Glucose-C14 incorporation into extractable and residual glycogen by liver slices.
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Glucose↗
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Tissue glucogen and blood glucose in irradiated rats. II. Effect of non-lethal doses of continuous gamma-radiation.
Male rats of the Wistar strain were continuously irradiated with an exposure of 0.57 Gy (60 R) of gamma-rays from a 60Co source. Irradiation lasted from 1 to 50 days in an experimental field, in which control animals shielded from radiation were also placed. After a 16-h starvation, concentration of glucose in the blood and of glycogen in the liver and heart was determined 1, 3, 7, 14, 21, 25, 32, 39 and 50 days after the beginning of irradiation. Concentration of blood glucose in irradiated rats did not practically differ from that of control animals during the whole period of investigation. Concentration of liver glycogen in irradiated animals was higher than that of the controls during all time intervals, except for day 1. Values of glycogen in the heart muscle were approximately identical in irradiated and control rats, except for day 21, on which they sharply increased in the irradiated animals. In addition to the investigation of blood glucose and tissue glycogen during continuous irradiation, we followed these parameters immediately, and 1, 6 and 12 months after continuous irradiation with a daily exposure of 0.57 Gy (60 R) up to a total exposure of 14.35 Gy (1 500 R) of gamma-rays. Considerably higher values of liver glycogen were detected in irradiated rats immediately and 1 and 6 months after the end of irradiation.
Animals↗
Effect of noradrenaline on triglyceride and glycogen concentrations in liver and muscle from man.
Fifteen male subjects aged 21-29 were given noradrenaline infusions for 4 hr. The noradrenaline infusions started at a rate of 0.1 mug/kg/min and were increased stepwise at hourly intervals. Blood was sampled before and at hourly intervals during and after the noradrenaline infusions. Needle biopsies were taken from the femoral muscle in 10 subjects and frim the liver in 8 subjects before and after the noradrenaline infusion. The concentrations of FFA in lasma and of beta-hydroxybutyric acid in blood were markedly elevated during noradrenaline infusion. The concentrations of plasma TG and blood glucose were slightly elevated. In liver the TG concentration increased from 23.1 to 32.7 mmole/kh (p smaller than 0.001). It was estimated that the de novo synthesis of TG in the liver could have required about 30% of the plasma FFA entering the slanchnic region. In muscle the TG concentration was 3.6 mmole/kh lower after the noradrenaline infusion (p smaller than 0.001). No change was found in the concentrations of cholesterol and phospholipids in muscle or of cholesterol in liver. The glycogen concentration in muscle did not change during noradrenaline infusion. The decrease in liver glycogen concentration was of the same order of magnitude as previously observed in fasting man. The results suggest that noradrenaline was without major net effects on the metabolism of glycogen in liver and muscle.
Adult↗
Glucose 6-phosphate plays a central role in the regulation of glycogen synthesis in a glycogen-storing liver cell line.
Two substrains of the epithelial liver cell line C1I, one storing large amounts of glycogen, the other one being very poor in glycogen were used as a model for studying glycogen synthesis. The glycogen content of glycogen-rich cells doubled during the proliferative phase and remained high in plateau phase although glycogen synthase I activity was not significantly altered during growth cycle and was too low to account for the increase in glycogen. However, the activity of the glucose 6-phosphate (Glc6-P)-dependent synthase rose continuously during growth cycle, and intracellular Glc6-P-concentration increased about 10-fold in log phase cells to 0.72 mumol g-1 wet weight. A0.5 of synthase for Glc6-P was 0.79 mM. It was also found that in contrast to the enzyme from normal liver, glycogen phosphorylase a from C1I cells was inhibited by Glc6-P, the apparent Ki being 0.45 mM. It was concluded that glycogen accumulation in C1I cells was due to stimulation of synthase and inhibition of phosphorylase by Glc6-P. Findings from the glycogen-poor cell line which revealed similar specific activities of synthase and phosphorylase but only low Glc6-P (0.056 mumol g-1 wet weight) supported this conclusion. Addition of glucose to starved cells resulted in a transient activation of synthase in both cell lines. Net glycogen synthesis, was, however, only observed in the cells with a high Glc6-P-content. Thus, modulation of synthase and phosphorylase by Glc6-P and not activation/inactivation of the enzymes seems to play a predominant role in glycogen accumulation in this cell line.
Animals↗
Role of adenosine monophosphate in regulation of metabolic pathways of perfused rat liver.
