Glycogen Synthetase Activity Research Articles

Investigation of activity of jnk kinases new potential inhibitors

JNK kinase - group stress-activated kinases that are involved in apoptosis, growth, development and differentiation of cells. JNK kinase activation is observed in the development of inflammatory processes, neurodegenerative disorders, insulin resistance, some types of cancer. Therefore, the search for new inhibitors of kinases JNK is an important and urgent problem. The purpose of this study was to investigate the activity of the new compounds, potential inhibitors of JNK kinases. Experiments were performed on isolated rat hepatocytes. It was determined the content of JNK and its active phosphorylated form (p-JNK), the activity of glycogen synthetase (GS) and alanine aminotransferase (ALT). It was found that substances G0003, G0004, G0006 and G0007 inhibited the activity of JNK, reducing the content of p-JNK, decreased GS activity and increased ALT activity. We have found that substances G0006 and G0007 showed the highest activity.

Investigation of activity of jnk kinases new potential inhibitors

JNK kinase - group stress-activated kinases that are involved in apoptosis, growth, development and differentiation of cells. JNK kinase activation is observed in the development of inflammatory processes, neurodegenerative disorders, insulin resistance, some types of cancer. Therefore, the search for new inhibitors of kinases JNK is an important and urgent problem. The purpose of this study was to investigate the activity of the new compounds, potential inhibitors of JNK kinases. Experiments were performed on isolated rat hepatocytes. It was determined the content of JNK and its active phosphorylated form (p-JNK), the activity of glycogen synthetase (GS) and alanine aminotransferase (ALT). It was found that substances G0003, G0004, G0006 and G0007 inhibited the activity of JNK, reducing the content of p-JNK, decreased GS activity and increased ALT activity. We have found that substances G0006 and G0007 showed the highest activity.

Polysaccharides from Liriopes Radix ameliorates hyperglycemia via various potential mechanisms in diabetic rats

Liriopes Radix, which is regarded as both drug and healthy diet, is drunk as tea and used in traditional Chinese medicine to treat diabetes. Based on our previous studies, investigated the hypoglycemic effects and explored the mechanisms of total polysaccharides from Liriope spicata var. prolifera (Liriopes Radix) in a diabetic rat model. TLSP reduced hyperglycemia in diabetic rats. The oral glucose tolerance test showed that TLSP could improve the glucose tolerance of diabetic rats. Damage to liver and pancreas tissue was inhibited after treatment with TLSP. Moreover, TLSP increased glycogen content, glucokinase (GK) and glycogen synthetase (GS) activities, and suppressed the elevation of glucose-6-phosphatase (G6Pase) and glycogen phosphorylase (GP) activities in liver. Compared with the diabetic control group, GK and GS mRNA expression were significantly elevated, while G6Pase and GP mRNA expression were decreased in TLSP groups. In addition, TLSP could inhibit glycogen synthase kinase-3β expression and increase insulin receptor, insulin receptor substrate-1, phosphoinositide 3-kinase, protein kinase B and glucose transport protein-4 expression in liver. TLSP showed hypoglycemic function. Improvement of glucose metabolism and insulin-signaling transduction were possible mechanisms.

Antidiabetic properties of purified polysaccharide fromHedysarum polybotrys

Hedysarum polybotrys polysaccharide (HPS) is the principal active fraction responsible for the antidiabetic properties of this species. The aim of this study was to determine the antidiabetic properties of 4 purified fractions of different molecular weight range HPSs (HPS1, HPS2, HPS3, HPS4). HPS3 was selected for examination of its hypoglycemic mechanism because of its significant hypoglycemic effect in alloxan-induced diabetic mice. The changes in blood glucose levels and oral glucose tolerance tests (OGTT) showed that hypoglycemia was more pronounced in HPS3-treated groups than in the diabetes mellitus model (DM) control group. The interleukin-6, tumor necrosis factor-alpha, leptin, and free fatty acid levels were significantly lower in the HPS3-treated groups and HPS3 + metformin (HPS3+MET) group than in the DM control group, while plasma insulin, hepatic glycogen, superoxide dismutase, and nitric oxide synthetase activity were significantly higher. Treatment with HPS3 or HPS3+MET also significantly lowered malonaldehyde levels compared with the DM control group, while it elevated the nitric oxide and total antioxidant capacity. HPS3 altered the plasma lipid levels by lowering cholesterol and triglyceride concentrations, while elevating the plasma high-density lipoprotein cholesterol level. Therefore, these results suggest that HPS3 may partly ameliorate hyperglycemia and hyperlipidemia associated with type 2 diabetes through increased insulin secretion, inhibition of lipid peroxidation, promotion of sensitivity to insulin, suppression of gluconeogenesis and reduction in the biosynthesis fatty acid, cholesterol and cell cytokines related to insulin resistance, and it could be a useful adjunct therapy to a proven first-line therapy for type 2 diabetes using metformin.

