A comparison of direct enzymatic determination of glycogen in liver and heart.
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Effects of lactation on circulating plasma metabolites in 'cafeteria-fed' rats.
1. The effects of 'cafeteria feeding' on primiparous Wistar rats during lactation have been studied by measuring circulating levels of glucose, amino acids, lactate, urea and ammonia as well as glycogen levels in liver and muscle. 2. No significant changes in glucose levels were observed despite alterations in blood glucose compartmentation. 3. Compared with controls, the dams given the cafeteria diet had higher liver glycogen stores which were more easily mobilized at the peak of lactation. 4. Rats given the cafeteria diet showed a lower amino acid utilization than controls and adequately maintained circulating levels, as determined by the lower circulating levels of ammonia and urea. 5. No significant differences in body-weight were observed in the period studied despite increasing dam weight after weaning in the cafeteria-fed group. 6. The size of pups of cafeteria-fed dams was greater than that of controls, and the differences were marked after weaning, when the metabolic machinery of the cafeteria pup maintained high protein accretion and body build-up using fat as the main energy substrate characteristic of the preweaning stage. The controls, however, changed to greater utilization of amino acids as an energy substrate and adapted to high-protein (low-biological-quality) diets with a significantly different pattern of circulating nitrogen distribution.
Amino Acids↗
Metabolic and hormonal changes following endotoxin administration to diabetic rats.
The aim of these investigations was to study the time course and cause of the altered metabolic response of diabetic rats to endotoxin administration. Escherichia coli endotoxin was administered to streptozotocin-diabetic and control normoglycemic rats. At 1, 2, 5, 8, and 24 h following endotoxin, animals were decapitated. Plasma samples were analyzed for glucose, lactate, insulin, glucagon, and corticosteroids. In addition, tissue glycogen content of liver and skeletal muscle was determined. Endotoxin caused an elevation of plasma glucose in both diabetic and normoglycemic rats by 1 h postinjection. The elevation was prolonged in diabetic rats for 8 h but lasted only 2 h in nondiabetic rats. Both endotoxin-treated groups demonstrated hyperlactacidemia following endotoxin. Endotoxin led to liver glycogen depletion in both diabetic and normoglycemic rats, whereas muscle glycogen content was only slightly affected. Plasma glucagon and corticosteroids rose immediately and remained elevated in both endotoxin-treated groups. A significant insulin response to rising plasma glucose was observed in nondiabetic but not in diabetic rats following endotoxin. These results suggest that the exaggerated and prolonged hyperglycemia observed in diabetic endotoxin-treated rats is due to hypersecretion of glucose-mobilizing hormones and elevated gluconeogenesis, unmatched by an adequate secretion of insulin to promote glucose uptake and utilization.
Adrenal Cortex Hormones↗
The effects of a high carbohydrate diet on postprandial energy expenditure during exercise in rats.
Whether or not a high intake of carbohydrate increases postprandial energy expenditure during exercise was studied in rats. The rats were meal-fed regularly twice a day (0800-0900 hours and 1800-1900 hours) on either a high carbohydrate (CHO) (carbohydrate/fat/protein = 70/5/25, % of energy) or high fat (FAT) (35/40/25) diet for 12 days. On the final day of the experiment, all of the rats in each dietary group were fed an evening meal containing equal amounts of energy (420 kJ.kg-1 body mass). After the meal, they were divided into three subgroups: pre-exercise control (PC), exercise (EX), and resting control (RC). The PC-CHO and PC-FAT groups were sacrificed at 2030 hours. The EX-CHO and EX-FAT groups were given a period of 3-h swimming, and then sacrificed at 2330 hours. The RC-CHO and RC-FAT groups rested after the meal and were sacrificed at 2330 hours. Total energy expenditure during the period 1.5 h from the commencement of exercise was higher in EX-CHO than in EX-FAT. The respiratory exchange ratio was also higher in EX-CHO than in EX-FAT, suggesting enhanced carbohydrate oxidation in the former. Compared with both PC-FAT and RC-FAT, the liver glycogen content of EX-FAT rats was significantly decreased by exercise. On the other hand, the liver glycogen content of both EX-CHO and RC-CHO was higher than that of PC-CHO rats. The glycogen content of soleus muscle of EX-FAT was slightly decreased during exercise, however, that of EX-CHO increased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Utilization of dietary amino acids for energy production in neonatal rat liver.
