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首页> 外文期刊>Life sciences >Acetylcholine affects rat liver metabolism via type 3 muscarinic receptors in hepatocytes.
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Acetylcholine affects rat liver metabolism via type 3 muscarinic receptors in hepatocytes.

机译：乙酰胆碱通过肝细胞中的3型毒蕈碱受体影响大鼠肝脏的代谢。

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摘要

Although the role of acetylcholine (Ach) in hepatic glucose metabolism is well elucidated, it is still unclear if it influences gluconeogenesis, glycogenolysis and high-energy phosphate metabolism, and if it does what the mechanisms of this influence are. Therefore, using isolated perfused rat liver as a model, we have studied the effect of Ach on oxygen consumption, synthesis of glucose from lactate and pyruvate, glycogen formation, mitochondrial oxidative phosphorylation and ATP-synthesis. We have established that effects of Ach on oxygen consumption depend on its concentration. When used at a concentration of 10(-7) M, Ach exerts maximum stimulatory effect, while its infusion at 10(-6) M causes a decrease of oxygen consumption by the liver. Moreover, when used at a concentration of 10(-6) M or 10(-7) M, Ach increases rates of glucose production from the gluconeogenic substrates lactate and pyruvate, leading to enhanced glycogen content in perfused liver. It was also shown that Ach possesses a stimulating effect on alanine and aspartate aminotransferases. As detected by 31P NMR spectroscopy, continuous liver perfusion with pyruvate and lactate in the presence of Ach leads to a significant decrease of ATP level, implying enhanced energy requirements for gluconeogenesis under these conditions. Elimination of the described effects of Ach by atropine, the antagonist of muscarinic receptors, and identification of the type 3 muscarinic receptors (m3) in isolated hepatocytes as well as in whole liver, imply that Ach may exert its effect on liver metabolism through m3 receptors.
机译：尽管乙酰胆碱（Ach）在肝葡萄糖代谢中的作用已得到很好的阐明，但仍不清楚它是否影响糖异生，糖原分解和高能磷酸盐代谢，以及它是否影响这种作用的机理。因此，以离体灌流大鼠肝脏为模型，我们研究了Ach对耗氧量，乳酸和丙酮酸合成葡萄糖，糖原形成，线粒体氧化磷酸化和ATP合成的影响。我们已经确定，Ach对耗氧量的影响取决于其浓度。当以10（-7）M的浓度使用时，Ach发挥最大的刺激作用，而以10（-6）M的浓度输注则会降低肝脏的耗氧量。此外，当以10（-6）M或10（-7）M的浓度使用时，Ach会增加从糖异生底物乳酸和丙酮酸产生的葡萄糖的速率，从而导致灌注肝脏中糖原含量的增加。还显示出Ach对丙氨酸和天冬氨酸转氨酶具有刺激作用。如通过31P NMR光谱检测到的，在Ach存在下用丙酮酸和乳酸连续进行肝脏灌注会导致ATP水平显着降低，这意味着在这些条件下糖异生的能量需求增加。消除了毒蕈碱受体的拮抗剂阿托品对Ach的影响，并鉴定了分离的肝细胞以及全肝中的3型毒蕈碱受体（m3），这意味着Ach可能通过m3受体发挥其对肝脏代谢的作用。

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