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PubMed1989

Application of the pyroantimonate method and electron probe microanalysis to the study of glycogen metabolism in liver.

Glycogen distribution in the liver of mouse under different metabolic conditions was studied by the pyroantimonate (PA) method combined with semi-quantitative electron probe microanalysis (EPMA). In the liver of animals subjected to a sugar-rich diet, glycogen granules were abundant and electron transparent. In fasted animals, they were less numerous and stained by PA, which indicates the presence of a complexed cation. This cation was identified as calcium by EPMA. In both cases, adjacent cytoplasmic areas contained "masked" calcium not revealed by PA but detected by EPMA, which is characteristic of a neutral complexed form; but in the case of the fasted animals, the calcium concentration was significantly lower. If the liver of fasted animals was dissected in 0.2% glucose-containing medium, the glycogen areas dramatically released calcium and lost their stainability by PA, whereas mitochondria and adjacent cytoplasm contained many PA precipitates rich in calcium and sodium, suggesting a sudden increase of intracellular [Ca2+]. In mitochondria, the sodium:calcium ratio was relatively constant, which suggests a process involving a coupling between these two elements. Our results could be explained in the light of physiological and biochemical data. We particularly noted that diffusible cations as calcium and sodium did not appear to be displaced over long distances from their likely source. This observation agrees with recent theories on the state of water and ion mobility in the cell.

Animals↗
PubMed1993

Livers from fasted rats acquire resistance to warm and cold ischemia injury.

Successful liver transplantation is dependent upon many factors, one of which is the quality of the donor organ. Previous studies have suggested that the donor nutritional status may affect the outcome of liver transplantation and starvation, due to prolonged stay in the intensive care unit, may adversely affect the liver. In this study we have used the orthotopic rat liver transplant model to measure how fasting the donor affects the outcome of liver transplantation. Rat livers were preserved with UW solution either at 37 degrees C (warm ischemia for 45-60 min) or at 4 degrees C (cold ischemia for 30 or 44 hr). After preservation the livers were orthotopically transplanted and survival (for 7 days) was measured, as well as liver functions 6 hr after transplantation. After 45 min of warm ischemia 50% (3 of 6) animals survived when the liver was obtained from a fed donor about 80% (4 of 5) survived when the liver was obtained from a three-day-fasted donor. After 60 min warm ischemia no animal survived (0 of 8, fed group). However, if the donor was fasted for 3 days 89% (8 of 9) of the animals survived for 7 days. Livers cold-stored for 30 hr were 50% viable (3 of 6) and fasting for 1-3 days did not affect this outcome. However, if the donor was fasted for 4 days 100% (9 of 9) survival was obtained. After 44-hr preservation only 29% (2/7) of the recipients survived for 7 days. If the donor was fasted for 4 days, survival increased to 83% (5/6). Liver functions, bile production, and serum enzymes were better in livers from the fasted rats than from the fed rats. Fasting caused a 95% decrease in liver glycogen content. Even with this low concentration of glycogen, liver viability (animal survival) after warm or cold ischemia was not affected, and livers with a low glycogen content were fully viable. Thus liver glycogen does not appear to be important in liver preservation. This study shows that fasting the donor does not cause injury to the liver after warm or cold ischemia. In fact, the livers appeared to be better able to tolerate ischemia when obtained from fasted rats. Thus donor nutritional status may be an important factor for outcome of liver transplantation. Livers from fasted donors may be capable of tolerating long-term preservation better than livers from fed donors.

Adenosine↗
PubMed1979

[The influence of ether anesthesia in white mice on the contents of cyclic nucleotides in their brain and of cyclic nucleotides and glycogen in their liver (author's transl)].