The 3-day-old rat has a high basal level of phosphoenolpyruvate carboxykinase (PEPCK), the activity of which is not increased upon starvation. The lower basal activity of the enzyme in 19-day-old rat liver can, however, be stimulated by starvation. Serum glucose levels increased from 3 days to 19 days of age, with a decrease to adult levels. Liver glycogen concentration increased from 3 days to 19 days of age, with no additional increase observed at 3 months. There was a decrease with age in the specific activity of liver glycogen (from [14C]alanine and [14C]leucine). In fed rats given [14C]alanine, 14CO2 expiration tended to decrease with age. The 14CO2 production from [14C]leucine was less than that from alanine, and also decreased with age. Three-day-old rats showed no change in serum glucose when starved for 4 hr. On the other hand, 19-day-old rats responded with a decrease in serum glucose; although the adult animal's basal level of serum glucose was less than that of the 19-day-old rats, starvation for 15 hr also caused a significant decrease. There was no statistically significant difference in liver glycogen concentration between the fed and starved 3-day-old animals. Liver glycogen concentration in the 19-day-old adult rats was affected, however, by starvation. The 3-day-or glycogen during starvation. Starvation resulted in a tremendous increase in the specific activity of hepatic glycogen in the 19-day-old and adult rats. Starvation decreased the percentage of labeled amino acid expired as 14CO2. The proportion expired also decreased with age. Urinary nitrogen concentration increased significantly between 3 and 19 days of age. Starvation produced differential effects in the animals, with no change being observed in either the 3-day or adult rats; a decrease was observed in the 19-day-old animals. Urinary nitrogen concentration was measured in adult carbohydrate-deprived rats and was significantly higher than control values. These rats had a high gluconeogenic rate, reflected in the increased urinary nitrogen concentration. The young rat is at the mercy of a continuous supply of substrate in that it has a limited capacity for directing substrat
Amino Acids↗
Inhibition of glucose production during hepatic nerve stimulation in regenerating rat liver perfused in situ. Possible involvement of gap junctions in the action of sympathetic nerves.
To explore the possible role of gap junctions in neural regulation of hepatic glucose metabolism, the effects of hepatic nerve stimulation on metabolic and hemodynamic changes were examined in normal and regenerating rat liver which was perfused in situ at constant pressure via the portal vein with a medium containing 5 mM glucose, 2 mM lactate and 0.2 mM pyruvate. 1. The content of connexin 32, a major component of gap junctions in rat liver, decreased transiently to about 25% of the control level in regenerating liver 48-72 h after partial hepatectomy and recovered to normal by the 11th day after the operation. 2. In normal liver, electrical stimulation of the hepatic nerves (10 Hz, 20 V, 2 ms) and infusion of noradrenaline (1 microM) both increased glucose and lactate output and reduced perfusion flow. 3. In early stage of regenerating liver 48 h and 72 h after partial hepatectomy, the increase in glucose output in response to nerve stimulation was almost completely inhibited, whereas the change in lactate balance was partially suppressed and the reduction of flow rate was retained. The response of glucose output to nerve stimulation recovered by the 11th day after partial hepatectomy. In contrast, exogenous application of noradrenaline increased glucose output even in the early stage of regenerating liver. 4. The increase in noradrenaline overflow during hepatic nerve stimulation in the early stage of regenerating liver was approximately the same as in normal liver. Liver glycogen was sufficiently preserved in the early stage of regenerating liver. However, noradrenaline infusion could no more increase glucose output both in normal and in regenerating livers after 24 h of fasting that depleted liver glycogen. These results suggest that the impaired effects of sympathetic nerve stimulation on glucose metabolism observed in regenerating liver are derived neither from reduced release of noradrenaline nor from depletion of liver glycogen, but rather from transient reduction of gap junctions which assist signal propagation of the nerve action through intercellular communication in rat liver.
Animals↗
Influence of the route of glucose administration on hepatic glycogen repletion.
