Decrease In Glycogen Research Articles

ATP catabolism and adenosine generation during ischemia in the aging heart

Myocardial injury following ischemia and reperfusion is increased in the aging heart. The mechanisms underlying the increased susceptibility of the aging heart to ischemic injury remain unknown. We investigated whether decreased glycogen utilization with a more rapid depletion of ATP occurred during ischemia in the aging heart. Isolated buffer-perfused hearts from adult (6 months old) and aging (24 months old) Fischer 344 rats were subjected to 0, 2, 5, 10, 15 or 25 min of global stop-flow ischemia following a 15 min equilibration period ( n = 5–6 for each ischemic time at each age). ATP levels were decreased at preischemic baseline in aging hearts. ATP levels remained lower in the aging heart throughout ischemia ( P < 0.001) with a similar pattern of decrease in both age groups. The decrease in tissue glycogen and increase in lactate contents was similar during ischemia in both age groups, suggesting that comparable glycogen utilization occurred during ischemia in adult and aging hearts. ATP catabolism leads to ADP, AMP and then adenosine. Tissue levels of adenosine, an important cardioprotective metabolite, were measured during ischemia. Tissue adenosine levels were decreased by 50% in the aging heart at 5 and 10 min, and remained depressed at 15 min and 25 min of ischemia compared to adult controls. Thus, increased ischemic injury in the aging heart is not related to differences in glycogen consumption. Lower tissue ATP levels and decreased adenosine levels were observed during ischemia. The differences in ATP content between adult and aging hearts occurred only during early ischemia and are unlikely to provide a mechanism for the increased damage observed following more prolonged periods of ischemia in the aging heart. The potential contribution of these decreases in tissue adenosine content to the increased injury observed in the aging heart will require further study.

Mitochondrial enzymes increase in muscle in response to 7-10 days of cycle exercise.

Endurance exercise training induces a significant increase in the respiratory capacity of skeletal muscle. This is reflected by a training-induced increase in mitochondrial enzyme activity. One consequence of this adaptation is that there is a decreased reliance on carbohydrate utilization with a concomitant increase in fat utilization, resulting in an improvement in endurance capacity. Recently it has been reported that 7-14 days of cycle ergometer exercise training does not induce an increase in mitochondrial enzyme levels in skeletal muscle but, nevertheless, results in smaller decreases in phosphocreatine and glycogen and smaller increases in Pi and lactate in muscle in response to the same exercise after compared with before training. However, previous studies in rats have shown that an adaptive increase in mitochondrial enzymes is already evident after only 2 days of exercise training. In view of this discrepency, the present study was performed to reevaluate the effect of short-term training (7-10 days) on mitochondrial enzymes in skeletal muscle of humans. Twelve subjects [6 men and 6 women, 27 +/- 5 (SE) yr old] underwent 7 (n = 5) or 10 days (n = 7) of cycle ergometer exercise for 2h/day at 60-70% of peak O2 consumption. Peak O2 consumption was increased by 9% (from 2.97 +/- 0.16 to 3.24 +/- 0.17 l/min) in response to training. Blood lactate levels were lower at the same absolute work rates after than before training. The activities of citrate synthase, beta-hydroxyacyl-CoA dehydrogenase, mitochondrial thiolase, and carnitine acetyltransferase were increased by approximately 30% in response to training. The results of the present study provide evidence that in humans, as in rats, the adaptive increase in mitochondrial enzymes in skeletal muscle occurs fairly rapidly in response to exercise training. They provide no support for the claim that this adaptive response is delayed for > 2 wk after the onset of training.

Potentiation of hypoxic injury in cultured rabbit hepatocytes by the quinoxalinone anxiolytic, panadiplon

