An enzyme that catalyzes the transfer of D-glucose from UDPglucose into 1,4-alpha-D-glucosyl chains. EC
Glycogen stored in the liver. (Dorland, 28th ed)
A glycogen synthase kinase that was originally described as a key enzyme involved in glycogen metabolism. It regulates a diverse array of functions such as CELL DIVISION, microtubule function and APOPTOSIS.
An enzyme that catalyzes the degradation of GLYCOGEN in animals by releasing glucose-1-phosphate from the terminal alpha-1,4-glycosidic bond. This enzyme exists in two forms: an active phosphorylated form ( PHOSPHORYLASE A) and an inactive un-phosphorylated form (PHOSPHORYLASE B). Both a and b forms of phosphorylase exist as homodimers. In mammals, the major isozymes of glycogen phosphorylase are found in muscle, liver and brain tissue.
A class of protein-serine-threonine kinases that was originally found as one of the three types of kinases that phosphorylate GLYCOGEN SYNTHASE. Glycogen synthase kinases along with CA(2+)-CALMODULIN DEPENDENT PROTEIN KINASES and CYCLIC AMP-DEPENDENT PROTEIN KINASES regulate glycogen synthase activity.
A class of glucosyltransferases that catalyzes the degradation of storage polysaccharides, such as glucose polymers, by phosphorolysis in animals (GLYCOGEN PHOSPHORYLASE) and in plants (STARCH PHOSPHORYLASE).
A group of inherited metabolic disorders involving the enzymes responsible for the synthesis and degradation of glycogen. In some patients, prominent liver involvement is presented. In others, more generalized storage of glycogen occurs, sometimes with prominent cardiac involvement.
1,4-alpha-D-Glucan-1,4-alpha-D-glucan 4-alpha-D-glucosyltransferase/dextrin 6 alpha-D-glucanohydrolase. An enzyme system having both 4-alpha-glucanotransferase (EC and amylo-1,6-glucosidase (EC activities. As a transferase it transfers a segment of a 1,4-alpha-D-glucan to a new 4-position in an acceptor, which may be glucose or another 1,4-alpha-D-glucan. As a glucosidase it catalyzes the endohydrolysis of 1,6-alpha-D-glucoside linkages at points of branching in chains of 1,4-linked alpha-D-glucose residues. Amylo-1,6-glucosidase activity is deficient in glycogen storage disease type III.
An ester of glucose with phosphoric acid, made in the course of glucose metabolism by mammalian and other cells. It is a normal constituent of resting muscle and probably is in constant equilibrium with fructose-6-phosphate. (Stedman, 26th ed)
A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.
An autosomal recessive disease in which gene expression of glucose-6-phosphatase is absent, resulting in hypoglycemia due to lack of glucose production. Accumulation of glycogen in liver and kidney leads to organomegaly, particularly massive hepatomegaly. Increased concentrations of lactic acid and hyperlipidemia appear in the plasma. Clinical gout often appears in early childhood.
An autosomal recessively inherited glycogen storage disease caused by GLUCAN 1,4-ALPHA-GLUCOSIDASE deficiency. Large amounts of GLYCOGEN accumulate in the LYSOSOMES of skeletal muscle (MUSCLE, SKELETAL); HEART; LIVER; SPINAL CORD; and BRAIN. Three forms have been described: infantile, childhood, and adult. The infantile form is fatal in infancy and presents with hypotonia and a hypertrophic cardiomyopathy (CARDIOMYOPATHY, HYPERTROPHIC). The childhood form usually presents in the second year of life with proximal weakness and respiratory symptoms. The adult form consists of a slowly progressive proximal myopathy. (From Muscle Nerve 1995;3:S61-9; Menkes, Textbook of Child Neurology, 5th ed, pp73-4)
The inactive form of GLYCOGEN PHOSPHORYLASE that is converted to the active form PHOSPHORYLASE A via phosphorylation by PHOSPHORYLASE KINASE and ATP.
The active form of GLYCOGEN PHOSPHORYLASE that is derived from the phosphorylation of PHOSPHORYLASE B. Phosphorylase a is deactivated via hydrolysis of phosphoserine by PHOSPHORYLASE PHOSPHATASE to form PHOSPHORYLASE B.
An isoenzyme of GLYCOGEN PHOSPHORYLASE that catalyzes the degradation of GLYCOGEN in liver tissue. Mutation of the gene coding this enzyme on chromosome 14 is the cause of GLYCOGEN STORAGE DISEASE TYPE VI.
An isoenzyme of GLYCOGEN PHOSPHORYLASE that catalyzes the degradation of GLYCOGEN in muscle. Mutation of the gene coding this enzyme is the cause of McArdle disease (GLYCOGEN STORAGE DISEASE TYPE V).
A key intermediate in carbohydrate metabolism. Serves as a precursor of glycogen, can be metabolized into UDPgalactose and UDPglucuronic acid which can then be incorporated into polysaccharides as galactose and glucuronic acid. Also serves as a precursor of sucrose lipopolysaccharides, and glycosphingolipids.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
A subtype of striated muscle, attached by TENDONS to the SKELETON. Skeletal muscles are innervated and their movement can be consciously controlled. They are also called voluntary muscles.
An autosomal recessive metabolic disorder due to deficient expression of amylo-1,6-glucosidase (one part of the glycogen debranching enzyme system). The clinical course of the disease is similar to that of glycogen storage disease type I, but milder. Massive hepatomegaly, which is present in young children, diminishes and occasionally disappears with age. Levels of glycogen with short outer branches are elevated in muscle, liver, and erythrocytes. Six subgroups have been identified, with subgroups Type IIIa and Type IIIb being the most prevalent.
Contractile tissue that produces movement in animals.
A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).
A normal intermediate in the fermentation (oxidation, metabolism) of sugar. The concentrated form is used internally to prevent gastrointestinal fermentation. (From Stedman, 26th ed)
In glycogen or amylopectin synthesis, the enzyme that catalyzes the transfer of a segment of a 1,4-alpha-glucan chain to a primary hydroxy group in a similar glucan chain. EC
Salts or esters of LACTIC ACID containing the general formula CH3CHOHCOOR.
