Effect of cobalt on the liver glycogen content in the streptozotocin-induced diabetic rats

Cobalt decreases blood glucose in diabetic rats but the mechanisms involved are unclear. To determine the contribution of glycogen metabolism to glycemia-lowering effect, glycogen contents of liver and muscle in the streptozotocin-induced diabetic rats were determined. The liver glycogen was depleted in diabetic rats. But when cobalt was administered to the rats, the glycogen returned to the level of healthy rats, concomitantly with the decrease in blood glucose. The cobalt treatment had no effect on the muscle glycogen in the diabetic rats. The tissue-specific responses of glycogen metabolism suggest the involvement of suppressed glucagon signaling due to cobalt treatment.     

Effect of indomethacin on hepatic glucose production in vitro: the impact of hepatic glycogen content

The effect of indomethacin (IND) on glucagon-induced hepatic glucose production (HGP) was studied in the isolated perfused livers of rats. Addition of IND (0.2 mM) to the perfusion medium had no effect on glucagon-stimulated HGP when compared to control experiments without added IND (1.02 +/- 0.17 vs. 1.00 +/- 0.26 mmol per (120 min X 100 g b.w.), respectively; NS). Intravenous pretreatment with both, IND (10 mg/kg b.w.), or vehicle resulted in a reduction in glucagon-induced HGP due to a decrease in hepatic glycogen content. A complete depletion of the hepatic glycogen pool and thus a lack in glucagon-stimulated HGP was observed when IND was given intraperitoneally. These results indicate that the changes in HGP observed after pretreatment with IND may largely if not completely be due to a non-specific depletion in hepatic glycogen content and that IND does not exert a direct influence on HGP.     

Dynamics of glycogen content in the normal and cirrhotic liver following glucose administration to starving rats

Using biochemical, cytofluorimetric and television cytophotometric methods, glycogen contents were studied in normal and cirrhotic rat liver at various intervals after glucose administration to fasting animals. The obtained data indicate that after a 48 h fasting glycogen contents in normal and cirrhotic liver are equally poor. A marked rise of glycogen content in cirrhotic liver was observed only 20-30 min after glucose administration to rats. It has been established that at all intervals after glucose administration to rats hepatocytes of the portal lobule zone, both in normal and in cirrhotic liver, accumulate more glycogen than those of the central zone. Again, the intensity of glycogen accumulation in cirrhotically altered liver is significantly lower than in normal liver, due, presumably, to a lower rate of glycogen synthesis in pathologically changed liver.     

Effect of exercise on glycogen level in muscles and liver in rats

The effect of exercise of glycogen level in skeletal muscles and liver was studied in Wistar rats. The previously untrained animals were subjected to one-time exercise in form of swimming in water at 32 degrees C for 10, 20 and 30 min. The glycogen level in the muscles (in g per 100 g of tissue) fell down during the first 10 minutes of the exercise by a mean value of 0.45 g. During the following 10 minutes the decrease was smaller amounting on the average to 0.1 g. After 30 min the glycogen level in the muscles was about 0.1 g/100 g of tissue. Respective falls of glycogen level in the liver were on the average 0.99 g and 0.40 g/100 g of tissue. After 30 min of exercise the glycogen level in the liver was 1.2 g/100 g of tissue. The fall of glycogen level in the muscles was similar at all times during exercise in all animals, but in the liver fairly significant differences were observed in the first 10 min between individual groups of rats. Later on during exercise the differences in the liver glycogen falls decreased.     

Melatonin increases muscle and liver glycogen content in nonexercised and exercised rats

The effects of melatonin on several parameters of carbohydrate and lipid metabolism were investigated in exercised and nonexercised rats. Animals were run to exhaustion on a rodent treadmill at 24 m/min and a 12% slope. Exercise resulted in a significant hypoglycemia and increased plasma levels of lactate and beta-hydroxybutyrate, together with a significant reduction of glycogen in muscle and liver. Muscle and liver glycogen content was elevated and plasma free fatty acid decreased in nonexercised animals receiving melatonin (0.5 or 2.0 mg/kg i.p). Melatonin at 2.0 mg/kg reduced plasma lactate and increased lactate concentration in liver. When compared to untreated exercised animals glycemia and muscle and liver glycogen content were significantly higher in melatonin-treated exercised animals, while plasma and liver lactate and plasma beta-hydroxybutyrate were significantly reduced. Our data indicate that melatonin preserves glycogen stores in exercised rats through changes in carbohydrate and lipid utilization.     