The quinoxalinone anxiolytic, panadiplon, produces hepatic metabolic inhibition (mitochondrial impairment), microvesicular steatosis and centrilobular necrosis in rabbits. Metabolic inhibition occurs in cultured hepatocytes without cytotoxicity, suggesting that hepatic injury is influenced by additional factors. The present experiments were conducted to determine if metabolic inhibition by panadiplon predisposed hepatocytes to hypoxic injury. Injury (cell death) was evaluated by lactate dehydrogenase (LDH) release from cells; ATP and glycogen levels were also evaluated. Under hypoxic conditions, control cultures showed a 6.5-fold increase in LDH release compared to normoxic controls, with a coincident 80% decrease in ATP and 50% decrease in glycogen levels. Under normoxic conditions, 10 μg/ml panadiplon treatment for 48 h reduced ATP and glycogen levels by 40% but did not cause an increase in LDH leakage. Cells treated with panadiplon, then exposed to hypoxia conditions, showed a significant level of injury compared to normoxic control cultures, and a further reduction in ATP. No additional decrease in glycogen was observed. In an attempt to prevent panadiplon-mediated injury, glycolytic substrates (dihydroxyacetone or pyruvate) were included during normoxic and hypoxic incubations. Both cotreatments reduced the level of LDH leakage produced by panadiplon during hypoxia. Cotreatment did not generally increase ATP or glycogen levels (compared to panadiplon treatment groups) during hypoxia, though individual experiments showed a slight increase in ATP levels. During normoxia both cotreatments with panadiplon resulted in significantly higher glycogen levels than in panadiplon cultures alone. These results suggest that cellular glycogen and subsequently ATP levels are reduced during panadiplon exposure, metabolically predisposing hepatocytes to hypoxic injury.

Occurrence and hormonal action of ecdysone on gametogenesis and energy utilization in the leech Nephelopsis obscura (Erpobdellidae)

AbstractThe present study provides novel information on the presence of compounds with ecdysone‐like activity and its involvement in the control of gonadal development in a leech. The presence of ecdysone was demonstrated in leech (Nephelopsis obscura) extract by means of high‐performance liquid chromatography (HPLC) in combination with radioimmunoassy. Leech extract was found to bind specifically to an anti‐ecdysone antiserum in a similar manner as standard ecdysone. Further HPLC purification demonstrated the presence of an immunoreactive fraction coeluting exactly with the standard ecdysone, strongly suggesting the presence of ecdysone in N. obscura. Addition of ecdysone to the ambient medium not only advanced leech gametogenesis but also influenced energy utilization. Both low (60 μg·L−1) and high (600 m̈g·L−1 concentrations of ecdysone increased testisac number, spermatogonia, 4th stage spermatogonia, ovisac size, and 2nd stage oogonia within 14 days compared to 35 days in the controls. Ecdysone also caused significant decreases in glycogen, total lipid, and triacylglycerols correlated with the energetic demands of gametogenesis. The findings provide support for the hypothesis that endogenous ecdysone is involved in the regulation of reproduction in N. obscura. © 1995 Wiley‐Liss, Inc.

Effect of hepatic vagotomy on plasma insulin levels during fasting in rats

The present investigation was designed to evaluate the effect of a selective hepatic vagotomy (HV) on the insulin response in rats fasted for 24 h when blood glucose levels were or were not maintained by a constant glucose infusion. Rats were divided into three dietary groups: one group of normally fed rats, one group of 24-h fasted rats, and one group of 24-h fasted rats infused with glucose throughout the fasting period. Each one of these groups was subdivided into HV and sham-operated (SHM) rats. Fasting without glucose infusion resulted in a significant ( p < 0.05) decrease in plasma glucose, liver glycogen, and insulin concentrations and in a significant ( p < 0.05) increase in β-hydroxybutyrate and FFA concentrations. Despite the maintenance of plasma glucose concentrations in the glucose-infused groups, the concentrations of liver glycogen and insulin were still decreased ( p < 0.01) and the concentrations of β-hydroxybutyrate were still increased ( p < 0.05) at the end of the fasting period. However, no significant differences in insulin or in β-hydroxybutyrate concentrations were found between HV and SHM rats. It is concluded that the decline in plasma glucose concentration during fasting does not totally explain the insulinopenic response to fasting, and that the liver, through the mediation of the hepatic vagus nerve does not seem to contribute to insulinopenia in 24-h fasted rats.

SOME BIOCHEMICAL STUDIES ON THE RODENTICIDE ZINC PHOSPHIDE

The present investigation is an attempt to study the hazardous effects associated with the use of the rodenticide zinc phosphide (Zn3,P2) in the albino rats as a useful model for man. The LD50 of Zn3, P2 205 mg/kg b.wt. caused a significant decrease (P < 0.05) of serum glucose and a highly significant decreases (P < 0.01) in liver and muscle glycogen. Total lipid contents, total protein contents, Aspartate amino transferase (AST) and Alanine aminotransferase (ALT) activities showed a great alterations. The sublethal dose of Zn3 P2 (102.5 mg/kd b.wt.) elicited a great deteriorations in all the above mentioned parameters in serum, liver and muscles. These deteriorating effects of Zn3 P2 may extend to the sixth day after its administration. Thus, the toxic effect of the rodenticide is not limited to the target animals, so it should be empolyed with a great care in rodent control.