1. By perfusion of rat livers with 3mm-AMP in the perfusion medium we obtain increased intracellular concentrations of AMP. 2. These high intracellular concentrations of AMP lead to an increased output of glucose and urea into the perfusion medium. 3. The increased output of glucose in livers from fed rats is brought about primarily by an AMP-stimulated breakdown of liver glycogen. In livers from starved rats the increase in glucose output is not as great, reflecting the low contents of glycogen in livers from starved rats. 4. AMP inhibits gluconeogenesis from lactate in perfused livers. In the presence of high concentrations of lactate, however, the counteracting effects of AMP to increase glycogenolysis and to inhibit gluconeogenesis result in little change in the net glucose output. 5. The increased urea output is brought about by increased breakdown of amino acids that are present in the perfusion medium. In livers from starved rats the overall urea production is much higher, indicating increased catabolism of amino acids and other nitrogenous substrates in the absence of carbohydrate substrates. 6. AMP causes an inhibition of incorporation of labelled precursors into protein and nucleic acid. This may result from increased catabolism of precursors of proteins and nucleic acids as reflected by the more rapid breakdown of nitrogenous compounds. In support of this hypothesis, cell-free systems for amino acid incorporation isolated from livers perfused with and without AMP are equally capable of supporting protein synthesis. 7. The labelling pattern of RNA in perfused livers corresponds very closely to those found by pulse-labelling in vivo. AMP in no way alters the qualitative nature of the labelling patterns. 8. We consider these results as supporting evidence for the role of the concentration ratio of AMP to ATP in controlling the metabolic pathways that lead to the formation of ATP.
Adenine Nucleotides↗
An endogenous glycogen-associated compound modulates glucose-6-phosphatase activity in rat liver microsomes.
Liver glycogen is closely associated with the endoplasmic reticulum, which contains the glucose-6-phosphatase enzyme system that catalyses the final step of hepatic glucose production. To examine whether this structural association has functional consequences, microsomes were isolated from 48 h fasted (n = 6) and ad lib fed rats (n = 3). Microsomes from fed rats had a higher glycogen content and lower enzyme activity than fasted rats. Overall, glucose-6-phosphatase activity was inversely proportional to microsomal glycogen content. Partially purified rabbit or rat liver glycogen, at physiological relevant concentrations (10-100 mM glucose equivalents), added directly to either intact or Triton-disrupted microsomes from fasted rats significantly decreased glucose-6-phosphatase activity. Inhibitory activity was present in native liver glycogen prepared by sedimentation and could be dissociated from glycogen by ion-exchange and ultrafiltration. These findings suggest that a low molecular weight (< 5000 D) compound closely associated with glycogen can modulate glucose-6-phosphatase and may have a physiologic role in the regulation of hepatic glucose production.
Animals↗
Metabolic changes after non-lethal x-irradiation of rats. I. Carbohydrates, hormones.
Male rats of the Wistar strain were fasted overnight prior to exposure to single total-body X-ray dose of 2.39 Gy (250 R). Irradiated and sham-irradiated rats were pair-fed for 5 days, in the next period they were fed ad libitum. The levels of corticosterone and immunoreactive insulin in serum, glucose in blood, glycogen in liver, heart and skeletal muscle were determined 1 and 6 h, 1, 2, 3, 7, 14, 28, and 38 days after irradiation and sham-irradiation. Irradiation of rats resulted, at one hour, in a decrease and, at two days, in an icrease in level of blood glucose. A marked increase in liver glycogen persisted from 6 h to 21 days after irradiation. The level of glycogen in the skeletal muscle was reduced at 6 h and increased on days 3 and 14. Heart muscle glycogen declined within the first 24 h and rose at 14 days after exposure. The kinetics of changes in the heart and skeletal muscle glycogen following non-lethal irradiation was similar and indicated an overlap of changes produced by fasting with those brought about by irradiation, particularly during the first week. Corticosterone in serum was markedly increased in rats at 24 and 72 h after irradiation compared to pair-fed controls. The serum insulin concentration did not change after irradiation, except for a single increase on day 21. Irradiation with non-lethal doses produced changes in the parameters of the carbohydrate metabolism studied, except for serum insulin, which reflected the changes in the nutrition regimen upon pair-feeding rather than the effect of ionizing irradiation.
Animals↗
Effects of insulin on glycogen metabolism in isolated and perfused catfish liver.
The isolated and perfused catfish liver showed (a) a decrease in liver glycogen, (b) a continuous increase in glucose output, and (c) a decrease of lactate in the medium. Insulin did not influence liver glycogen decay during the first 2 hr; thereafter the hormone induced an increase of glycogen, particularly when glucose was added into perfusate. In insulin treated liver, the glucose output was lower than controls in the first hours of perfusion; thereafter a re-uptake of glucose occurred. After 2-3 hr of perfusion, the lactate present in the medium was increased by insulin towards the starting level. The long lasting effects of insulin on catfish in vivo were confirmed.
Animals↗
[Influence of dexamethasone and epinephrine on glycogen content and cytosol glucocorticoid receptors in hyperthyroid rat liver].
