an accumulation of beta-hydroxybutyrate in the liver. The effects of nerve stimulation were inhibited by the alpha 1-antagonist bunazosin (10 microM). However, noradrenaline, a typical sympathetic neurotransmitter, at a concentration of 1 microM decreased the output of acetoacetate but did not affect beta-hydroxybutyrate output. Prostaglandin F2 alpha at a concentration of 10 microM produced an effect similar to treatment with noradrenaline, without a decrease in beta-hydroxybutyrate output. ATP at 50 microM, however, decreased the output of both acetoacetate and beta-hydroxybutyrate and increased the tissue concentration of beta-hydroxybutyrate, mimicking the effect of nerve stimulation. Moreover, in the presence of 0.2 microM ATP, a concentration that produced neither metabolic nor hemodynamic changes, noradrenaline (1 microM) was shown to decrease the beta-hydroxybutyrate output. These results indicate the possible involvement of ATP in the action of hepatic sympathetic nerves on beta-hydroxybutyrate output from the liver, presumably through its interaction with noradrenaline.
在原位灌注的大鼠肝脏中研究了肝交感神经对酮体输出的调节机制。用1 mM辛酸富集灌注培养基可使肝脏的基础酮体输出增加至1.5 μmol·min⁻¹·g肝脏⁻¹。在这些条件下，电刺激肝神经（20 V，20 Hz，2 ms）可降低乙酰乙酸和β-羟基丁酸的输出，并伴有肝脏中β-羟基丁酸的积累。神经刺激的作用被α1拮抗剂布那唑嗪（10 μM）抑制。然而，典型的交感神经递质去甲肾上腺素在浓度为1 μM时可降低乙酰乙酸的输出，但不影响β-羟基丁酸的输出。浓度为10 μM的前列腺素F2α产生的作用与去甲肾上腺素处理相似，β-羟基丁酸的输出没有降低。然而，50 μM的ATP可降低乙酰乙酸和β-羟基丁酸的输出，并增加组织中β-羟基丁酸的浓度，模拟神经刺激的作用。此外，在0.2 μM ATP存在的情况下，该浓度既不产生代谢变化也不产生血流动力学变化，结果显示去甲肾上腺素（1 μM）可降低β-羟基丁酸的输出。这些结果表明，ATP可能参与肝交感神经对肝脏β-羟基丁酸输出的作用，可能是通过其与去甲肾上腺素的相互作用。