An autosomal recessive metabolic disorder due to a deficiency in expression of glycogen branching enzyme 1 (alpha-1,4-glucan-6-alpha-glucosyltransferase), resulting in an accumulation of abnormal GLYCOGEN with long outer branches. Clinical features are MUSCLE HYPOTONIA and CIRRHOSIS. Death from liver disease usually occurs before age 2.
A salt of lithium that has been used experimentally as an immunomodulator.
The release of GLUCOSE from GLYCOGEN by GLYCOGEN PHOSPHORYLASE (phosphorolysis). The released glucose-1-phosphate is then converted to GLUCOSE-6-PHOSPHATE by PHOSPHOGLUCOMUTASE before entering GLYCOLYSIS. Glycogenolysis is stimulated by GLUCAGON or EPINEPHRINE via the activation of PHOSPHORYLASE KINASE.
Glycogenosis due to muscle phosphorylase deficiency. Characterized by painful cramps following sustained exercise.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
Enzymes that catalyze the transfer of glucose from a nucleoside diphosphate glucose to an acceptor molecule which is frequently another carbohydrate. EC 2.4.1.-.
An enzyme that catalyzes the conversion of phosphorylated, inactive glycogen synthase D to active dephosphoglycogen synthase I. EC
A metabolic process that converts GLUCOSE into two molecules of PYRUVIC ACID through a series of enzymatic reactions. Energy generated by this process is conserved in two molecules of ATP. Glycolysis is the universal catabolic pathway for glucose, free glucose, or glucose derived from complex CARBOHYDRATES, such as GLYCOGEN and STARCH.
Biosynthesis of GLUCOSE from nonhexose or non-carbohydrate precursors, such as LACTATE; PYRUVATE; ALANINE; and GLYCEROL.
An isoenzyme of GLYCOGEN PHOSPHORYLASE that catalyzes the degradation of GLYCOGEN in brain tissue.
Glucose in blood.
An enzyme that catalyzes the conversion of ATP and PHOSPHORYLASE B to ADP and PHOSPHORYLASE A.
An enzyme that catalyzes the conversion of D-glucose 6-phosphate and water to D-glucose and orthophosphate. EC
Enzymes that catalyze the exohydrolysis of 1,4-alpha-glucosidic linkages with release of alpha-glucose. Deficiency of alpha-1,4-glucosidase may cause GLYCOGEN STORAGE DISEASE TYPE II.
A eukayrotic protein serine-threonine phosphatase subtype that dephosphorylates a wide variety of cellular proteins. The enzyme is comprised of a catalytic subunit and regulatory subunit. Several isoforms of the protein phosphatase catalytic subunit exist due to the presence of multiple genes and the alternative splicing of their mRNAs. A large number of proteins have been shown to act as regulatory subunits for this enzyme. Many of the regulatory subunits have additional cellular functions.
A form of stimulus sensitive myoclonic epilepsy inherited as an autosomal recessive condition. The most common presenting feature is a single seizure in the second decade of life. This is followed by progressive myoclonus, myoclonic seizures, tonic-clonic seizures, focal occipital seizures, intellectual decline, and severe motor and coordination impairments. Most affected individuals do not live past the age of 25 years. Concentric amyloid (Lafora) bodies are found in neurons, liver, skin, bone, and muscle (From Menkes, Textbook of Childhood Neurology, 5th ed, pp111-110)
A group of enzymes removing the SERINE- or THREONINE-bound phosphate groups from a wide range of phosphoproteins, including a number of enzymes which have been phosphorylated under the action of a kinase. (Enzyme Nomenclature, 1992)
Serves as the glycosyl donor for formation of bacterial glycogen, amylose in green algae, and amylopectin in higher plants.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
The rate dynamics in chemical or physical systems.
A 29-amino acid pancreatic peptide derived from proglucagon which is also the precursor of intestinal GLUCAGON-LIKE PEPTIDES. Glucagon is secreted by PANCREATIC ALPHA CELLS and plays an important role in regulation of BLOOD GLUCOSE concentration, ketone metabolism, and several other biochemical and physiological processes. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1511)
Lengthy and continuous deprivation of food. (Stedman, 25th ed)
A protein-serine-threonine kinase that is activated by PHOSPHORYLATION in response to GROWTH FACTORS or INSULIN. It plays a major role in cell metabolism, growth, and survival as a core component of SIGNAL TRANSDUCTION. Three isoforms have been described in mammalian cells.
Five-carbon furanose sugars in which the OXYGEN is replaced by a NITROGEN atom.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
A group of enzymes that catalyzes the conversion of ATP and D-glucose to ADP and D-glucose 6-phosphate. They are found in invertebrates and microorganisms, and are highly specific for glucose. (Enzyme Nomenclature, 1992) EC
Abstaining from all food.
Carbohydrates present in food comprising digestible sugars and starches and indigestible cellulose and other dietary fibers. The former are the major source of energy. The sugars are in beet and cane sugar, fruits, honey, sweet corn, corn syrup, milk and milk products, etc.; the starches are in cereal grains, legumes (FABACEAE), tubers, etc. (From Claudio & Lagua, Nutrition and Diet Therapy Dictionary, 3d ed, p32, p277)
A CALMODULIN-dependent enzyme that catalyzes the phosphorylation of proteins. This enzyme is also sometimes dependent on CALCIUM. A wide range of proteins can act as acceptor, including VIMENTIN; SYNAPSINS; GLYCOGEN SYNTHASE; MYOSIN LIGHT CHAINS; and the MICROTUBULE-ASSOCIATED PROTEINS. (From Enzyme Nomenclature, 1992, p277)
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
An enzyme that catalyzes the conversion of ATP and a D-hexose to ADP and a D-hexose 6-phosphate. D-Glucose, D-mannose, D-fructose, sorbitol, and D-glucosamine can act as acceptors; ITP and dATP can act as donors. The liver isoenzyme has sometimes been called glucokinase. (From Enzyme Nomenclature, 1992) EC