Role of liver nerves and adrenal medulla in glucose turnover of running rats

Sympathetic control of glucose turnover was studied in rats running 35 min at 21 m X min-1 on the level. The rats were surgically liver denervated, adrenodemedullated, or sham operated. Glucose turnover was measured by primed constant infusion of [3-3H]glucose. At rest, the three groups had identical turnover rates and concentrations of glucose in plasma. During running, glucose production always rose rapidly to steady levels. The increase was not influenced by liver denervation but was halved by adrenodemedullation. Similarly, hepatic glycogen depletion was identical in denervated and control rats but reduced after adrenodemedullation. Early in exercise, glucose uptake rose identically in all groups and, in adrenodemedullated rats, matched glucose production. Accordingly, plasma glucose concentration increased in liver-denervated and control rats but was constant in adrenodemedullated rats. Compensatory changes in hormone or substrate levels explaining the lack of effect of liver denervation were not found. In rats with intact adrenals, the plasma epinephrine concentration was increased after 2.5 min of running. It is concluded that, in rats carrying out exercise of moderate intensity and duration, hepatic glycogenolysis and glucose production are not influenced by the autonomic liver nerves but are enhanced by circulating epinephrine.     

Effect of growth hormone on liver glycogen accumulation in suckling rats.

The regulation of liver glycogen turnover in the neonatal period differs from that of the adult state. Little is also known about the regulation exerted by GH in the first period of life. To shed light on the regulation of glycogen production and in particular to study the role of GH on liver glycogen accumulation, we investigated the effect of GH administration in control or GH-deficient neonatal rats. A slow-release GH preparation was injected subcutaneously on days 9 and 12 of life, in normal and neonatally treated rats with thyroxine or cortisol. Seventy-two hours after the last GH administration, liver glycogen was increased without concomitant elevation of plasma insulin and corticosterone levels and in addition without sequential inactivation of glycogen synthase. These data strongly suggest that the current concepts on the regulation of the hepatic synthesis of glycogen should be revised.     

Effect of prolonged restraint on glycogen content and activities of four enzymes of carbohydrate metabolism in the liver of rats

Triphasic changes in glycogen content and activities of four enzymes of carbohydrate metabolism (glucose-6-phosphatase, phosphoenolpyruvate carboxykinase, hexokinase, and glucose-6-phosphate dehydrogenase) were studied in the liver of male Wistar rats exposed to 1, 5, 10, 15, 20, 30, 45, 60, 70 and 90-day movement restrain in pencil cases. It was assumed that these three phases corresponded to the alarm, resistance and exhaustion stages of Selye's general adaptation syndrome. In hypokinetic rats, however, a transition of the alarm reaction to the resistance stage was registered later, and hepatic glycogen accumulation was reduced in comparison with the standard pattern observed in chronic stress.     

Effect of the acclimation to high environmental temperature on the activity of hepatic glycogen phosphorylase (a+b and a), liver glycogen content and blood glucose level in rats

(1) Changes in the activity of hepatic glycogen phosphorylase a+b and a (GPh-ase a+b and a), liver glycogen content and blood glucose level during acclimation to moderate high environmental temperature (35±1 °C) were studied. (2) Experiments were carried out on adult fed Wistar rats of both sexes, previously given either short-term (1, 4 and 7 days) or long-term (14, 21, 30 and 60 days) exposure to high environmental temperature. The controls were continuously kept at room temperature (20±2 °C). (3) The results obtained showed that in the period of short-term exposure the liver glycogen content was decreased significantly (after the first and fourth days in male rats and after first day in female rats) and the GPh-ase a activity increased (after first day in male rats and after first, fourth and seventh day in female rats). Long-term exposure caused significant increased liver glycogen content (beginning from the 14th day in male rats and the 21st day in female rats) until the end of the acclimation period (60 days). The elevated activity of GPh-ase a persists after 14th day of exposure only in female rats while there are no significant changes over the rest of the acclimation period in both sexes. There were no significant changes in total GPh-ase activity during the whole period of exposure. Blood glucose level was significantly decreased throughout the whole period of acclimation to high environmental temperature, in both sexes (except in the 1 day exposed groups). (4) The increased activity of hepatic GPh-ase a and decreased glycogen content suggested that the short-term exposure to heat stimulates the glycogenolytical processes. Decreased blood glucose level, and elevated liver glycogen content (r=-0.7467 in male and r=-0.6548 in female rats) suggested that prolonged exposure to high environmental temperature stimulated glycogenogenesis, without changes in the GPh-ase activity.