During ether narcosis (10% diethyl ether v/v) of 30 min in white mice, the brain content of cAMP and cGMP is significantly diminished. By contrast, the liver cAMP and cGMP concentrations are increased 5 and 30 min after beginning narcosis but there is no or little difference, respectively, as compared to controls after 60 min. Liver glycogen content is elevated after 5 min but is diminished after 30 and 60 min as compared to controls. Pretreatment of the animals with the alpha-blocking agent phentolamine and the beta-blocking agent propranolol, respectively, prevents neither the increase in liver cAMP nor the decrease in liver glycogen during ether narcosis. It may be assumed that the changes in the liver and brain contents of cAMP and cGMP during ether application are due to physico-chemical alterations at the cell membrane which result in changes of the activity of the enzymes adenylate cyclase and guanylate cyclase in brain and liver tissue.

Anesthesia↗
PubMed1985

A study of glycogen in the liver of metal-fed rats.

Liver glycogen was estimated after feeding heavy metals to rats. With the exception of copper (CU) and zinc (Zn) these metals i.e. lead (Pb), mercury (Hg), cadmium (Cd), chromium (Cr), manganese (Mn), molybdenum (Mo) and cobalt (Co) depleted liver glycogen. These results are discussed in relation to glycogenolysis, gluconeogenesis, hypo- and hyperglycemic conditions. The role of the responsible enzymes is also discussed.

Animals↗
PubMed1990

Purification and partial characterization of glycogen synthase kinase-3 from rabbit liver.

Glycogen synthase kinase-3 (GSK-3) was purified from rabbit liver to homogeneity by ultracentrifugation, ion-exchange chromatography on DEAE-cellulose, Cellulose phosphate, CM-Sephadex and Fast Protein Liquid Chromatography (FPLC) on Mono-S column. The enzyme was purified approximately 20,000 fold with an approximate 2% recovery. The purified enzyme showed a single band on SDS-polyacrylamide gel electrophoresis. GSK-3 is a monomeric enzyme with a molecular weight of 50,000-52,000 as derived from SDS-polyacrylamide gel electrophoresis and gel filtration. The purified enzyme was indeed a GSK-3 since it phosphorylated three sites, i.e., 3a, 3b, and 3c on liver glycogen synthase. GSK-3 incorporated up to 2.6 mol Pi/mol glycogen synthase subunit with a concomitant inactivation of glycogen synthase activity.

Animals↗
PubMed1983

Adrenal hormones and liver cAMP in exercising rats--different modes of anesthesia.

We have compared five different modes of anesthesia (iv and ip pentobarbital sodium, ether, CO2, and cervical dislocation) with respect to their effects on liver glycogen, liver adenosine 3',5'-cyclic monophosphate (cAMP), blood glucose and lactate, plasma corticosterone, norepinephrine, and epinephrine in resting rats and in rats run on a treadmill at 26 m/min for 30 min. Ether, CO2, and cervical dislocation were found to be unsuitable due to the marked elevation in plasma catecholamines seen in both resting and exercising rats. Injection of pentobarbital sodium ip required an average of 8 min before onset of surgical anesthesia as opposed to less than 5 s for iv pentobarbital. Exercising rats anesthetized with ip pentobarbital showed markedly lower plasma catecholamines compared with rats given iv pentobarbital. Hepatic cAMP increased in response to exercise in all groups except the ip pentobarbital group. This is most likely due to the long delay between the end of the exercise and freezing of the liver in the ip pentobarbital-anesthetized animals. We conclude that iv injection of pentobarbital is the most suitable method of anesthesia for obtaining accurate measurements of plasma stress hormones, substrates, and metabolites and of hepatic cAMP and glycogen in resting and exercising rats.

Adrenal Cortex Hormones↗
PubMed1997

Sex differences in response to dietary manipulation in rats with hypertension and myocardial hypertrophy.