Amylin regulation of carbohydrate metabolism.

This review describes how amylin may work in the control of carbohydrate metabolism by actions on gastric emptying and on muscle glycogen metabolism. Amylin, which is co-secreted with insulin from pancreatic beta-cells in response to nutrient stimuli, affects both carbohydrate absorption and carbohydrate disposal. Amylin appears to regulate carbohydrate metabolism as a partner to insulin. Defending fuel stores tends to be hierarchical; plasma glucose is defended first, then muscle glycogen, then liver glycogen, then fat. Fuel stores are replenished by both incorporating ingested nutrient and by translocating nutrient stores among body sites. Lactate may better be regarded as a vector of fuel transfer rather than a 'dead end' in metabolism. Amylin can promote the translocation of lactate from muscle to liver. The amylin effect, illustrated by the simultaneous decrease in muscle glycogen and increase in liver glycogen [53, 56], is similar to the catecholamine effect observed by Cori et al. [57]. Amylin thus may be important in maintaining liver glycogen stores via the Cori cycle and the 'indirect' glycogen synthesis pathway [58,59]. Unlike catecholamines, amylin does not mobilize fat or impede insulin action in adipose tissue [30,35]. It can supply lactate to the liver, and because lactate is a preferred lipogenic substrate [60], may thereby favour fat storage. Amylin may also help to control carbohydrate absorption via an 'entero-insular loop' to ensure that absorption from the gut remains within the regulatory limits for carbohydrate disposal by peripheral tissues. This regulatory system is essential for normal control of plasma glucose and appears to be disrupted in type-1 diabetes, an amylin-deficient state.

1015-71 Lower Adenosine Levels During Early Ischemia: Cause of Increased Injury in the Aging Heart?

Myocardial injury following ischemia and reperfusion is increased in the aging heart, including in the aging 24 mo Fischer 344 rat (mean survival 29 mo) compared to the Fischer 344 adult (6 mo). Adenosine (ADO) has been increasingly appreciated as a cardioprotective agent in myocardial ischemia. We hypothesized that a potential mechanism of the increased injury in the aging heart is decreased production of ADO in response to ischemia. Isolated buffer perfused (glucose 5 mM — insulin 5 μ /1) hearts from aging and adult Fischer 344 rats were subjected to stop-flow ischemia for either 2, 5, 10, 15 or 25 min after a 15 min equilibration phase. ADO and hypoxanthine (HX) were measured by HPLC. Tissue total adenylates, ATP, glycogen and lactate were measured. Ischemia Pre-ischemia 2 min 5 min 10 min 15 min 25 min (n = 5) (n = 5) (n = 5) (n = 5) (n = 5) (n = 5) ADO 6 mo 0.2 ± 0.1 0.7 ± 0.1 0.7 ± 0.1 2.2 ± 0.2 37 ± 0.6 4.5 ± 0.3 24 mo 0.2 ± 0.1 05 ± 0.1 0.3 ± 0.1 * 1.1 ± 0.3 * 2.1 ± 0.3 * 3.5 ± 0.4 HX 6 mo 2.0 ± 0.2 1.6 ± 0.2 2.3 ± 0.3 2.2 ± 0.1 25 ± 0.2 2.8 ± 0.2 24 mo 1.9 ± 0.2 1.4 ± 0.1 1.4 ± 0.2 * 2.1 ± 0.2 2.2 ± 0.8 3.5 ± 0.3 (Mean ± SE, nmol/mg protein) * p &lt; 0.05 vs 6 mo ADO levels were 50% lower in the aging heart at 5 and 10 min, remained depressed at 15 min and had not fully equalized to adult levels by 25 min of ischemia. HX was decreased at 5 min, consistent with decreased ADO production at that time. The change in total adenylate pool was similar in both groups. The decrease in tissue glycogen and increase in lactate were similar during ischemia in both groups, suggesting comparable glycolytic activity. ATP levels were decreased in aging hearts at 5 min (11.1 ± 2.3 vs 18.7 ± 1.9 nmol/mg protein), but reached levels similar to adult hearts as ischemia progressed. Thus, decreased ADO levels during early ischemia may reflect reduced production of ADO in the aging heart, and increase the susceptibility of the aging heart to damage during ischemia and reperfusion.