Seasonal variation of the glycogen enzyme activity in diploid and triploid Pacific oyster gonad during sexual maturation

The glycogen content and the activities of two key enzymes in glycogen metabolism, glycogen phosphorylase and glycogen synthetase, in the gonad of diploid and triploid Pacific oysters (Crassostrea gigas) were compared during maturation. The glycogen content in the gonad of diploids decreased with gametogenesis (by 85.7%), but the glycogen content in the gonad of triploids did not vary significantly. Activity of glycogen phosphorylase (GP) in the gonad of diploids decreased with gametogenesis (by 55.5%), while GP activity of triploids did not vary significantly during maturation. Activity of glycogen synthetase (GS) in the gonad of diploids increased slightly with gametogenesis, reaching a peak in June. Activity of GS declined sharply from June to July, which might be due to gonad spawning. GS activity of triploid oysters in spawning time (July and August) was significantly higher than that in other months, which might be explained with a ‘compensating’ mechanism for the higher glycogen content in triploids.

ラットの糖質及び脂質代謝に及ぼすガーリック抽出物腹腔内投与の効果

The effects of garlic components extracted with organic solvents on the carbohydrate and fat metabolism of rats were investigated. Rats fed on a diet prepared according to the AIN-76 formula were given either the garlic extract or saline for 5 weeks via an intra-peritoneal injection. The liver weight of the garlic group decreased, but their thyroid glands increased significantly in wet weight compared to the control group. The weight of the carcass was suppressed in the garlic group, and crude fat content in the carcass significantly decreased. The glycogen synthetase activity in the liver cytosol of the garlic-supplemented rats was also significantly decreased, as was the plasma insulin concentration, while the plasma glucagon concentration of the garlic group was elevated. It is suggested from these data that dietary supplementation with the garlic extract might have promoted the catabolism of glucose and/or fatty acid (combustion) in the rats.

Long-term oral nicotine administration reduces insulin resistance in obese rats

This study aimed to investigate the effect of long-term oral nicotine administration on insulin resistance in an animal model of obesity. Eight-week-old male Zucker fatty rats (ZFRs) were administered nicotine tartrate dihydrate (4.6 mg/kg/day) in the drinking water. The control group was pair-fed. The body weights and food intake over 8 weeks were similar in both groups. Plasma glucose levels at 3, 6, 9, 12, and 15 min after insulin administration (0.5 U/kg) in the nicotine group were significantly lower than those in the control group. The calculated K ITT value for the nicotine group was significantly higher than that for the control group. Wet weight of the liver in the nicotine group was significantly lower than that in the control group. Transaminases and histological examination of the liver revealed no alteration by nicotine administration. Glycogen, glycogen synthetase activity and gluconeogenesis in the liver in the nicotine group were significantly lower than those in the control group. Phosphorylase-a activity of the liver in the nicotine group was significantly higher than that in the control group. Glycogen, glycogen synthetase, and phosphorylase-a activity of skeletal muscle were similar in both groups. These results suggest that long-term oral nicotine administration may reduce insulin resistance in obese diabetic rats through a reduced hepatic glucose release and, in part, contribute to lowering blood glucose levels.