Phenols substituted in any position by an amino group.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Cellular processes in biosynthesis (anabolism) and degradation (catabolism) of CARBOHYDRATES.
An enzyme that catalyzes the formation of UDPglucose from UTP plus glucose 1-phosphate. EC
A hepatic GLYCOGEN STORAGE DISEASE in which there is an apparent deficiency of hepatic phosphorylase (GLYCOGEN PHOSPHORYLASE, LIVER FORM) activity.
Adenine nucleotide containing one phosphate group esterified to the sugar moiety in the 2'-, 3'-, or 5'-position.
A multi-functional catenin that participates in CELL ADHESION and nuclear signaling. Beta catenin binds CADHERINS and helps link their cytoplasmic tails to the ACTIN in the CYTOSKELETON via ALPHA CATENIN. It also serves as a transcriptional co-activator and downstream component of WNT PROTEIN-mediated SIGNAL TRANSDUCTION PATHWAYS.
An ATP-dependent enzyme that catalyzes the addition of ADP to alpha-D-glucose 1-phosphate to form ADP-glucose and diphosphate. The reaction is the rate-limiting reaction in prokaryotic GLYCOGEN and plant STARCH biosynthesis.
The chemical reactions involved in the production and utilization of various forms of energy in cells.
Expenditure of energy during PHYSICAL ACTIVITY. Intensity of exertion may be measured by rate of OXYGEN CONSUMPTION; HEAT produced, or HEART RATE. Perceived exertion, a psychological measure of exertion, is included.
A ketotriose compound. Its addition to blood preservation solutions results in better maintenance of 2,3-diphosphoglycerate levels during storage. It is readily phosphorylated to dihydroxyacetone phosphate by triokinase in erythrocytes. In combination with naphthoquinones it acts as a sunscreening agent.
A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.
An element in the alkali metals family. It has the atomic symbol Li, atomic number 3, and atomic weight [6.938; 6.997]. Salts of lithium are used in treating BIPOLAR DISORDER.
A monosaccharide in sweet fruits and honey that is soluble in water, alcohol, or ether. It is used as a preservative and an intravenous infusion in parenteral feeding.
FATTY ACIDS found in the plasma that are complexed with SERUM ALBUMIN for transport. These fatty acids are not in glycerol ester form.
Stable carbon atoms that have the same atomic number as the element carbon, but differ in atomic weight. C-13 is a stable carbon isotope.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
A glucose transport protein found in mature MUSCLE CELLS and ADIPOCYTES. It promotes transport of glucose from the BLOOD into target TISSUES. The inactive form of the protein is localized in CYTOPLASMIC VESICLES. In response to INSULIN, it is translocated to the PLASMA MEMBRANE where it facilitates glucose uptake.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Intracellular signaling protein kinases that play a signaling role in the regulation of cellular energy metabolism. Their activity largely depends upon the concentration of cellular AMP which is increased under conditions of low energy or metabolic stress. AMP-activated protein kinases modify enzymes involved in LIPID METABOLISM, which in turn provide substrates needed to convert AMP into ATP.
Diet modification and physical exercise to improve the ability of animals to perform physical activities.
Benzopyrroles with the nitrogen at the number one carbon adjacent to the benzyl portion, in contrast to ISOINDOLES which have the nitrogen away from the six-membered ring.
The protein constituents of muscle, the major ones being ACTINS and MYOSINS. More than a dozen accessory proteins exist including TROPONIN; TROPOMYOSIN; and DYSTROPHIN.
The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.
A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein.
An autosomal recessive glycogen storage disease in which there is deficient expression of 6-phosphofructose 1-kinase in muscle (PHOSPHOFRUCTOKINASE-1, MUSCLE TYPE) resulting in abnormal deposition of glycogen in muscle tissue. These patients have severe congenital muscular dystrophy and are exercise intolerant.
A large group of membrane transport proteins that shuttle MONOSACCHARIDES across CELL MEMBRANES.
An enzyme that catalyzes the hydrolysis of terminal 1,4-linked alpha-D-glucose residues successively from non-reducing ends of polysaccharide chains with the release of beta-glucose. It is also able to hydrolyze 1,6-alpha-glucosidic bonds when the next bond in sequence is 1,4.
An X-linked dominant multisystem disorder resulting in cardiomyopathy, myopathy and INTELLECTUAL DISABILITY. It is caused by mutation in the gene encoding LYSOSOMAL-ASSOCIATED MEMBRANE PROTEIN 2.
An enzyme that deactivates glycogen phosphorylase a by releasing inorganic phosphate and phosphorylase b, the inactive form. EC
2-Deoxy-D-arabino-hexose. An antimetabolite of glucose with antiviral activity.
Elements of limited time intervals, contributing to particular results or situations.
Spectroscopic method of measuring the magnetic moment of elementary particles such as atomic nuclei, protons or electrons. It is employed in clinical applications such as NMR Tomography (MAGNETIC RESONANCE IMAGING).
The time span between the beginning of physical activity by an individual and the termination because of exhaustion.
An endogenous substance found mainly in skeletal muscle of vertebrates. It has been tried in the treatment of cardiac disorders and has been added to cardioplegic solutions. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1996)
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
A highly branched glucan in starch.
Maintenance of a constant blood glucose level by perfusion or infusion with glucose or insulin. It is used for the study of metabolic rates (e.g., in glucose, lipid, amino acid metabolism) at constant glucose concentration.
A scaffolding protein that is a critical component of the axin signaling complex which binds to ADENOMATOUS POLYPOSIS COLI PROTEIN; GLYCOGEN SYNTHASE KINASE 3; and CASEIN KINASE I.