Changes in oxidative metabolism in selected tissues of the crab ( Scylla serrata) in response to cadmium toxicity

Changes in oxidative metabolism were studied in hepatopancreas, muscle, and hemolymph of the edible crab Scylla serrata, exposed to a sublethal concentration (2.5 ppm) of cadmium chloride. A significant decrease in glycogen, total carbohydrates, and pyruvate and an increase in lactate levels in hepatopancreas and muscle were observed. Hemolymph sugar levels were increased in experimental crabs. An increase in phosphorylase suggested increased glycogenolysis during cadmium toxicity. The decrease in lactate dehydrogenase activity and the increase in lactate content indicated reduced mobilization of pyruvate into the citric acid cycle. Krebs cycle enzymes such as succinate dehydrogenase and malate dehydrogenase were found to be decreased, suggesting impairment of mitochondrial oxidative metabolism as a consequence of cadmium toxicity. Glucose-6-phosphate dehydrogenase activity was increased, suggesting enhanced oxidation of glucose by the HMP pathway. Cytochrome-c oxidase and Mg 2+ ATPase activity levels decreased, indicating impaired energy synthesis during cadmium stress. Acid and alkaline phosphatase activities increased, suggesting enhanced breakdown of phosphates to release energy in view of impaired ATPase system during cadmium exposure. A significant decrease in protein and free amino acid and an increase in ammonia, urea, and glutamine levels were observed in the tissues during exposure. An increase in protease, alanine aminotransaminase, and asparate aminotransaminase suggested increased proteolysis and transamination of amino acids. The increase in glutamate dehydrogenase, AMP deaminase, and adenosine deaminase indicated increased ammonia production. The increased arginase and glutamine synthetase suggested the detoxification or mobilization of ammonia toward the production of urea and glutamine. These results suggest that cadmium affects oxidative metabolism and induces hyperammonemia, and crabs switch over their metabolic profiles toward compensatory mechanisms for the survivability in cadmium-polluted habitats.

NMDA and Not Non-NMDA Receptor Antagonists Are Protective against Seizures Induced by Homocysteine in Neonatal Rats

Homocysteine induces seizures in adult, as well as in immature, experimental animals, but the mechanism of its action is still unknown. The aim of the present study was to examine whether homocysteine in immature animals may act via excitatory amino acids receptors. Seizures were induced in 7-day-old rats by ip administration of homocysteine (16.5 mmol/kg) and the effects of selected antagonists at NMDA and non-NMDA receptor sites were investigated. The anticonvulsant effect was evaluated not only in terms of behavioral changes, but also in terms of some indicators of brain energy metabolism. Rat pups were sacrificed during generalized clonic-tonic seizures, corresponding approximately to 15-30 min after homocysteine administration. Comparable time intervals were used for sacrificing pups in the groups with protective drugs. Non-NMDA antagonists, l-glutamic acid diethylester (GDEE) (4 mmol/kg, ip) and 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo (F) quinoxaline (NBQX) (two doses, 30 mg/kg each, ip), failed to protect neonatal rats against homocysteine-induced seizures. Although NBQX prevented the tonic phase, the severity of clonic movements was even more pronounced. Metabolic changes accompanying the seizures (decreases of glucose and glycogen and a rise of lactate) were also not influenced by GDEE or NBQX pretreatment. On the contrary, NMDA antagonists, both competitive (AP7, 0.33 mmol/kg, ip) and noncompetitive (MK-801, 0.5 mg/kg, ip), had a clear-cut anticonvulsant effect. They not only suppressed the behavioral signs of seizures, but also prevented most of the metabolic changes accompanying seizures. Whether incomplete normalization of lactate levels reflects subclinical seizure activity or whether it is due to the effect of anatagonists (AP7, MK-801) themselves is not clear. All drugs, besides GDEE, when given alone caused a rise in brain glucose. This is the first demonstration that seizures induced by homocysteine can be blocked by NMDA antagonists. The findings thus suggest that, at least in neonatal rats, enhanced activation of NMDA receptors is implicated in homocysteine-induced seizures.