Effects of food deprivation on 24 h‐changes in brain and liver carbohydrate and ketone body metabolism of rainbow trout

Plasma glucose, lactate and acetoacetate, brain glycogen and acetoacetate, and liver acetoacetate, glycogen and lactate in fed rainbow trout exhibited daily changes. However, no daily changes were observed in the activities of the brain enzymes glycogen synthetase, 6‐phosphofructo 1‐kinase, and lactate dehydrogenase. Depending on the length of the previous fasting period most daily changes observed in the metabolic parameters of fed fish disappeared, except for liver acetoacetate levels, which displayed daily changes in both fed and fasted fish. These results suggest that feeding is an important factor regulating most daily changes in the brain and liver carbohydrate and ketone body metabolism of rainbow trout.

Time course for cryoprotectant synthesis in the freeze-tolerant chorus frog, Pseudacris triseriata

Increases in liver glycogen phosphorylase activity, along with inhibition of glycogen synthetase and phosphofructokinase-1, are associated with elevated cryoprotectant (glucose) levels during freezing in some freeze-tolerant anurans. In contrast, freeze-tolerant chorus frogs, Pseudacris triseriata, accumulate glucose during freezing but exhibit no increase in phosphorylase activity following 24-h freezing bouts. In the present study, chorus frogs were frozen for 5- and 30-min and 2- and 24-h durations. After freezing, glucose, glycogen, and glycogen phosphorylase and synthetase activities were measured in leg muscle and liver to determine if enzyme activities varied over shorter freezing durations, along with glucose accumulation. Liver and muscle glucose levels rose significantly (5–12-fold) during freezing. Glycogen showed no significant temporal variation in liver, but in muscle, glycogen was significantly elevated after 24 h of freezing relative to 5 and 30 min-frozen treatments. Hepatic phosphorylase a and total phosphorylase activities, as well as the percent of the enzyme in the active form, showed no significant temporal variation following freezing. Muscle phosphorylase a activity and percent active form increased significantly after 24 h of freezing, suggesting some enhancement of enzyme function following freezing in muscle. However, the significance of this enhanced activity is uncertain because of the concurrent increase in muscle glycogen with freezing. Neither glucose 6-phosphate independent (I) nor total glycogen synthetase activities were reduced in liver or muscle during freezing. Thus, chorus frogs displayed typical cryoprotectant accumulation compared with other freeze-tolerant anurans, but freezing did not significantly alter activities of hepatic enzymes associated with glycogen metabolism.

Differential response of rat skeletal muscle glycogen metabolism to testosterone and estradiol

Although reports on sex steroids have implicated them as promoting protein synthesis and also providing extra strength to the skeletal muscle, it remains unclear whether sex steroids affect glycogen metabolism to provide energy for skeletal muscle functions, since glycogen metabolism is one of the pathways that provides energy for the skeletal muscle contraction and relaxation cycle. The purpose of the current study was to show that testosterone and estradiol act differentially on skeletal muscles from different regions, differentially with reference to glycogen metabolism. To study this hypothesis, healthy mature male Wistar rats (90-120 days of age, weighing about 180-200 g) were castrated (a bilateral orchidectomy was performed to test the significance of skeletal muscle glycogen metabolism in the absence of testosterone). One group of castrated rats was supplemented with testosterone (100 microg/100 g body weight, i.m., for 30 days from day 31 postcastration onwards). To test whether estradiol has any effect on male skeletal muscle glycogen metabolism 17beta-estradiol (5 microg/100 g body weight, i.m., for 30 days from day 31 postcastration onwards) was administered to orchidectomized rats. To test whether these sex steroids have any differential effect on skeletal muscles from different regions, skeletal muscles from the temporal region (temporalis), muscle of mastication (masseter), forearm muscle (triceps and biceps), thigh muscle (vastus lateralis and gracilis), and calf muscle (gastrocnemius and soleus) were considered. Castration enhanced blood glucose levels and decreased glycogen stores in skeletal muscle from head, jaw, forearm, thigh, and leg regions. This was accompanied by diminished activity of glycogen synthetase and enhanced activity of muscle phosphorylase. Following testosterone supplementation to castrated rats, a normal pattern of all these parameters was maintained. Estradiol administration to castrated rats did not bring about any significant alteration in any of the parameters. The data obtained suggest a stimulatory effect of testosterone on skeletal muscle glycogenesis and an inhibitory effect on glycogenolysis. Estradiol did not play any significant role in the skeletal muscle glycogen metabolism of male rats.