Role of glutamine in human carbohydrate metabolism in kidney and other tissues. (1/3146)

Glutamine is the most abundant amino acid in the human body and is involved in more metabolic processes than any other amino acid. Until recently, the understanding of many aspects of glutamine metabolism was based on animal and in vitro data. However, recent studies using isotopic and balance techniques have greatly advanced the understanding of glutamine metabolism in humans and its role in glucose metabolism in the kidney and other tissues. There is now evidence that in postabsorptive humans, glutamine is an important glucose precursor and makes a significant contribution to the addition of new carbon to the glucose carbon pool. The importance of alanine for gluconeogenesis, viewed in terms of the addition of new carbons, is less than previously assumed. It appears that glutamine is predominantly a renal gluconeogenic substrate, whereas alanine gluconeogenesis is essentially confined to the liver. As shown recently, renal gluconeogenesis contributes 20 to 25% to whole-body glucose production. Moreover, glutamine has been shown not only to stimulate net muscle glycogen storage but also to stimulate gluconeogenesis in normal humans. Finally, in humans with type II diabetes, conversion of glutamine to glucose is increased (more so than that of alanine). The available evidence on the hormonal regulation of glutamine gluconeogenesis in kidney and liver and its alterations under pathological conditions are discussed.  (+info)

Glucose kinetics during prolonged exercise in highly trained human subjects: effect of glucose ingestion. (2/3146)