To delineate the role of the route of glucose administration on liver glycogen synthesis, we administered [1-13C]glucose either by intravenous or intraduodenal infusion to chronically catheterized 24-h fasted rats and performed 1) intravenous-hyperglycemic clamp (group I, n = 9), portal vein plasma glucose and insulin concentrations were 216 +/- 6 mg/dl and 23.9 +/- 4.2 ng/ml; 2) intraduodenal-hyperglycemic infusion (group II, n = 8), portal vein glucose and insulin concentrations were 219 +/- 6 mg/dl and 17.5 +/- 2.7 ng/ml; and 3) intravenous-hyperglycemic-suprahyperinsulinemic clamp (group III, n = 5), portal vein glucose and insulin concentrations were 203 +/- 12 mg/dl and 44.6 +/- 5.0 ng/ml. The mean glucose infusion rates (mumol.kg-1.min-1) and glycogenic rates (mumol.g liver-1.min-1) were 201 +/- 8, 0.34 +/- 0.05; 129 +/- 3, 0.73 +/- 0.11; and 269 +/- 19, 0.38 +/- 0.08 in groups I-III, respectively. The percent of glycogen synthesized by the direct pathway was group I = 43 +/- 6%, group II = 44 +/- 6%, and group III = 46 +/- 7%. In conclusion, despite similar or lower portal vein insulin and glucose concentrations, the intraduodenal route of glucose administration (group II), compared with the intravenous route (groups I and III), markedly increased the total amount of liver glycogen synthesized without altering the percent of the direct vs. indirect pathways by which liver glycogen was repleted.
Animals↗
The liver and glycogen metabolism.
It was shown that the liver is not the major site of removal of glucose after a carbohydrate meal in man. Fractional extractions varied from 5 to 10%. Alternative substrates for postprandial hepatic glycogen synthesis were therefore sought. It was demonstrated than, in man, about 60% of hepatic glycogen was formed from gluconeogenetic substrates. Since significant excursions occur only in plasma lactate after glucose loading, this was deemed the most likely substrate under these circumstances. By differential sampling across the liver and the gut in a conscious pig model, it was found that the liver takes up enough lactate (fractional extraction of 40-50%) to account for the gluconeogenetic production of glycogen. Forty percent of this arises from the gut. Muscle (as represented by the forearm in man) does not contribute lactate during glucose loading, suggesting that other tissues such as the skin are of importance. The gluconeogenetic process may be an important site for the obligatory tissue production of lactate.
Animals↗
Relationships among prehatch and posthatch physiological parameters in early nutrient restricted broilers hatched from eggs laid by young breeder hens.
The objective of this study was to establish relationships among various physiological parameters in early (through 72 h posthatch) nutrient restricted broiler chicks from young breeder hens. Despite a 19% decrease in mean BW between 0 and 72 h posthatch, there were no chick mortalities. Liver glycogen peaked at 24 h, and peaks in rectal temperature, plasma glucose, and plasma refractive index occurred at 48 h. By 24 h, negative correlations were noted between BW and relative liver weight and between liver glycogen and both refractive index and rectal temperature. By 24 h, positive correlations were noted between relative liver weight and liver glycogen, BW and plasma glucose, rectal temperature and plasma glucose, and rectal temperature and body fat loss score. Mean daily relative egg weight loss between 0 and 19 d of incubation (RIEWL) was positively correlated with rectal temperature at 0 h but was negatively correlated with rectal temperature at 24 h and liver glycogen at 24 and 48 h. Furthermore, mean relative hatching chick weight (RHCW) had significantly positive correlations with plasma glucose at 6 h and rectal temperature at 48 and 72 h. Broilers having a greater RHCW after hatching from eggs with a lower RIEWL may maintain higher metabolic rates between 24 and 72 h posthatch despite nutrient deprivation. However, broiler chicks from eggs exhibiting a higher than optimal RIEWL may have greater dependence on gluconeogenesis, thus requiring stricter management during initial brooding.
Aging↗
Metabolic and hormonal effects of exercise in mild streptozotocin diabetes.
Metabolic and hormonal changes produced by muscular exercise were studied in rats with mild streptozotocin diabetes. In both diabetic and control animals the mean blood glucose increased and liver glycogen decreased during exercise. The postexercise blood glucose level correlated with the liver glycogen content in diabetic rats. A decrease of blood glucose occurred in some diabetic animals, and these also showed a decrease of liver glycogen to very low levels during exercise. During exercise the rise of plasma glycerol was higher in diabetic than in control animals, but changes in circulating free fatty acids, acetone bodies, insulin, corticosterone, lactate, and acid-base equilibrium were similar in the two groups. The results indicate that the only abnormal metabolic response to exercise in rats with mild diabetes is a slight increase of lipid mobilization.
Animals↗
Substrate utilization during acute exercise in obese Zucker rats.
