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猪蛔虫肌肉中肌肉活动与糖原代谢的相关性

Correlation of muscle activity with glycogen metabolism in muscle of Ascaris suum.

作者信息

Donahue M J, Yacoub N J, Harris B G

出版信息

Am J Physiol. 1982 May;242(5):R514-21. doi: 10.1152/ajpregu.1982.242.5.R514.

Abstract

Isolated muscle segments from the parasitic roundworm Ascaris suum were shown to contract when perfused with acetylcholine (ACh). The muscle responded to ACh concentrations of 1 microM and was maximally contracted at 50 microM ACh. In fed muscle segments perfused with saturating levels of ACh the glycogen synthase Ka values for glucose 6-phosphate increased from 0.5 to 0.95 mM. In starved segments stimulated by ACh, the muscle utilized glycogen at a rate that was 1.41 micrograms.min-1.g tissue-1 greater than the saline-perfused controls. The cyclic AMP (cAMP) levels remained relatively constant at 0.34 +/- 0.08 nmol/g muscle during perfusion with ACh. Contraction in the muscle could be inhibited in a dose-dependent manner by gamma-aminobutyric acid (GABA). The presence of GABA in starved muscle prevented the decrease in Ka values and phosphorylase activity ratios brought about by glucose. Perfusion of GABA did not change cAMP levels in the muscle. Starved muscle perfused with GABA utilized glycogen at a rate that was 0.41 microgram.min-1.g-1 greater than saline-perfused controls. The results indicated that muscle contraction could be elicited by ACh, and that the energy for this process was derived from endogenous glycogen stores, which were depleted during contraction. Muscle contraction was also correlated with inactivation of glycogen synthase and activation of phosphorylase. These processes appeared to function via a cAMP-independent mechanisms.

摘要

研究表明,来自寄生蛔虫猪蛔虫的离体肌肉段在灌注乙酰胆碱(ACh)时会收缩。该肌肉对1微摩尔/升的ACh浓度有反应,在50微摩尔/升的ACh浓度下达到最大收缩。在用饱和水平的ACh灌注的喂食肌肉段中,葡萄糖6-磷酸的糖原合酶Ka值从0.5毫摩尔/升增加到0.95毫摩尔/升。在由ACh刺激的饥饿段中,肌肉利用糖原的速率比用生理盐水灌注的对照高1.41微克·分钟⁻¹·克组织⁻¹。在灌注ACh期间,环磷酸腺苷(cAMP)水平在0.34±0.08纳摩尔/克肌肉中保持相对恒定。肌肉收缩可被γ-氨基丁酸(GABA)以剂量依赖的方式抑制。饥饿肌肉中GABA的存在可防止由葡萄糖引起的Ka值和磷酸化酶活性比的降低。灌注GABA不会改变肌肉中的cAMP水平。用GABA灌注的饥饿肌肉利用糖原的速率比用生理盐水灌注的对照高0.41微克·分钟⁻¹·克⁻¹。结果表明,ACh可引发肌肉收缩,并且该过程的能量来自内源性糖原储备,其在收缩过程中被耗尽。肌肉收缩还与糖原合酶的失活和磷酸化酶的激活相关。这些过程似乎通过不依赖cAMP的机制起作用。

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