1. The objectives of this study were (1) to investigate whether glucose ingestion during prolonged exercise reduces whole body muscle glycogen oxidation, (2) to determine the extent to which glucose disappearing from the plasma is oxidized during exercise with and without carbohydrate ingestion and (3) to obtain an estimate of gluconeogenesis. 2. After an overnight fast, six well-trained cyclists exercised on three occasions for 120 min on a bicycle ergometer at 50 % maximum velocity of O2 uptake and ingested either water (Fast), or a 4 % glucose solution (Lo-Glu) or a 22 % glucose solution (Hi-Glu) during exercise. 3. Dual tracer infusion of [U-13C]-glucose and [6,6-2H2]-glucose was given to measure the rate of appearance (Ra) of glucose, muscle glycogen oxidation, glucose carbon recycling, metabolic clearance rate (MCR) and non-oxidative disposal of glucose. 4. Glucose ingestion markedly increased total Ra especially with Hi-Glu. After 120 min Ra and rate of disappearance (Rd) of glucose were 51-52 micromol kg-1 min-1 during Fast, 73-74 micromol kg-1 min-1 during Lo-Glu and 117-119 micromol kg-1 min-1 during Hi-Glu. The percentage of Rd oxidized was between 96 and 100 % in all trials. 5. Glycogen oxidation during exercise was not reduced by glucose ingestion. The vast majority of glucose disappearing from the plasma is oxidized and MCR increased markedly with glucose ingestion. Glucose carbon recycling was minimal suggesting that gluconeogenesis in these conditions is negligible.  (+info)

alpha-adrenergic stimulation mediates glucose uptake through phosphatidylinositol 3-kinase in rat heart. (3/3146)

We examined whether insulin and catecholamines share common pathways for their stimulating effects on glucose uptake. We perfused isolated working rat hearts with Krebs-Henseleit buffer containing [2-3H]glucose (5 mmol/L, 0.05 microCi/mL) and sodium oleate (0.4 mmol/L). In the absence or presence of the phosphatidylinositol 3-kinase (PI3-K) inhibitor wortmannin (3 micromol/L), we added insulin (1 mU/mL), epinephrine (1 micromol/L), phenylephrine (100 micromol/L) plus propranolol (10 micromol/L, selective alpha-adrenergic stimulation), or isoproterenol (1 micromol/L) plus phentolamine (10 micromol/L, selective beta-adrenergic stimulation) to the perfusate. Cardiac power was found to be stable in all groups (between 8.07+/-0.68 and 10.7+/-0. 88 mW) and increased (25% to 47%) with addition of epinephrine, but not with selective alpha- and beta-adrenergic stimulation. Insulin and epinephrine, as well as selective alpha- and beta-receptor stimulation, increased glucose uptake (the following values are in micromol/[min. g dry weight]: basal, 1.19+/-0.13; insulin, 3.89+/-0.36; epinephrine, 3.46+/-0.27; alpha-stimulation, 4.08+/-0.40; and beta-stimulation, 3.72+/-0.34). Wortmannin completely inhibited insulin-stimulated and selective alpha-stimulated glucose uptake, but it did not affect the epinephrine-stimulated or selective beta-stimulated glucose uptake. Sequential addition of insulin and epinephrine or insulin and alpha-selective stimulation showed additive effects on glucose uptake in both cases. Wortmannin further blocked the effects of insulin on glycogen synthesis. We conclude that alpha-adrenergic stimulation mediates glucose uptake in rat heart through a PI3-K-dependent pathway. However, the additive effects of alpha-adrenergic stimulation and insulin suggest 2 different isoforms of PI3-K, compartmentation of PI3-K, potentiation, or inhibition by wortmannin of another intermediate of the alpha-adrenergic signaling cascade. The stimulating effects of both the alpha- and the beta-adrenergic pathways on glucose uptake are independent of changes in cardiac performance.  (+info)

Effect of ambient temperature on human skeletal muscle metabolism during fatiguing submaximal exercise. (4/3146)

To examine the effect of ambient temperature on metabolism during fatiguing submaximal exercise, eight men cycled to exhaustion at a workload requiring 70% peak pulmonary oxygen uptake on three separate occasions, at least 1 wk apart. These trials were conducted in ambient temperatures of 3 degrees C (CT), 20 degrees C (NT), and 40 degrees C (HT). Although no differences in muscle or rectal temperature were observed before exercise, both muscle and rectal temperature were higher (P < 0.05) at fatigue in HT compared with CT and NT. Exercise time was longer in CT compared with NT, which, in turn, was longer compared with HT (85 +/- 8 vs. 60 +/- 11 vs. 30 +/- 3 min, respectively; P < 0.05). Plasma epinephrine concentration was not different at rest or at the point of fatigue when the three trials were compared, but concentrations of this hormone were higher (P < 0.05) when HT was compared with NT, which in turn was higher (P < 0.05) compared with CT after 20 min of exercise. Muscle glycogen concentration was not different at rest when the three trials were compared but was higher at fatigue in HT compared with NT and CT, which were not different (299 +/- 33 vs. 153 +/- 27 and 116 +/- 28 mmol/kg dry wt, respectively; P < 0.01). Intramuscular lactate concentration was not different at rest when the three trials were compared but was higher (P < 0.05) at fatigue in HT compared with CT. No differences in the concentration of the total intramuscular adenine nucleotide pool (ATP + ADP + AMP), phosphocreatine, or creatine were observed before or after exercise when the trials were compared. Although intramuscular IMP concentrations were not statistically different before or after exercise when the three trials were compared, there was an exercise-induced increase (P < 0.01) in IMP. These results demonstrate that fatigue during prolonged exercise in hot conditions is not related to carbohydrate availability. Furthermore, the increased endurance in CT compared with NT is probably due to a reduced glycogenolytic rate.  (+info)

