RESUMEN

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.

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RESUMEN

PURPOSE: To investigate the accumulation of glycogen in cirrhotic rat liver at several time intervals after per os administration of glucose to fasted animals. METHODS: Liver cirrhosis was produced by inhalation of the hepatotropic poison CCl4. Glycogen concentration in the liver was determined biochemically. Glycogen content in hepatocytes was measured cytofluorimetrically in the smears stained with a fluorescent PAS reaction. Glycogen content in the hepatocytes of the portal and the central zone of the liver lobule was determined by absorption cytophotometry. RESULTS: Rats poisoned with CCl4 for 6 months developed typical liver cirrhosis characterized by a fourfold (p < 0.001) increase in the proportion of the connective tissue. In the cirrhotic rats fasted for 48 h, glycogen concentration in the liver and glycogen content in hepatocytes were lower as compared with the control by 36 and 27 % (p < 0.01), respectively. According to data obtained by different methods, the control animals accumulated glycogen at a high rate. In particular, the glycogen content in hepatocytes increased by 34 % after 10 min (p < 0.01). In the cirrhotic rats, glycogen content remained at the same level for 20 min. In both groups of animals, hepatocytes of the portal zone accumulated more glycogen than those of the central zone. CONCLUSIONS: Glycogen accumulation in cirrhotic rats starts after a delay and proceeds at a lower rate than in the norm.

RESUMEN

The effect of the actoprotector bemithyl (2-ethylthiobenzimidazole hydrobromide) on the content of glycogen and activities of glycogen synthase, glycogen phosphorylase, and glucose-6-phosphatase was studied in the cirrhotic rat liver. The content of glycogen and its fraction was determined by a cytofluorimetric method (Kudryavtseva et al. 1974). It has been shown that in cirrhosis the content of total glycogen in hepatocytes increases about 3 times and the content of its stable fraction increases 7.5 times. The activity of glucose-6-phosphatase fell to a level as low as 25% of normal. Activities of glycogen synthase and glycogen phosphorylase in the cirrhotic liver did not differ from normal. In the cirrhotic liver, bemithyl produced a decrease of the total glycogen content which was associated with a decrease of the glycogen synthase activity and an increase of the glucose-6-phosphatase and glycogen phosphorylase activities. Thus, the results of our studies indicate a favorable effect of bemithyl on the cirrhotic liver.

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