Changes in the activity levels of glutamine synthetase, glutaminase and glycogen synthetase in rats subjected to hypoxic stress.

Exposure to high altitude causes loss of body mass and alterations in metabolic processes, especially carbohydrate and protein metabolism. The present study was conducted to elucidate the role of glutamine synthetase, glutaminase and glycogen synthetase under conditions of chronic intermittent hypoxia. Four groups, each consisting of 12 male albino rats (Wistar strain), were exposed to a simulated altitude of 7620 m in a hypobaric chamber for 6 h per day for 1, 7, 14 and 21 days, respectively. Blood haemoglobin, blood glucose, protein levels in the liver, muscle and plasma, glycogen content, and glutaminase, glutamine synthetase and glycogen synthetase activities in liver and muscle were determined in all groups of exposed and in a group of unexposed animals. Food intake and changes in body mass were also monitored. There was a significant reduction in body mass (28-30%) in hypoxia-exposed groups as compared to controls, with a corresponding decrease in food intake. There was rise in blood haemoglobin and plasma protein in response to acclimatization. Over a three-fold increase in liver glycogen content was observed following 1 day of hypoxic exposure (4.76 +/- 0.78 mg.g-1 wet tissue in normal unexposed rats; 15.82 +/- 2.30 mg.g-1 wet tissue in rats exposed to hypoxia for 1 day). This returned to normal in later stages of exposure. However, there was no change in glycogen synthetase activity except for a decrease in the 21-days hypoxia-exposed group. There was a slight increase in muscle glycogen content in the 1-day exposed group which declined significantly by 56.5, 50.6 and 42% following 7, 14, and 21 days of exposure, respectively. Muscle glycogen synthetase activity was also decreased following 21 days of exposure. There was an increase in glutaminase activity in the liver and muscle in the 7-, 14- and 21-day exposed groups. Glutamine synthetase activity was higher in the liver in 7- and 14-day exposed groups; this returned to normal following 21 days of exposure. Glutamine synthetase activity in muscle was significantly higher in the 14-day exposed group (4.32 mumol gamma-glutamyl hydroxamate formed.g protein-1.min-1) in comparison to normal (1.53 mumol gamma-glutamyl hydroxamate formed.g protein-1.min-1); this parameter had decreased by 40% following 21 days of exposure. These results suggest that since no dramatic changes in the levels of protein were observed in the muscle and liver, there is an alteration in glutaminase and glutamine synthetase activity in order to maintain nitrogen metabolism in the initial phase of hypoxic exposure.

Regulation of Enzymes of Carbohydrate Metabolism during Anoxia in the Salt Marsh BivalveGeukensia demissus

The effects of anoxia exposure (2 or 12 h at 5°C) on the tissue-specific responses by enzymes of carbohydrate metabolism were analyzed in the mantle, gill, hepatopancreas, and adductor muscle of the intertidal bivalve Geukensia demissus demissus. Reversible enzyme phosphorylation has been identified in other species of marine molluscs as a mechanism for coordinating the suppression of metabolic rate and the redirection of carbon into fermentative pathways under anoxic conditions. The present study shows patterns of response to anoxia by five enzymes of carbohydrate metabolism, including glycogen synthetase (GS) and pyruvate dehydrogenase (PDH), whose responses to anoxia have not before been analyzed in marine molluscs. Anoxia-induced changes in properties, consistent with reversible phosphorylation modification of the enzymes, were found for pyruvate kinase (PK) and PDH in all tissues and in selected tissues for glycogen phosphorylase (GP) and GS. However, phosphofructokinase did not appear to be modified in any tissue during anoxia. Within 2 h ofanoxia exposure, PK showed a sharp drop in the activity ratio (at subsaturating vs. saturating PEP concentrations) that indicated a stable modification of enzyme Km for PEP; for example, in the gill, the ratio (determined at 0.75 and 7.5 mM PEP) fell from 0.39 ± 0.08 for aerobic controls to 0.08 ± 0.01 after 2 h anoxia. The percentage of PDH in the active a form also dropped significantly in anoxia from 80%-84% PDHa in controls to 65%-75% PDHa in anoxic tissues. Changes in both of these enzymes are consistent with anoxia-induced metabolic rate suppression. By contrast, anoxia exposure increased GP activity in the gill and adductor muscle, indicating a need for increased glycogenolysis during anoxia in these tissues. Total phosphorylase (a + b) activity increased in both tissues, as did the percentage of a in the adductor; for example, in the adductor, active GPa content rose from 0.09 ± 0.02 U/g wet wt in controls to 0.24 ± 0.01 U/g wet wt after 2 h and to 0.16 ± 0.02 U/g wet wt after 12 h of anoxia exposure. Glycogen synthetase behaved oppositely in hepatopancreas, showing a significant decrease in total activity in 12-h anoxic tissue, but GS was unaffected by anoxia in the gill or the adductor muscle. In the mantle, oppositely directed changes in total GS activity and the percentage active resulted in no net change in the activity of the active I form during anoxia.