The influence of hyperthyroidism on the action of drugs affecting rat liver glycogen content and its mechanism were investigated. The thyroid-induced hyperthyroidism of rat served as the model. In normal rats, dexamethasone (5 mg.kg-1, ip) increased the content of liver glycogen and decreased the Bmax of glucocorticoid receptors (GCR) in liver cytosol. These effects were minimized or even disappeared in hyperthyroid rat models. On the other hand, in normal rats, epinephrine (0.20 mg.kg-1, ip) decreased the content of liver glycogen. This effect was potentiated in hyperthyroid rat models. Epinephrine did not affect the Bmax of GCR in liver cytosol of normal and hyperthyroid rats. These results suggested that hyperthyroidism may be one of the causes effecting the individual differences of drug action, and that the influence of hyperthyroidism on the glycogen-increasing action of dexamethasone correlated well with the changes in glucocorticoid receptor. The mechanism of the influence of hyperthyroidism on the glycogen-decreasing action of epinephrine is to be further explored.
Animals↗
Glucose homeostasis during the perinatal period in normal rats and rats with a glycogen storage disorder.
The fetal rat mobilizes liver glycogen during parturition for use as a glucose source until the onset of gluconeogenesis at 2 h after birth. A rat strain (NZR/Mh) unable to mobilize liver glycogen because of a phosphorylase b kinase deficiency has been used to assess the importance of liver glycogen in glucose homeostasis of the newborn. In normal rats the mean blood glucose concentration of the fetus measured at various times up to 24 h after natural birth ranged between 3.7 and 5.4 mM. In contrast, fetuses of the affected rats were hypoglycemic before birth (2.02 +/- 0.15 mM), and by 1 h after birth the blood glucose had decreased to 0.74 +/- 0.14 mM. Concentrations increased by 4 h to 1.48 +/- 0.17 mM and by 24 h reached values not significantly different from the normal newborn rats. Changes in plasma insulin over the perinatal period were similar in both groups although concentrations were always significantly lower in the affected rts. The findings demonstrate the crucial role of the fetal liver glycogen store in the maintenance of normoglycemia in the newborn. The normal rat does not develop hypoglycemia when born naturally and left with the mother after birth (in contrast to other studies in which the newborn were taken by cesarian delivery 1 d prematurely and kept in an artificial environment without food). The rats with the glycogen storage disorder experienced severe hypoglycemia without any apparent effects, which raises questions concerning alternative fuels available to and utilized by the newborn.
Animals↗
[The effect of ultrasonic waves on liver cell glycogen and Kupffer's astrocytes].
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Astrocytes↗
Time course of insulin action on tissue-specific intracellular glucose metabolism in normal rats.
We investigated the time course of insulin action in conscious rats exposed to constant physiological hyperinsulinemia (approximately 100 mU/l) while maintaining euglycemia (approximately 100 mg/dl) for 0, 0.5, 2, 4, 8, or 12 h. [3-3H]glucose was infused to quantitate whole body glucose disposal (rate of disappearance, Rd), glycolysis (generation of 3H2O in plasma), hepatic glucoses production (HGP), and skeletal muscle and liver glycogen synthesis ([3-3H]glucose incorporation into glycogen and time-dependent change in tissue glycogen concentration). The basal Rd, which equals HGP, was 6.0 +/- 0.3 mg.kg-1.min-1. With increased duration of hyperinsulinemia from 0 to 0.5 to 2 to 4 h, Rd increased from 6.0 +/- 0.3 to 21.0 +/- 1.1 to 24.1 +/- 1.5 to 26.6 +/- 0.6 mg.kg-1.min-1 (P < 0.05 for 2 and 4 h vs. 0.5 h). During the first 2 h the increase in Rd was explained by parallel increases in glycolysis and glycogen synthesis. From 2 to 4 h the further increase in Rd was entirely due to an increase in glycolysis without change in glycogen synthesis. From 4 to 8 to 12 h of hyperinsulinemia, Rd decreased by 19% from 26.6 +/- 0.6 to 24.1 +/- 1.1 to 21.6 +/- 1.8 mg.kg-1.min-1 (P < 0.05 for 8 h vs. 4 h and 12 h vs. 8 h). The progressive decline in Rd, in the face of constant hyperinsulinemia, occurred despite a slight increase (8-14%) in glycolysis and was completely explained by a marked decrease (64%) in muscle glycogen synthesis. In contrast, liver glycogen synthesis increased fourfold, indicating an independent regulation of muscle and liver glycogen synthesis by long-term hyperinsulinemia. In the liver, during the entire 12-h period of insulin stimulation, the contribution of the direct (from glucose) and the indirect (from C-3 fragments) pathways to net glycogen formation remained constant at 77 +/- 5 and 23 +/- 5%, respectively. HGP remained suppressed throughout the 12-h period of hyperinsulinemia.
Adipose Tissue↗
Isolation of glycogen from buffalo liver.