Studies of the effect of sex on the metabolic state of rats with chronic hypertension and concomitant myocardial hypertrophy were conducted. Female and male spontaneously hypertensive rats (SHRs) with early myocardial hypertrophy (5.5 mo old) were used. Serum fatty acids, liver glycogen, and myocardial glycogen were measured at baseline and after the rats were deprived of food for 24 h. The metabolic effects of progressive myocardial hypertrophy in females were assessed in additional groups of female SHRs (5.5 or 12 mo old) under the following conditions: control, food deprived, or food deprived and refed with equienergetic lipid-rich (38.9% of total energy) or carbohydrate-rich (76.5% of total energy) diets. Despite no differences in serum fatty acids, females had significantly higher baseline myocardial glycogen and liver glycogen concentrations than males. In response to food deprivation, females continued to have significantly higher myocardial glycogen and fatty acid concentrations than males, whereas there were no sex differences in liver glycogen, which was depleted in both males and females. Older hypertensive females had higher baseline fatty acid concentrations and lower liver glycogen concentrations than younger females, whereas there were no differences in myocardial glycogen. Food deprivation doubled fatty acid concentrations, depleted liver glycogen, and increased myocardial glycogen in both age groups. In both age groups, fatty acid concentrations and liver glycogen did not return to baseline values after food deprivation and refeeding. In both age groups, fatty acid concentrations increased further after the lipid-rich diet whereas liver glycogen concentrations returned to approximately 50% of baseline values after the carbohydrate-rich diet. Refeeding with either diet did not significantly increase myocardial glycogen further. Thus, the metabolic response to dietary manipulation was influenced by both sex and, in females, progressive pathology.

Aging↗
PubMed1985

Glycogen synthase in prenatal rat liver.

Glycogen synthase first appears in significant levels in fetal rat liver on day 18 of gestation (22 day term), but in a mostly inactive, phospho- form. This was reflected in a decreased affinity for its allosteric activator (increased A0.5 for glucose-6-phosphate), and with limited glycogen synthesis and accumulation. Peak glycogen synthesis occurs on day 21 of gestation, and glycogen synthase is in a more dephospho-form with decreased A0.5 for G6P and increased -G6P/+G6P activity ratio. The data suggest that a significant change in phosphorylation state of synthase occurs in late gestation to facilitate the large increase in glycogen synthesis and accumulation.

Animals↗
PubMed1976

The manipulation of circadian rhythms.

In a study on male Wistar (TNO) rats kept under phase-shifted light-dark (12:12) conditions, it was demonstrated that the circadian rhythms of the following functions were effectively synchronized to the new lighting regimen: (a) body temperature, gross motor activity (after 1 week of acclimatization); (b) stomach weight, liver weight, liver glycogen, liver protein and acid phosphatase activity; serum corticosterone, glucose, total protein and inorganic phosphatase (after 4-6 weeks; as concluded from the data pooled of a sex of identical experiments); (c) the in vivo toxicity of approximately LD50 amounts (i.p.) for antimycin A and of E 600. In the individual experiments the various normal functions appeared to be different with respect to sensitivity to light. The overall pooled results indicated that, except for glycogen, the 24-h means of the normal values in the stomach, liver and serum were slightly decreased when compared to the respective means obtained from standard LD (= light: 6:00-18:00)-conditioned control groups (P less than 0.001 for liver weight, liver protein, serum protein and inorganic phosphate). The experimental animals revealed an intermediate or persisting decrease of the growth rate. From the serial biological and toxicological studies performed in the course of 1 year, it is concluded that the synchronizing effect of an altered lighting regiment may be influenced by seasonal factors...

Animals↗
PubMed1988

Effect of the exercise-induced increase in glucocorticoids on endurance in the rat.

To investigate the effect of the increase in glucocorticoids during exercise on endurance, rats were either sham operated (SO) or adrenalectomized. All adrenalectomized rats were given a subcutaneously implanted corticosterone pellet at the time of adrenalectomy. Adrenalectomized rats were injected with corticosterone (ADX Cort) or corn oil (ADX) 5 min before exercise. Rats were killed at rest or after running on a treadmill (21 m/min, 15% grade) until exhaustion. SO rats ran 138 +/- 6 min compared with 114 +/- 9 min for ADX Cort and 89 +/- 8 min for ADX. All differences in run times were significant (P less than 0.05). Corticosterone levels were similar in exhausted SO and ADX Cort groups. ADX exhausted rats had corticosterone levels similar to resting values in SO and ADX rats. Inhibition of the rise in glucocorticoids during exercise had no effect on liver glycogen, liver adenosine 3',5'-cyclic monophosphate, plasma insulin, blood glucose, lactate, glycerol, or 3-hydroxybutyrate, plasma norepinephrine, or red quadriceps and soleus glycogen. Plasma free fatty acids were significantly depressed at exhaustion in ADX rats compared with SO. These data show that glucocorticoids exert effects within the time frame of a prolonged exercise bout and play a role in increasing endurance.