Effects of Salbutamol, a β2-Adrenergic Agonist, on Muscles of Growing Pigs Fed Different Levels of Dietary Protein: II. Aerobic and Glycolytic Capacities and Glycogen Metabolism of the Longissimus Dorsi Muscle

Abstract Dietary inclusion of salbutamol (3 ppm), a β2-adrenergic agonist, to growing pigs from 25 to 90 kg body weight reduced the activities of citrate synthetase (CS) (P<0.01) and 3-OH-acyl-CoA-dehydrogenase (HAD) (P<0.07) by 10 and 8%, respectively, measured on needle biopsies obtained from the fast-twitch-glycolytic longissimus dorsi muscle at 25, 45, 60 and 90 kg body weight. These reductions by salbutamol were induced at 60 kg body weight and remained unchanged. On the other hand, salbutamol did not affect the activities of lactate dehydrogenase (LDH), total glycogen synthetase (GS), the glucose-6-phosphate independent form of GS, and muscle glycogen content. The activity of LDH increased by 41% from 25 to 90 kg body weight (P<0.001), with the steepest increase from 25 to 45 kg body weight, while the activities of CS and HAD decreased by 25 (P<0.001) and 19% (P<0.001) in control animals, respectively. The total GS activity was decreased at 60 and 90 kg body weight by 24% (P<0.01), whereas the independent form of GS did not change in the body weight range examined. The glycogen content was reduced by 20% (P<0.05) at 90 kg body weight compared to the other body weights. These results indicate that salbutamol treatment decreases muscle oxidative capacity. In addition, a marked shift in the metabolic profile towards a higher glycolytic and a lower oxidative capacity occurs in the longissimus dorsi muscle during growth in pigs.

Hypoglycaemic effect of Coccinia indica: mechanism of action.

The hypoglycaemic effect of orally administered extracts of leaves and roots of Coccinia indica has been reported earlier. The oral administration of the pectin isolated from the fruit of the above plant at a dose of 200 mg/100 g BW/day showed a significant hypoglycaemic action in normal rats. Pectins isolated from many other plants have also been reported to have hypoglycaemic actions. The pectin administration resulted in a significant reduction in blood glucose and an increase in the liver glycogen. Glycogen synthetase activity was highly significant. Incorporation of labelled glucose into hepatic glycogen was also found to be higher. A significant reduction in phosphorylase activity was noted in the pectin-administered groups.

Influence of oral administration of estradiol-17? and testosterone on growth, digestion, food conversion and metabolism in the underyearling red sea bream, Chrysophrys major

Estradiol-17β (E2) administered in the diet to the red sea bream Chrysophrys major did not affect appetite, food conversion efficiency, protein efficiency ratio and specific growth rate. Serum concentrations of total protein, albumin, globulin, vitellogenin, α-amino acids, total lipid, free fatty acids, cholesterol and calcium were elevated. The hepatosomatic index was also increased. Activities of hepatic enzymes including lactate dehydrogenase, isocitrate dehydrogenase and glutamate-pyruvate transaminase were higher than found in untreated control fish. Intestinal activity of leucine aminopeptidase was augmented. However, there were no changes in muscle water, protein, lipid and glycogen content. In contrast, testosterone (T) given by the same route increased appetite, food conversion efficiency, protein efficiency ratio and specific growth rate. There were no alterations in serum protein and calcium concentrations but serum glucose, ammonia and triglyceride levels were elevated. Hepatic glycogen content was increased. The activities of hepatic fructose- 1,6-diphosphatase, glucose-6-phosphatase and glycogen synthetase and intestinal activities of alkaline phosphatase and τ-glutamyltransferase were higher than noted on control fish. The results reveal that estradiol-17β and testosterone exerted different metabolic effects in the red sea bream and they suggest that testosterone exerts its anabolic actions by increasing appetite, food conversion efficiency and activities of digestive enzymes.