Lung parenchyma and type II cell morphometrics: effect of surfactant treatment on preterm ventilated lamb lungs

The effect of exogenous surfactant treatment on lung and type II cell structure of ventilated lambs of 137-138 days gestational age was studied. Thirty-four lambs were delivered and randomized to control or 100 mg/kg of natural sheep surfactant treatment groups. Lungs from one group of lambs not treated with surfactant were fixed before ventilation, and the other animals were ventilated to maintain normal blood gas values for 3, 24, or 48 h. Morphometric assessment of the inflation-fixed lung parenchyma of ventilated lungs was compared with the architectural appearance of alveoli and alveolar ducts in the unventilated lungs. Mechanical ventilation resulted in distension of alveolar ducts accompanied by the shallowing and loss of well-defined alveoli and areas of atelectasis at 3 h. These abnormalities increased in severity after 24 and 48 h of ventilation. Surfactant treatment before ventilation significantly reduced the extent and degree of dilatation and concomitant atelectasis. The fraction of normal parenchyma was 38 +/- 7% in untreated lambs vs. 64 +/- 6% in treated lambs after 24 h of ventilation. After 48 h of ventilation, significant differences between control (39 +/- 6%) and surfactant-treated (55 +/- 6%) lambs were still evident. Alveolar type II cells contained approximately 15% lamellar bodies by volume. Neither surfactant treatment nor time of ventilation altered the volume density of lamellar bodies or other organelles, except for a decrease in glycogen from 8% in nonventilated lungs to 2.5% in lungs ventilated for 24 h. These findings indicate that a surfactant treatment at birth results in the maintenance of more normal parenchyma with less atelectasis during prolonged ventilation of the immature lung.(ABSTRACT TRUNCATED AT 250 WORDS)

Biochemistry and physiology of overwintering in the mature larva of the sunflower stem weevil, Cylindrocopturus adspersus (Coleoptera: Curculionidae) in the Northern Great Plains

The sunflower stem weevil, Cylindrocopturus adspersus (LeConte), overwinters as a mature larva at the base of the stalk and in the root crown of cultivated sunflower plants. Sunflower stalks from fields known to be infested with C. adspersus larvae were collected in southeastern North Dakota in October 1991. Larvae from stalks kept outdoors accumulated a high whole-body concentration of trehalose (up to 69 μg/mg wet wt) at the expense of glycogen with the onset of winter followed by a partial reconversion of trehalose to glycogen with the onset of spring. Larvae from stalks acclimated to 0°C also accumulated a high level of trehalose (∼69 μg/mg wet wt) with a concomitant decrease in glycogen. Those larvae from stalks kept at 20°C showed an initial sharp increase in whole-body trehalose that then stabilized but at a concentration well below that of larvae acclimated to 0°C. This indicates that there exists in the larva an underlying developmental component to trehalose accumulation which is further enhanced by low temperature (0°C) exposure. The mean temperature of crystallization ( T c) of larvae exposed to outdoor conditions showed an abrupt drop from October (−25.0 ± 1.3°C) to November (−28.2 ± 0.6°C) with a minimum in February (−29.1 ± 0.3°C). The level of trehalose accumulated by the sunflower stem weevil larva is to our knowledge the highest reported in an overwintering insect.

Changes in host muscles induced by excretory/secretory products of larvalTrichinella spiralisandTrichinella pseudospiralis

Excretory/secretory (ES) products obtained by in vitro culture of infective-stage larvae of Trichinella spiralis and T. pseudospiralis were injected intramuscularly at various intervals into mice. Mini-osmotic pumps containing T. spiralis ES products were also implanted subcutaneously and intraperitoneally into rats. The introduction of ES materials into muscles elicited extensive lesions which included dissolution of myofibres, mobilization of mononuclear and polymorphonuclear leucocytes, angiogenesis, hypertrophy of myonuclei, myotube formation, mitosis, muscle bundles becoming rounded and separated from each other, disappearance of Z, I and A bands of sarcomeres, increase in endoplasmic reticulum and Golgi complexes, decrease in glycogen and relocation of mitochondria. These are considered as degenerative/regenerative changes of muscles to injury. Immunodominant epitopes of specific 45-53 kDa glycoproteins in ES antigens of T. spiralis could not be detected in hypertrophic nuclei of injected muscles by using polyclonal and monoclonal antibodies and immunocytochemical methods. ES products of T. spiralis failed to stimulate unsensitized lymphocytes in the lymphocyte transformation test. Infective-stage larvae of T. spiralis released from muscles were found capable of forming nurse cells after injection subcutaneously into rats. It is postulated that the invasion of muscles by trichinellids elicits two independent events, i.e. a general degenerative/regenerative response of muscles and a specific change in genomic expression of myonuclei. The two events are probably mediated by different effector molecules.