The glycogen has been isolated from buffalo (Bos Bubalus bubalis) liver, purified several-fold, and characterized to compare with rabbit and oyster glycogen. Once-purified buffalo glycogen has been found to contain 1.3% protein, 0.16% nitrogen, 0.69% phosphorous, no lipids, and nucleic acids sufficient to cause absorption at 260 mu. The buffalo glycogen may be used as a potential substitute for rabbit and oyster glycogen after two-or three- purifications and a treatment with DEAE-cellulose.
Animals↗
[Changes in carbohydrate metabolism in hens experimentally infected with Pasteurella multocida kokoshki].
Studied were the concentration of blood sugar, the activity of glucose-6-phosphatase and glucose-6-phosphatedehydrogenase, and the level of glycogen in the liver of P. multocida infected chickens. An abrupt decrease of the liver glycogen was found as well as a negligible rise of the blood sugar. The activity of glucose-6-phosphatase remained unchanged, and that of glucose-6-dehydrogenase was twice as high. It is concluded that the intense exhaustion of liver glycogen is in connection with the activation of the pentosephosphate pathway.
Animals↗
[Formation of liver and muscle glycogen from xylitol, sorbitol and glucose in healthy and alloxan-diabetic rats].
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Alloxan↗
[Behavior of the liver and muscle glycogen after roentgen irradiation in 2 different strains of rats].
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Animals↗
Enhancement of the gluconeogenic flux of hepatic glycogen repletion by a phenacyl imidazolium compound in vivo.
The effect of a phenacyl imidazolium compound (LY177507 or Proglycosyn, Eli Lilly) on the direct (glucose-->glucose-6-phosphate-->glycogen) and indirect (three-carbon compounds-->glucose-6-phosphate-->glycogen) pathways of liver glycogen synthesis was studied in conscious rats. [1-13C]Glucose (99% enriched) was infused intraduodenally into chronically catheterized Proglycosyn-treated (n = 7) and saline-treated (n = 7) rats for 120 min. Net hepatic glycogen synthetic rates were increased twofold in drug-treated rats compared with saline-treated controls. The percentage of liver glycogen synthesized by the direct pathway was calculated by comparing the 13C isotopic enrichment in the C1 and C6 positions of hepatic glycogen and plasma glucose using 13C nuclear magnetic resonance spectroscopy and gas chromatography-mass spectroscopy techniques and was found to be 59 +/- 5% and 39 +/- 2% (P < 0.05) in the saline treated and Proglycosyn-treated groups, respectively. Net flux rates for the direct and indirect pathways were calculated to be 0.24 +/- 0.04 and 0.17 +/- 0.03 mumol/g liver per min, respectively, in the saline-treated group and 0.30 +/- 0.04 (P = NS) and 0.46 +/- 0.06 (P < 0.05) mumol/g liver per min, respectively, in the Proglycosyn-treated group. Thus, Proglycosyn increases net hepatic glycogen synthesis in vivo exclusively through augmentation of the indirect pathway.
Animals↗
Diminished ketosis and triglyceridemia during fasting in odd-carbon enriched pregnant rats.
The lipolysis, ketosis and hypertriglyceridemia of fasted rats in late pregnancy may be related to decreased insulin secretion geared to decreased glucose availability. In odd-carbon fatty acid enriched (OCE) rats, the odd-carbon fatty acids (OCFA) mobilized during fasting provide terminal three-carbon residues which are glucogenic, thereby permitting blood glucose and insulin to be maintained close to fed levels. The present study has used OCE rats to evaluate the role of insulin in the altered fat metabolism of the fasted rats in late pregnancy. The adipose tissue of 24 female Sprague-Dawley rats was enriched to more than 25% undecanoate (c11:0) and higher OCFA by feeding them a complete diet high in triundecanoin content for six weeks. Twenty-four female controls were fed a similar diet except that the fat was exclusively corn oil. Both OCE and control rats were than mated and on day 18 of pregnancy were divided into four groups: one group was killed fed, one after a 24 h fast, and one after a 48 h fast; the fourth group was fed to day 20 of pregnancy and then killed. In the fed state, the concentrations of glucose, ketones, and cholesterol in serum, as well as that of glycogen in liver, were the same in control and OCE rats. Insulin and triglycerides were similarly elevated in the two groups. After two days of fasting, serum glucose, insulin, and liver glycogen concentrations were significantly higher in OCE than in control rats, while ketones and triglycerides were significantly lower. No significant changes occurred in serum cholesterol. The results are consistent with a predominantly insulin effect in the pregnant OCE rats in diminsihing the marked fasting lipolysis, hyperketonemia and hypertriglyceridemia observed in controls, but do not rule out inhibition of FFA release by in situ re-esterification to glycerol derived from glucose or propionic acid.
Acidosis↗