The regulation of glycogen synthesis in the fetal rat liver in the near term

In order to clarify the mechanism of regulation of glycogen metabolism in fetal rat liver during gestation, we measured glycogen synthetase activity, and the binding capacity of the insulin receptor. We also examined the possibility of glycogen synthesis through gluconeogenesis. Major findings are as follows: 1) Glycogen content in fetal liver increased dramatically during gestation and peaked on Day 21 of gestation (one day before delivery). 2) Both the total glycogen synthetase activity (a: active enzyme+b: inactive enzyme) and the ratio of the activities of a to a+b also rose during gestation, suggesting that an increase in the active form of glycogen synthetase is a major cause of the increase in the amount of glycogen in fetal liver. 3) Insulin is known to stimulate glycogen synthesis by activating glycogen synthetase. However, the number and the affinity constant of the insulin receptor in fetal liver did not changed, although the concentration of serum insulin increased during gestation. 4) The ratio of glycogen synthesized from serum glycerol relative to that from serum glucose plus glycerol increased from 8% on Day 19 to 22% on Day 21. Since stimulation of gluconeogenesis is considered to result in an accumulation of glucose-6-phosphate, a potent activator for glycogen synthetase, glyconeogenesis from glycerol may play an important role in glycogen storage in fetal liver.

Changes in muscle carbohydrate metabolism in domesticated rainbow trout ( Oncorhynchus mykiss) after transfer to seawater

1. 1. A study of glycogen and glucose levels, as well as the activities of glycogen phosphorylase (GPase), glycogen synthetase (GSase), fructose 1,6-bisphosphatase (FBPase), phosphofructokinase (PFD) and glucose 6-phosphate dehydrogenase (G6PDH) was carried out in white and red muscle of domesticated rainbow trout ( Oncorhynchus mykiss) of two different weights [small(80g) and large (140g)] after transfer to seawater (28 p.p.t.) for 21 days. 2. 2. A fall in glycogen levels for both sizes assessed was observed in both types of muscle. 3. 3. Glucose levels followed opposite trends in both tissues in seawater animals: they were higher in red muscle, but smaller in white muscle when compared with those of freshwater animals. 4. 4. An increase in glycolytic activity was only observed in white muscle. 5. 5. These results seem to indicate that seawater adaptation of rainbow trout induces glycogenolysis in white and red muscle, with the glucose produced in white muscle being used in situ through glycolysis.

Glycogenesis in the cultured fetal and adult rat hepatocyte is differently regulated by medium glucose.

We examined the glycogenic response to glucose in cultured fetal and adult rat hepatocytes. After a 48-h culture in Dulbecco's modified Eagle's medium, 1 mM glucose, insulin, and cortisol, cells were cultured for 4 h in serum-free medium containing glucose (1-30 mM) and U-14C-glucose. Incorporation of 14C-glucose into glycogen was greater in fetal hepatocytes compared with adult hepatocytes at all glucose concentrations (p < 0.001). Net glycogenic rate in fetal cells was greatest between 1 and 8.3 mM (7.7- +/- 1.1-fold increase) compared with a 3.8- +/- 0.6-fold increase in adult cells. In contrast, there was a 19.4- +/- 2.7-fold increase in glycogen accumulated between 8.3 and 30 mM glucose in the adult and a 1.6 +/- 0.1-fold increase in the fetus. Total glycogen synthetase activity was higher in fetal than adult hepatocytes (p < 0.001), but the active a form was similar in fetal and adult hepatocytes. Glycogen synthase a/+b was stimulated at 8.3 mM or greater glucose in fetal hepatocytes, and 5.7 mM or greater in adult hepatocytes (p < 0.05). Total phosphorylase did not change with medium glucose, but glycogen phosphorylase a/a4+b decreased in adult hepatocytes incubated in 5.7 mM glucose or greater (p < 0.05). Fetal phosphorylase a/a+b was increased at 8.3 mM or greater glucose (p < 0.05). In contrast, both adult and fetal phosphorylase were activated by glycogen. A glucose-induced increase in active phosphorylase may induce the decrease in net glycogenic rate at high glucose in fetal hepatocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of cortisol and thyroid hormone treatment on the glycogen metabolism of selected tissues of domesticated rainbow trout, Oncorhynchus mykiss