A comparative study on the responses of the gills of two mudskippers to hypoxia and anoxia

A comparison of branchial enzyme profiles indicates that the gills of Periophthalmodon schlosseri would have a greater capacity for energy metabolism through glycolysis than those of Boleophthalmus boddaerti. Indeed, after exposure to hypoxia, or anoxia, there were significant increases in the lactate content in the gills of P. schlosseri. In addition, exposure to hypoxia or anoxia significantly lowered the glycogen level in the gills of this mudskipper. It can be deduced from these results that the glycolytic flux was increased to compensate for the decrease in ATP production through anaerobic glycolysis. Different from P. schlosseri, although there was an increase in lactate production in the gills of B. boddaerti exposed to hypoxia, there was no significant change in the branchial glycogen content, indicating that a reversed Pasteur effect might have occurred under such conditions. In contrast, anoxia induced an accumulation of lactate and a decrease in glycogen in the gills of B. boddaerti. Although lactate production in the gills of these mudskippers during hypoxia was inhibited by iodoacetate, the decreases in branchial glycogen contents could not account for the amounts of lactate formed. The branchial fructose-2,6-bisphosphate contents of these mudskippers exposed to hypoxia or anoxia decreased significantly, leaving phosphofructokinase and glycolytic rate responsive to cellular energy requirements under such conditions. The differences in response in the gills of B. boddaerti and P. schlosseri to hypoxia were possibly related to the distribution of phosphofructokinase between the free and bound states.

No effect of carbohydrate feeding on glycogen synthase in human muscle during exercise.

The effect of carbohydrate (CHO) feedings on exercise-mediated changes in glycogen synthase fractional (GSF) activity has been investigated. Subjects cycled at approximately 70% of maximal oxygen uptake on two occasions: the first to fatigue (135 +/- 17 min; mean +/- SE) (control, CON), and the second at the same workload and duration as the first, but with the addition of frequent ingestion of CHO during exercise (0.27 g kg-1 body weight every 15 min). Biopsies were taken from the quadriceps femoris muscle before and immediately after exercise. Plasma glucose and insulin decreased during CON exercise, but remained elevated throughout CHO exercise (end of exercise: glucose = 4.4 +/- 0.2 mM CON vs. 5.8 +/- 0.2 CHO, P < 0.01; insulin = 9 +/- 1 uU ml-1 CON vs. 19 +/- 3 CHO, P < 0.05). Glycogen decreased to approximately 10% of the basal value during CON and to approximately 20% during CHO, and there was no significant difference in net glycogenolysis between treatments. GSF activity averaged 0.25 +/- 0.03 and 0.22 +/- 0.05 at rest, and increased to 0.51 +/- 0.08 and 0.48 +/- 0.09 after exercise in CON and CHO, respectively (P > 0.05 between treatments). It is concluded that under the present conditions CHO feedings do not alter the exercise-mediated changes in GSF activity. The increase in GSF during exercise is attributed at least in part to the decrease in muscle glycogen (which increases the suitability of GS as substrate for GS phosphatase).

Facultative Physiological Adaptation and Compensation to Winter Stresses in the Predatory Leech Nephelopsis obscura

Influences of acclimation to winter, winter stresses (5°C, severe hypoxia) and reacclimation to summer conditions (20°C, normoxia) on life-history traits and energy allocation were determined in small and large Nephelopsis obscura. Acclimation to winter did not affect feeding but resulted in decreased growth and enhanced energy allocation to glycogen (GN), triaclyglycerols (TAG) and total lipid (TL). Winter stresses resulted in a significant decrease in GN, TAG and TL which were subsequently rapidly replenished in both small and large N. obscura. 3. Even with very low feeding rates during winter stresses energy derived from GN, TAG and TL was adequate to maintain body weight

Hypoxia causes glycogenolysis without an increase in percent phosphorylase a in rat skeletal muscle