Adrenalectomy↗
PubMed1967

Studies on glycogen synthesis in pigeon liver homogenates. Glycogen synthesis from glucose monophosphates and uridine diphosphate glucose.

Comparative time-course studies of glycogen synthesis from glucose 6-phosphate, glucose 1-phosphate and UDP-glucose show that glucose 1-phosphate forms glycogen at an initial rate faster than that obtained with glucose 6-phosphate and UDP-glucose. After 5min. the rates from glucose monophosphates are considerably slower. 2,4-Dinitrophenol decreases glycogen synthesis from both glucose monophosphates, whereas arsenate and EDTA increase glycogen synthesis from glucose 1-phosphate and inhibit the reaction from glucose 6-phosphate, galactose and galactose 1-phosphate. Mitochondria-free pigeon liver cytoplasmic fraction forms less glycogen from glucose monophosphates than does the whole homogenate. 2-Deoxyglucose 6-phosphate inhibits glycogen synthesis from glucose monophosphates. Glycogen formation from UDP-glucose is relatively unaffected by dinitrophenol, by arsenate, by EDTA, by 2-deoxyglucose 6-phosphate and by the removal of mitochondria from the whole homogenate.

Animals↗
PubMed1966

Studies on lipogenesis in vivo. Effect of dietary fat or starvation on conversion of [14]glucose into fat ad turnover of newly synthsized fat.

1. Lipogenesis was studied in vivo by giving mice 250mg. meals of [U-(14)C]glucose and measuring the disposition and incorporation of label. About 48% of the (14)C dose was eliminated as (14)CO(2) in the first 2hr. At 60min. after administration, 1.0, 1.9 and 11.9% of the dose was recovered as liver glycogen, liver fatty acid and carcass fatty acid respectively. Of the [(14)C]glucose converted into fat in the epididymal pads about 90% was present as glyceride fatty acid and 10% as glyceride glycerol. 2. Hepatic synthesis of fatty acid was depressed by dietary fat to a much greater extent than was synthesis outside the liver. Both feeding with fat and starvation decreased the proportion of the label taken up by adipose tissue present as fat (triglyceride) and increased the proportion of triglyceride label present as glyceride glycerol. These results are consistent with the hypothesis that the primary action of both these conditions in decreasing fat synthesis is to inhibit synthesis of fatty acids. 3. Turnover of body fat labelled in vivo from [U-(14)C]glucose was estimated from the decline in radioactivity measured over the first 24hr. of the experiment. The half-life of liver and extrahepatic fatty acids (excluding epididymal fat) was 16hr. and 3 days respectively. In contrast, no measurable decrease in radioactivity of the fatty acids of epididymal fat was observed for 7 days after administration of the [U-(14)C]glucose.

Adipose Tissue↗
PubMed1987

Patterns of glycogen turnover in liver characterized by computer modeling.

We used a computer model of liver glycogen turnover to reexamine the data of Devos and Hers, who reported the time course of accumulation in and loss from glycogen of label originating in [1-14C]galactose injected at different times after the start of refeeding of 40-h fasted mice or rats. In the present study computer representation of individual glycogen molecules was utilized to account for growth and degradation of glycogen according to specific hypothetical patterns. Using this model we could predict the accumulation and localization within glycogen of labeled glucose residues and compare the predictions with the previously published data. We considered three specific hypotheses of glycogen accumulation during refeeding: 1) simultaneous, 2) sequential, and 3) accelerating growth. Hypothetical patterns of glycogen degradation were 1) ordered and 2) random degradation. The pattern of glycogen synthesis consistent with experimental data was a steadily increasing number of growing glycogen molecules, whereas during degradation glycogen molecules are exposed to degrading enzymes randomly, rather than in a specific reverse order of synthesis. These patterns predict the existence of a specific mechanism for the steadily increasing "seeding" of new glycogen molecules during synthesis.