A tentative mechanism of the ternary complex formation between phosphorylase kinase, glycogen phosphorylase b and glycogen. (5/3146)

The kinetics of rabbit skeletal muscle phosphorylase kinase interaction with glycogen has been studied. At pH 6.8 the binding of phosphorylase kinase to glycogen proceeds only in the presence of Mg2+, whereas at pH 8.2 formation of the complex occurs even in the absence of Mg2+. On the other hand, the interaction of phosphorylase kinase with glycogen requires Ca2+ at both pH values. The initial rate of the complex formation is proportional to the enzyme and glycogen concentrations, suggesting the formation of the complex with stoichiometry 1:1 at the initial step of phosphorylase kinase binding by glycogen. According to the kinetic and sedimentation data, the substrate of the phosphorylase kinase reaction, glycogen phosphorylase b, favors the binding of phosphorylase kinase with glycogen. We suggest a model for the ordered binding of phosphorylase b and phosphorylase kinase to the glycogen particle that explains the increase in the tightness of phosphorylase kinase binding with glycogen in the presence of phosphorylase b.  (+info)

Contributions of net hepatic glycogenolysis and gluconeogenesis to glucose production in cirrhosis. (6/3146)

Net hepatic glycogenolysis and gluconeogenesis were examined in normal (n = 4) and cirrhotic (n = 8) subjects using two independent methods [13C nuclear magnetic resonance spectroscopy (NMR) and a 2H2O method]. Rates of net hepatic glycogenolysis were calculated by the change in hepatic glycogen content before ( approximately 11:00 PM) and after ( approximately 7:00 AM) an overnight fast using 13C NMR and magnetic resonance imaging. Gluconeogenesis was calculated as the difference between the rates of glucose production determined with an infusion of [6,6-2H2]glucose and net hepatic glycogenolysis. In addition, the contribution of gluconeogenesis to glucose production was determined by the 2H enrichment in C-5/C-2 of blood glucose after intake of 2H2O (5 ml/kg body water). Plasma levels of total and free insulin-like growth factor I (IGF-I) and IGF-I binding proteins-1 and -3 were significantly decreased in the cirrhotic subjects (P < 0.01 vs. controls). Postprandial hepatic glycogen concentrations were 34% lower in the cirrhotic subjects (P = 0.007). Rates of glucose production were similar between the cirrhotic and healthy subjects [9.0 +/- 0.9 and 10.0 +/- 0.8 micromol. kg body wt-1. min-1, respectively]. Net hepatic glycogenolysis was 3.5-fold lower in the cirrhotic subjects (P = 0.01) and accounted for only 13 +/- 6% of glucose production compared with 40 +/- 10% (P = 0.03) in the control subjects. Gluconeogenesis was markedly increased in the cirrhotic subjects and accounted for 87 +/- 6% of glucose production vs. controls: 60 +/- 10% (P = 0.03). Gluconeogenesis in the cirrhotic subjects, as determined from the 2H enrichment in glucose C-5/C-2, was also increased and accounted for 68 +/- 3% of glucose production compared with 54 +/- 2% (P = 0.02) in the control subjects. In conclusion, cirrhotic subjects have increased rates of gluconeogenesis and decreased rates of net hepatic glycogenolysis compared with control subjects. These alterations are likely important contributing factors to their altered carbohydrate metabolism.  (+info)

Effect of fast duration on disposition of an intraduodenal glucose load in the conscious dog. (7/3146)

The effects of prior fast duration (18 h, n = 8; 42 h, n = 8) on the glycemic and tissue-specific responses to an intraduodenal glucose load were studied in chronically catheterized conscious dogs. [3-3H]glucose was infused throughout the study. After basal measurements, glucose spiked with [U-14C]glucose was infused for 150 min intraduodenally. Arterial insulin and glucagon were similar in the two groups. Arterial glucose (mg/dl) rose approximately 70% more during glucose infusion after 42 h than after an 18-h fast. The net hepatic glucose balance (mg. kg-1. min-1) was similar in the two groups (basal: 1.8 +/- 0.2 and 2.0 +/- 0.3; glucose infusion: -2.2 +/- 0.5 and -2.2 +/- 0.7). The intrahepatic fate of glucose was 79% glycogen, 13% oxidized, and 8% lactate release after a 42-h fast; it was 23% glycogen, 21% oxidized, and 56% lactate release after an 18-h fast. Net hindlimb glucose uptake was similar between groups. The appearance of intraduodenal glucose during glucose infusion (mg/kg) was 900 +/- 50 and 1,120 +/- 40 after 18- and 42-h fasts (P < 0.01). CONCLUSION: glucose administration after prolonged fasting induces higher circulating glucose than a shorter fast (increased appearance of intraduodenal glucose); liver and hindlimb glucose uptakes and the hormonal response, however, are unchanged; finally, an intrahepatic redistribution of carbons favors glycogen deposition.  (+info)

