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正常及肝硬化大鼠肝脏在由葡萄糖或果糖合成糖原过程中糖原合酶和糖原磷酸化酶的活性

Activity of glycogen synthase and glycogen phosphorylase in normal and cirrhotic rat liver during glycogen synthesis from glucose or fructose.

作者信息

Bezborodkina Natalia N, Chestnova Anna Yu, Okovity Sergey V, Kudryavtsev Boris N

机构信息

Laboratory of Cellular Pathology, Institute of Cytology, Russian Academy of Sciences, St. Petersburg, Russia.

Laboratory of Cellular Pathology, Institute of Cytology, Russian Academy of Sciences, St. Petersburg, Russia.

出版信息

Exp Toxicol Pathol. 2014 Mar;66(2-3):147-54. doi: 10.1016/j.etp.2013.12.001. Epub 2013 Dec 25.

Abstract

Cirrhotic patients often demonstrate glucose intolerance, one of the possible causes being a decreased glycogen-synthesizing capacity of the liver. At the same time, information about the rates of glycogen synthesis in the cirrhotic liver is scanty and contradictory. We studied the dynamics of glycogen accumulation and the activity of glycogen synthase (GS) and glycogen phosphorylase (GP) in the course of 120min after per os administration of glucose or fructose to fasted rats with CCl4-cirrhosis or fasted normal rats. Blood serum and liver pieces were sampled for examinations. In the normal rat liver administration of glucose/fructose initiated a fast accumulation of glycogen, while in the cirrhotic liver glycogen was accumulated with a 20min delay and at a lower rate. In the normal liver GS activity rose sharply and GPa activity dropped in the beginning of glycogen synthesis, but 60min later a high synthesis rate was sustained at the background of a high GS and GPa activity. Contrariwise, in the cirrhotic liver glycogen was accumulated at the background of a decreased GS activity and a low GPa activity. Refeeding with fructose resulted in a faster increase in the GS activity in both the normal and the cirrhotic liver than refeeding with glucose. To conclude, the rate of glycogen synthesis in the cirrhotic liver is lower than in the normal one, the difference being probably associated with a low GS activity.

摘要

肝硬化患者常表现出葡萄糖不耐受,其可能原因之一是肝脏糖原合成能力下降。与此同时,关于肝硬化肝脏中糖原合成速率的信息匮乏且相互矛盾。我们研究了给四氯化碳诱导肝硬化的禁食大鼠或禁食正常大鼠经口给予葡萄糖或果糖后120分钟内糖原积累的动态变化以及糖原合酶(GS)和糖原磷酸化酶(GP)的活性。采集血清和肝组织样本进行检测。在正常大鼠肝脏中,给予葡萄糖/果糖会引发糖原的快速积累,而在肝硬化肝脏中,糖原积累延迟20分钟且速率较低。在正常肝脏中,糖原合成开始时GS活性急剧上升,GP活性下降,但60分钟后,在高GS和高GP活性的背景下维持着高合成速率。相反,在肝硬化肝脏中,糖原是在GS活性降低和GP活性较低的背景下积累的。用果糖重新喂食导致正常肝脏和肝硬化肝脏中GS活性的增加都比用葡萄糖重新喂食更快。总之,肝硬化肝脏中糖原合成速率低于正常肝脏,这种差异可能与低GS活性有关。

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