The purpose of the present study was to compare the carbohydrate use of insulin-resistant obese Zucker rats with that of their lean littermates during steady-state exercise. Obese and lean rats were randomly assigned to a sedentary group or to a run group in which rats ran at 72-73% of their maximal O2 consumption, with the duration of exercise set to require an energy expenditure of 2.1-2.2 kcal. During the run the respiratory exchange ratio was significantly higher in the obese than in the lean rats [0.94 +/- 0.01 (SE) and 0.86 +/- 0.01, respectively], which indicate that the obese rats required 54% more carbohydrate than the lean rats. Total muscle glycogen utilization in the soleus, plantaris, and red and white gastrocnemius was not different between groups. Obese rats had total liver glycogen values five times greater than those of lean rats (833.38 +/- 101.4 and 152.8 +/- 37.5 mg, respectively) and utilized twice as much liver glycogen as their lean littermates (193.5 and 90.4 mg, respectively). The obese rats exhibited higher blood glucose and insulin concentrations than the lean rats during the run. These findings indicate that, despite their characteristic insulin resistance, the obese Zucker rats had a greater dependency on carbohydrate as a substrate during exercise than their lean littermates and that the major source of this carbohydrate was liver glycogen.
Animals↗
Carbohydrate metabolism in fructose-fed and food-restricted running rats.
In chronically catheterized rats hepatic glycogen was increased by fructose (approximately 10 g/kg) gavage (FF rats) or lowered by overnight food restriction (FR rats). [3-3H]- and [U-14C]glucose were infused before, during, and after treadmill running. During exercise the increase in glucose production (Ra) was always directly related to work intensity and faster than the increase in glucose disappearance, resulting in increased plasma glucose levels. At identical work-loads the increase in Ra and plasma glucose as well as liver glycogen breakdown were higher in FF and control (C) rats than in FR rats. Breakdown of muscle glycogen was less in FF than in C rats. Incorporation of [14C]glucose in glycogen at rest and mobilization of label during exercise partly explained that 14C estimates of carbohydrate metabolism disagreed with chemical measurements. In some muscles glycogen depletion was not accompanied by loss of 14C and 3H, indicating futile cycling of glucose. In FR rats a postexercise increase in liver glycogen was seen with 14C/3H similar to that of plasma glucose, indicating direct synthesis from glucose. In conclusion, in exercising rats the increase in glucose production is subjected to feedforward regulation and depends on the liver glycogen concentration. Endogenous glucose may be incorporated in glycogen in working muscle and may be used directly for liver glycogen synthesis rather than after conversion to trioses. Fructose ingestion may diminish muscular glycogen breakdown. The [14C]glucose infusion technique for determination of muscular glycogenolysis is of doubtful value in rats.
Animals↗
[Effect of food carbohydrate quality on monosaccharide utilization for the biosynthesis of glycogen, fat and proteins in the rat liver].
The inclusion of 3H-6-glucose and 14C-fructose metabolites into the rat liver glycogen, lipids and protein was studied in male rats receiving the rations containing 56% of carbohydrates, 18% protein, 26% fat, necessary amount of mineral substances and vitamins, during 25 days. Animals given the ration with starch, as a carbohydrate, were used as controls. In the ration of animals in groups 2, 3 and 4 some portion of starch (30% calorific value) was substituted for glucose, sucrose of the mixture of glucose and fructose (1:1). It was found that in the liver of animals given pure starch, radioactivity from 3H-6-glucose was included mainly into proteins, when starch was partly substituted for monosaccharide--mainly into lipids. These regularities were recorded in the distribution of radioactivity from 14C-fructose, all the parameters being shifted in the direction of increased inclusion of radioactivity into lipids. Partial substitution of starch for sucrose specifically changed the radioactivity distribution between proteins and lipids, thus revealing a distinct "disaccharide" effect.
Animals↗
Use of deuterium labelled glucose in evaluating the pathway of hepatic glycogen synthesis.
Deuterium labelled glucose has been used to study the pathway of hepatic glycogen synthesis during the fasted-refed transition in rats. Deuterium enrichment of liver glycogen was determined using nuclear magnetic resonance as well as mass spectroscopy. Sixty minutes after oral administration of deuterated glucose to fasted rats, the portal vein blood was fully enriched with deuterated glucose. Despite this, less than half of the glucose molecules incorporated into liver glycogen contained deuterium. The loss of deuterium label from glucose is consistent with hepatic glycogen synthesis by an indirect pathway requiring prior metabolism of glucose. The use of deuterium labelled glucose may prove to be a useful probe to study hepatic glycogen metabolism. Its use may also find application in the study of liver glycogen metabolism in humans by a noninvasive means.