Effect of artemether on glucose uptake and glycogen content in Schistosoma japonicum. (8/3146)

AIM: To study the effect of artemether (Art) on glucose uptake and glycogen content in schistosomes. METHODS: Schistosomes recovered from mice treated intragastrically with Art 300 for 24-48 h, were incubated in the drug-free medium containing [U-14C]glucose 11.1 MBq.L-1. The glycogen content, [U-14C]glucose uptake, and incorporation of [U-14C]glucose into worm glycogen in both male and female worms were determined. RESULTS: When above-mentioned schistosomes were exposed to drug-free medium containing [U-14C]glucose for 1-24 h, the glycogen contents of male and female worms decreased 27%-61% and 39%-78%, respectively. Only 3 out of 6 male worm groups showed 23%-35% decrease in glucose uptake, while much less glucose uptake was found in female worms in all groups with reduction rates of 18%-38%. Apart from 2 male groups no apparent change in the incorporation of [U-14C]glucose into the worm glycogen was seen. CONCLUSIONS: Art-induced glycogen reduction in schistosomes was related to an inhibition of glycolysis rather than an interference with glucose uptake.  (+info)

Glycogen availability can influence glucose transporter 4 (GLUT4) expression in skeletal muscle through unknown mechanisms. The multisubstrate enzyme AMP-activated protein kinase (AMPK) has also been shown to play an important role in the regulation of GLUT4 expression in skeletal muscle. During contraction, AMPK [alpha]2 translocates to the nucleus and the activity of this AMPK isoform is enhanced when skeletal muscle glycogen is low. In this study, we investigated if decreased pre-exercise muscle glycogen levels and increased AMPK [alpha]2 activity reduced the association of AMPK with glycogen and increased AMPK [alpha]2 translocation to the nucleus and GLUT4 mRNA expression following exercise. Seven males performed 60 min of exercise at ~70% [VO.sub.2] peak on 2 occasions: either with normal (control) or low (LG) carbohydrate pre-exercise muscle glycogen content. Muscle samples were obtained by needle biopsy before and after exercise. Low muscle glycogen was associated with elevated AMPK ...
Purpose: To evaluate the efficacy of using combined glucose and fructose (GF) ingestion as a means to stimulate short-term (4 h) postexercise muscle glycogen synthesis compared to glucose only (G). Methods: On two separate occasions, six endurance-trained men performed an exhaustive glycogen-depleting exercise bout followed by a 4-h recovery period. Muscle biopsy samples were obtained from the vastus lateralis muscle at 0, 1, and 4 h after exercise. Subjects ingested carbohydrate solutions containing G (90 gIhj1) or GF (G = 60 gIhj1; F = 30 gIhj1) commencing immediately after exercise and every 30 min thereafter. Results: Immediate postexercise muscle glycogen concentrations were similar in both trials (G = 128 T 25 mmolIkgj1 dry muscle (dm) vs GF = 112 T 16 mmolIkgj1 dm; P 9 0.05). Total glycogen storage during the 4-h recovery period was 176 T 33 and 155 T 31 mmolIkgj1 dm for G and GF, respectively (G vs GF, P 9 0.05). Hence, mean muscle glycogen synthesis rates during the 4-h recovery period ...
TY - JOUR. T1 - Influence of muscle glycogen availability on ERK1/2 and Akt signaling after resistance exercise in human skeletal muscle. AU - Creer, Andrew. AU - Gallagher, Philip. AU - Slivka, Dustin. AU - Jemiolo, Bozena. AU - Fink, William. AU - Trappe, Scott. PY - 2005/9. Y1 - 2005/9. N2 - Two pathways that have been implicated for cellular growth and development in response to muscle contraction are the extracellular signal-regulated kinase (ERK1/2) and Akt signaling pathways. Although these pathways are readily stimulated after exercise, little is known about how nutritional status may affect stimulation of these pathways in response to resistance exercise in human skeletal muscle. To investigate this, experienced cyclists performed 30 repetitions of knee extension exercise at 70% of one repetition maximum after a low (2%) or high (77%) carbohydrate (LCHO or HCHO) diet, which resulted in low or high (∼174 or ∼591 mmol/kg dry wt) preexercise muscle glycogen content. Muscle biopsies ...
TY - JOUR. T1 - Epinephrine regulation of skeletal muscle glycogen metabolism. Studies utilizing the perfused rat hindlimb preparation. AU - Dietz, M. R.. AU - Chiasson, J. L.. AU - Soderling, T. R.. AU - Exton, J. H.. PY - 1980/12/1. Y1 - 1980/12/1. N2 - Studies of rat skeletal muscle glycogen metabolism carried out in a perfused hindlimb system indicated that epinephrine activates phosphorylase via the cascade of phosphorylation reactions classically linked to the β-adrenergic receptor/adenylate cyclase system. The β blocker propranolol completely blocked the effects of epinephrine on cAMP, cAMP-dependent protein kinase, phosphorylase, and glucose-6-P, whereas the α blocker phentolamine was totally ineffective. Omission of glucose from the perfusion medium did not modify the effects of epinephrine. Glycogen synthase activity in control perfused and nonperfused muscle was largely glucose-6-P-dependent (-glucose-6-P/+glucose-6-P activity ratios of 0.1 and 0.2, respectively). Epinephrine ...
