Fournier P A, Guderley H
Département de Biologie, Université Laval, Ste-Foy, Quebec, Canada.
Am J Physiol. 1992 Feb;262(2 Pt 2):R245-54. doi: 10.1152/ajpregu.1992.262.2.R245.
Although the ability of isolated frog muscle to synthesize glycogen from lactate has long been known, it has never been demonstrated that this metabolic activity occurs in the intact frog. Our results clearly indicate that lactate glycogenesis in frog muscle occurs to a significant extent in vivo. During recovery from strenuous exercise, most of the lactate accumulated by frogs seems to be recycled into muscle glycogen because the lactate that disappears during recovery could account nearly stoichiometrically for the glycogen that accumulates in muscle. Furthermore, the decrease in body lactate and the increase in muscle glycogen follow corresponding time courses, suggesting a precursor-product relationship between lactate and glycogen. During recovery from intense exercise, hepatectomized and normal frogs have nearly identical extents of lactate elimination and glycogen synthesis. This suggests that muscle is the main tissue responsible for the recycling of lactate into muscle glycogen and that liver plays a negligible role in lactate disposal. The negligible hepatic contribution to lactate recycling results in part from the liver's incapacity to produce glucose from lactate. In support of this proposition, we show that frog liver perfused in vitro is unable to incorporate any detectable labeled lactate into glucose despite its excellent physiological integrity. Changes in dietary status, training state, season at which the experiments were done, exercise status, and composition of the perfusion media (pH, hormonal composition, physiological saline vs. culture medium) did not give rise to lactate gluconeogenesis. Because frog liver contains all the regulatory enzymes of the gluconeogenic pathway, its inability to synthesize glucose from lactate is not due to an absence of pyruvate carboxylase. A limited ability for lactate uptake may explain why frog liver cannot produce glucose from lactate.
虽然离体青蛙肌肉从乳酸合成糖原的能力早已为人所知,但从未有人证明这种代谢活动在完整的青蛙体内发生。我们的结果清楚地表明,青蛙肌肉中的乳酸糖异生在体内有显著程度的发生。在剧烈运动后的恢复过程中,青蛙积累的大部分乳酸似乎被循环利用形成肌肉糖原,因为恢复过程中消失的乳酸几乎能按化学计量关系解释肌肉中积累的糖原。此外,体内乳酸的减少和肌肉糖原的增加遵循相应的时间进程,表明乳酸和糖原之间存在前体 - 产物关系。在剧烈运动后的恢复过程中,肝切除的青蛙和正常青蛙的乳酸消除和糖原合成程度几乎相同。这表明肌肉是负责将乳酸循环利用形成肌肉糖原的主要组织,而肝脏在乳酸处理中起的作用可忽略不计。肝脏对乳酸循环利用的贡献可忽略不计部分是因为肝脏无法从乳酸产生葡萄糖。为支持这一观点,我们表明,尽管体外灌注的青蛙肝脏生理完整性良好,但仍无法将任何可检测到的标记乳酸掺入葡萄糖。饮食状态、训练状态、实验进行的季节、运动状态以及灌注介质的成分(pH值、激素组成、生理盐水与培养基)的变化均未导致乳酸糖异生。由于青蛙肝脏含有糖异生途径的所有调节酶,其无法从乳酸合成葡萄糖并非由于缺乏丙酮酸羧化酶。有限的乳酸摄取能力可能解释了青蛙肝脏为何无法从乳酸产生葡萄糖。