Computer Simulation↗
PubMed1983

Isolation and characterization of glycogen branching enzyme from rabbit liver.

Glycogen branching enzyme was isolated from rabbit liver. The highly purified enzyme shows a monomer molecular weight of 71 000 by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and apparent molecular weights of 93 000 by sucrose density gradient sedimentation and 52 000 by gel-exclusion chromatography on Sephacryl S-300. No glucosamine, mannosamine, galactosamine, or sialic acid was detected in the protein. An amino acid analysis is reported. The spectrum of branching enzyme is that of a simple polypeptide, with A1%280nm = 24.6. Highly purified branching enzyme consists of several closely related active enzyme forms that can be resolved by isoelectric focusing in polyacrylamide gel. The major species of pI 5.7 is flanked by less abundant forms of pI 5.6 and 5.8. Seemingly identical enzyme forms are observed in crude extracts of rabbit liver, skeletal muscle, brain, and heart, although the absolute and relative concentrations vary among the tissues. Branching enzyme apparently does not exhibit tissue-specific isoenzymes.

1,4-alpha-Glucan Branching Enzyme↗
PubMed1991

Resistance of hepatic glycogen to depletion in obese Zucker rats.

Glycogen stores (liver and carcass) have been studied in lean and obese Zucker rats. The animals were submitted to one of three feeding conditions: ad libitum, a 48-h fast, or a 48-h fast and food ad libitum for 24 h, and to two environmental conditions, either thermoneutrality or an acute cold exposure (2 days at 4-7 degrees C). After a 2-day fast at 25 degrees C, the liver glycogen store was reduced by 45 times in the lean rats, while it was decreased by only 3 times in the obese rats. Under these conditions, the liver glycogen store was 45 times higher in the obese than in the lean rats. After 2 days in the cold, liver glycogen store was 4.4 times higher in obese rats than in lean rats. After a 2-day fast in the cold, the liver glycogen store in the obese rats was 30 times higher than in the lean rats. In comparison to fasting at thermoneutrality, fasting in the cold did not lead to a further reduction in hepatic glycogen in obese Zucker rats. The differences observed in the mobilization of the hepatic glycogen store between obese and lean rats have not been found in the mobilization of the carcass glycogen store. Drastic conditions, such as a 2-day fast in the cold, did not exhaust the glycogen store in obese Zucker rats. The present observations point out that obese Zucker rats cannot mobilize the entire hepatic glycogen store, as seen in lean control rats. The role of this abnormality in the high hyperlipogenesis that maintains the obese state is still to be evaluated.

Analysis of Variance↗
PubMed1985

[Regulation of glycogen metabolism in fetal rat liver of IUGR rats].

Fetal liver glycogen content, glycogen synthetase and phosphorylase activity were measured in growth retarded fetuses on 20th day of gestation of pregnant rats. The effects of administration of dexamethasone to the mother were also examined in both enzyme activities in livers of fetal rats. The results obtained were as follows. The incidence of IUGR rats by ligation of maternal uterine vessels on the 17th day of gestation was 85.8%. No changes in fetal body and liver weights were found after the administration of dexamethasone to the mother. In the IUGR fetuses, liver glycogen content was decreased about 25% compared with the control. However, the decreased liver glycogen levels in IUGR fetuses increased to the control level following the administration of dexamethasone. In IUGR fetuses, liver glycogen synthetase activity of both a-form and a + b form decreased. Dexamethasone markedly increased the a-form of glycogen synthetase. The effects of dexamethasone in glycogen phosphorylase activity of fetal liver were unchanged in IUGR fetuses.

Animals↗