Stimulation of skeletal muscle to contract activates phosphorylase b-to-a conversion and glycogenolysis. Despite reversal of the increase in percentage of phosphorylase a after a few minutes, continued glycogen breakdown can occur during strenuous exercise. Hypoxia causes sustained glycogenolysis in skeletal muscle without an increase in percentage of phosphorylase a. We used this model to obtain insights regarding how glycogenolysis is mediated in the absence of an increase in percentage of phosphorylase a. Hypoxia caused a 70% decrease in glycogen in epitrochlearis muscles during an 80-min incubation despite no increase in percentage of phosphorylase a above the basal level of approximately 10%. Muscle Pi concentration increased from 3.8 to 8.6 mumol/g muscle after 5 min and 15.7 mumol/g after 20 min. AMP concentration doubled, attaining a steady state of 0.23 mumol/g in 5 min. Incubation of oxygenated muscles with 0.1 microM epinephrine induced an approximately sixfold increase in percentage of phosphorylase a but resulted in minimal glycogenolysis. Muscle Pi concentration was not altered by epinephrine. Despite no increase in percentage of phosphorylase a, hypoxia resulted in a fivefold greater depletion of glycogen over 20 min than did epinephrine. To evaluate the role of phosphorylase b, muscles were loaded with 2-deoxyglucose 6-phosphate, which inhibits phosphorylase b. The rate of glycogenolysis during 60 min of hypoxia was reduced by only approximately 14% in 2-deoxyglucose 6-phosphate-loaded muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Post mortem changes in glycogen, ATP, hypoxanthine and [formula omitted] absorbance ratio in extracts of adductor muscles from Aulacomya ater ater (Molina) at different biological conditions

1. 1. Post mortem changes in glycogen, ATP, hypoxanthine levels and 260 250 absorbance ratio in extracts of adductor muscles from Aulacomya in different biological condition, were investigated. 2. 2. Glycogen and ATP levels were higher in muscles from specimens in good biological condition. The rate of decrease of both glycogen and ATP was not dependent on the biological condition of Aulacomya. 3. 3. The 260 250 absorbance ratio values in muscle extracts from specimens in poor biological condition were significantly lower ( P < 0.05 at 0 and 24 hr; P < 0.01 at 48, 72, 96 and 120 hr of storage) than in those from specimens in good condition. 4. 4. Irrespective of the biological condition, hypoxanthine levels remained unchanged for 72 hr of storage and increased thereafter.

Effect of starvation on glycogen and glucose metabolism in different areas of the rat brain

We have studied the changes in concentration of glucogen, glucose and the bisphosphorylated sugars, glucose 1,6-P 2 and fructose 2,6-P 2, in several rat brain regions during 72 h of starvation. The animals were killed by focused microwave irradiation. The activities of glycogen metabolizing enzymes in the different areas were measured. A large decrease in glycogen and glucose concentration was observed in all areas. The concentrations of bisphosphorylated sugars changed, suggesting that an increase in glycolysis could take place at the beginning of starvation, with blood glucose as a major energy source. Differences in metabolite concentration before starvation disappeared after 72 h. The activities of glycogen synthase, glycogen phosphorylase and glycogen phosphorylase kinase were similar in all areas, and they did not change during starvation.

Dynamics of Energy Storage in a Freshwater Predator (Nephelopsis obscura) following Winter Stresses

Two groups of Nephelopsis obscura were maintained under identical conditions (20 °C, 100% dissolved oxygen, 12 h light: 12 h dark regime, ad libitum food) from post-hatchling size (10–11 mg) to sexual maturity (500–700 mg). One group (winter N. obscura) had overwintered in the field and degrown to 10–11 mg, while the other group (summer N. obscura) had hatched in the laboratory. The winter N. obscura at post-hatchling size had significantly lower accumulations of total lipid (3.9%), total protein (50.7%), free amino acids (1.6%), and glycogen (3.4%) than summer leeches, indicating that winter stresses (low water temperatures, low dissolved oxygen, restricted prey availability) had reduced energy stores and caused degrowth. The cryoprotective glycerol concentration, however, was significantly higher (1.9%) in winter leeches. At or just prior to sexual maturity, both winter and summer leeches showed decreases in total protein, glycogen, and total lipid which were attributed to the increased energetic demands of gametogenesis and maturation. The effects of, and compensation for, winter stresses were evident throughout the development of the winter leeches which exhibited enhanced energy allocation to storage compared with summer leeches.