Glycogen, glucose, protein and glycogen phosphorylase and glycogen synthetase activity in liver, white muscle and kidney were determined in domesticated rainbow trout ( Oncorhynchus mykiss) treated with 3,5,3′-triiodo-L-thyronine (T 3), thyroxine (T 4) and cortisol and combinations of all these hormones for 10 days. Plasma protein and glucose levels were also determined. Declines in liver glycogen and glucose were observed after cortisol treatment as compared to values obtained in controls (controls: 27.54 ± 1.73 mg glycogen/g and 16.81 ± 1.50 mg glucose/g) such as 15.94 ± 2.64 mg glycogen/g and 8.63 ± 1.22 mg glucose/g. T 4 treatment did not produce any effects on the measured parameters. T 3 plus T 4 treatment caused a fall in hepatic glycogen and glucose levels ( 11.97 ± 1.27 mg glycogen/g and 8.98 ± 2.06 mg/g, respectively). All cortisol and thyroid hormone combinations produced a fall in liver glycogen levels (range between 6.07 ± 1.19 and 16.38 ± 1.56 mg glycogen/g) as well as an increase (from 37 to 44%) in glycogen phosphorylase activity. No changes were observed in any of the measured parameters for the different hormone treatments assessed in white muscle and kidney. Under our experimental conditions, cortisol and probably T 3 are involved in liver glycogen mobilization and apparently do not elicit a response in white muscle and kidney.

Alterations of Polymorphonuclear Leukocyte Glycogen Metabolism and Glucose Uptake in Dialysis Patients

Human polymorphonuclear leukocytes (PMNs) are activated during extracorporeal circulation. An indicator of PMN activation may be the glycogen-degrading enzyme phosphorylase. It is unknown whether dialysis therapy may influence PMN carbohydrate metabolism. Therefore, PMNs were isolated from healthy control subjects, patients undergoing continuous ambulatory peritoneal dialysis (CAPD), and patients undergoing regular hemodialysis therapy (RDT) before, during, and at the end of hemodialysis (HD) treatment using dialyzers made of polysulfone or polymethylmethacrylate (PMMA). Nifedipine (NIF) was continuously infused during HD with PMMA in 5 patients at a dose of 18 micrograms/kg body weight per hour. Glycogen, activity of glycogen synthetase and phosphorylase (active and inactive forms of both enzymes), and glucose uptake with and without stimulation with the chemotactic peptide FMLP were determined in these PMNs. During HD with PMMA, there was a significant increase of PMN phosphorylase "a" activity 15 and 30 minutes after the start of HD. HD with polysulfone did not stimulate the active "a" form of the glycogen-degrading enzyme in PMNs. HD with PMMA significantly inhibited the active I-form of glycogen synthetase, whereas polysulfone activated glycogen synthetase I. NIF inhibited phosphorylase "a" activation during HD with PMMA. PMN glycogen content and glucose uptake were improved during HD with polysulfone, but not with PMMA. PMN glycogen content, activity of glycogen synthetase, and glucose uptake were significantly lower also in CAPD patients compared with healthy controls. These data show that HD with PMMA activates PMN glycogenolysis. This effect can be inhibited by calcium channel blockers. PMN glycogen content of RDT and CAPD patients is significantly lower compared with healthy controls due to inhibition of glycogen synthesis. Elimination of dialyzable factor(s) improves, but does not restore, PMN glycogen synthesis and glucose uptake.