Animals↗
Short-term hormonal control of protein phosphatases involved in hepatic glycogen metabolism.
The prominent protein phosphatases involved in liver glycogen metabolism are the AMD (ATP, Mg-dependent, type-1) and PCS (polycation-stimulated, type-2A) phosphatases. The glycogen synthase phosphatase activity, measured from the rate of activation of liver glycogen synthase, is virtually accounted for by AMD phosphatases; the bulk of the activity belongs to the glycogen-bound protein phosphatase G and a small part is present in the cytosol. The major part of the phosphorylase phosphatase activity present in the post-mitochondrial supernatant is shared by protein phosphatase G and cytosolic enzymes, and a minor part belongs to a microsomal AMD phosphatase. In the liver cytosol, the phosphorylase phosphatase activity is about equally distributed between AMD and PCS phosphatases. Studies in vivo as well as on isolated, perfused livers have shown that glucagon (which raises the level of cyclic AMP) as well as vasopressin (which increases the cytosolic Ca2+ concentration) decrease the phosphorylase phosphatase activity in liver extract or cytosol (filtered through Sephadex G-25) by about 25% within a few minutes. These effects were not additive, and the activity of glycogen synthase phosphatase was not affected. Conversely, insulin as well as glucose increased both phosphatase activities by about 25%, and these effects were additive. Vanadate mimicked the effect of insulin on the perfused liver. All the activity changes were only observed when the assays were performed at high tissue concentration. Upon subcellular fractionation all the effects were well expressed in the cytosol, but not in the particulate fraction (glycogen and microsomes). However, quantitatively the hormonal responses were largely lost during the fractionation procedure; they could be restored by recombination of the liver cytosol from a hormone-treated rat with the particulate fraction from either a treated or an untreated animal. It appears that the effects of glucagon, insulin and glucose are mediated by cytosolic, transferable effectors of the Vmax of protein phosphatases. These effectors are eluted in the void volume of a Sephadex G-25 column. Rats of the gsd/gsd strain, which have a genetic deficiency of hepatic phosphorylase kinase, responded to an injection of insulin plus glucose with a normal increase in the cytosolic phosphorylase phosphatase activity. In contrast, they failed to respond to glucagon as well as vasopressin. A transient 80% inhibition of the phosphorylase phosphatase activity could be induced in vitro in a concentrate liver cytosol from Wistar rats upon addition of MgATP.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Long-term treatment with 2,5-hexanedione has no effect on the specific activity of some brain and liver glycolytic enzymes of adult rats.
Prolonged exposure to hexacarbon compounds is neurotoxic to humans and animals. As various hexacarbon compounds inhibit glycolytic enzymes in vitro, it has been suggested that this may underlie their neurotoxic effects in vivo. In the present investigation we examined whether long-term treatment with 2,5-hexanedione (200 mg/kg,sc) for 40 days affects the specific activity of brain and liver enolase, lactic dehydrogenase and malate dehydrogenase in female Wistar rats (150-170 g). Glycemia and liver glycogen levels were also determined. The specific activity of all enzymes tested, liver glycogen content and glycemia were not affected by chronic treatment with 2,5-hexanedione. Rats treated with 2,5-hexanedione weighed significantly less than control rats starting on day 18 of treatment (183 +/- 3.4 g for the vehicle group vs 171 +/- 3.2 g for the 2,5-hexanedione group). 2,5-Hexanedione also increased water intake (46% when compared to vehicle-treated rats). Prolonged treatment of rats with the non-neurotoxic hexacarbon 1,6-hexanediol (207 mg/kg, sc) significantly increased liver glycogen content (5.9 +/- 0.6 g/100 g for the vehicle group vs 9.0 +/- 1.1 g/100 g for the 1,6-hexanediol group) as well as food intake (44.0 +/- 1.5 g 100 g-1 6 days-1 for the vehicle vs 50.0 +/- 1.1 g 100 g-1 6 days-1 for the 1,6-hexanediol group).(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Formaldehyde extraction of glycogen from liver.
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Formaldehyde↗
Two methods for the determination of glycogen in liver.
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Glycogen↗