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饥饿对小鼠胍基化合物代谢的影响。

Effects of starvation on guanidino compound metabolism in mice.

作者信息

Shindo S, Watanabe Y, Mori A

出版信息

Res Commun Chem Pathol Pharmacol. 1986 Oct;54(1):73-85.

PMID:3797807
Abstract

Arginine levels diminished markedly in the plasma during starvation, suggesting that plasma arginine level principally depends on food intake. Organ arginine levels were relatively stable except for an extraordinary increase in the pancreas at 96 h. Guanidinoacetic acid decreased dramatically in all organs within 24 h and low level were maintained thereafter, except for the brain (and plasma). Creatinine output increased after 24h of starvation. The increased creatinine output recovered to the control level after 48 h. A small but significant amount of guanidinosuccinic acid was detected in the normal liver and decreased transitorily after 24 h and increased after 48 h starvation, corresponded with an increased output in the 24 h urine excretion. Otherwise this decrease may be related to the transitory decrease in arginine level in the liver over the same time course. Methylguanidine in the muscle and gamma-guanidinobutyric acid in the liver decreased gradually during starvation. These results suggest that guanidino compounds levels in mouse organs are principally dependent on exogenous nitrogen.

摘要

饥饿期间血浆中的精氨酸水平显著降低,这表明血浆精氨酸水平主要取决于食物摄入量。除了在96小时时胰腺中出现异常增加外,器官中的精氨酸水平相对稳定。胍基乙酸在24小时内所有器官中均急剧下降,此后维持在低水平,但大脑(和血浆)除外。饥饿24小时后肌酐排出量增加。饥饿48小时后,增加的肌酐排出量恢复到对照水平。在正常肝脏中检测到少量但显著量的胍基琥珀酸,饥饿24小时后短暂下降,48小时后增加,这与24小时尿液排泄量的增加相对应。否则,这种下降可能与同一时间进程中肝脏中精氨酸水平的短暂下降有关。饥饿期间肌肉中的甲基胍和肝脏中的γ-胍基丁酸逐渐减少。这些结果表明,小鼠器官中胍基化合物的水平主要依赖于外源性氮。

相似文献

1
Effects of starvation on guanidino compound metabolism in mice.饥饿对小鼠胍基化合物代谢的影响。
Res Commun Chem Pathol Pharmacol. 1986 Oct;54(1):73-85.
2
Guanidino compounds that are increased in cerebrospinal fluid and brain of uremic patients inhibit GABA and glycine responses on mouse neurons in cell culture.在尿毒症患者的脑脊液和大脑中含量增加的胍基化合物会抑制细胞培养中小鼠神经元对γ-氨基丁酸(GABA)和甘氨酸的反应。
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