Glycogen plays a major role in supporting the energy demands of skeletal muscles during high intensity exercise. Despite its importance, the amount of glycogen stored in skeletal muscles is so small that a large fraction of it can be depleted in response to a single bout of high intensity exercise. For this reason, it is generally recommended to ingest food after exercise to replenish rapidly muscle glycogen stores, otherwise ones ability to engage in high intensity activity might be compromised. But what if food is not available? It is now well established that, even in the absence of food intake, skeletal muscles have the capacity to replenish some of their glycogen at the expense of endogenous carbon sources such as lactate. This is facilitated, in part, by the transient dephosphorylation-mediated activation of glycogen synthase and inhibition of glycogen phosphorylase. There is also evidence that muscle glycogen synthesis occurs even under conditions conducive to an increased oxidation of ...
In Saccharomyces cerevisiae, nutrient levels control multiple cellular processes. Cells lacking the SNF1 gene cannot express glucose-repressible genes and do not accumulate the storage polysaccharide glycogen. The impaired glycogen synthesis is due to maintenance of glycogen synthase in a hyperphosphorylated, inactive state. In a screen for second site suppressors of the glycogen storage defect of snf1 cells, we identified a mutant gene that restored glycogen accumulation and which was allelic with PHO85, which encodes a member of the cyclin-dependent kinase family. In cells with disrupted PHO85 genes, we observed hyperaccumulation of glycogen, activation of glycogen synthase, and impaired glycogen synthase kinase activity. In snf1 cells, glycogen synthase kinase activity was elevated. Partial purification of glycogen synthase kinase activity from yeast extracts resulted in the separation of two fractions by phenyl-Sepharose chromatography, both of which phosphorylated and inactivated glycogen ...
1. A description is given of the hour-to-hour variation in the liver glycogen content in adult male mice, and it is shown that the concentration is highest while the animals are asleep and lowest while they are awake.. 2. A similar cycle is also described in the glycogen content of the skin. Histologically it is shown that a high proportion of the skin glycogen lies in the cytoplasm of the epidermal cells, and that during sleep both the epidermal glycogen content and the epidermal mitotis rate increase considerably. The skin glycogen content and the epidermal mitotic activity also show a marked increase after a subcutaneous injection of 20 mg. starch, while they are both abnormally depressed after two injections of 1/50 unit insulin.. 3. These results, together with others previously reported, are in agreement with the theory that at the onset of sleep glucose is deposited from the blood into the tissues where it appears in the form of glycogen. Since it is known that glucose, or glycogen, is a ...
Glycogen synthase (UDP-glucose-glycogen glucosyltransferase) is a key enzyme in glycogenesis, the conversion of glucose into glycogen. It is a glycosyltransferase (EC that catalyses the reaction of UDP-glucose and (1,4-α-D-glucosyl)n to yield UDP and (1,4-α-D-glucosyl)n+1. In other words, this enzyme combines excess glucose residues one by one into a polymeric chain for storage as glycogen. Glycogen synthase concentration is highest in the bloodstream 30 to 60 minutes following intense exercise. Much research has been done on glycogen degradation through studying the structure and function of glycogen phosphorylase, the key regulatory enzyme of glycogen degradation. On the other hand, much less is known about the structure of glycogen synthase, the key regulatory enzyme of glycogen synthesis. The crystal structure of glycogen synthase from Agrobacterium tumefaciens, however, has been determined at 2.3 A resolution. In its asymmetric form, glycogen synthase is found as a dimer, whose ...
Muscle glycogen resynthesis rate in humans after supplementation of drinks containing carbohydrates with low and high molecular masses ...
Eccentric contractions induce muscle damage, which impairs recovery of glycogen and adenosine tri-phosphate (ATP) content over several days. Leucine-enriched essential amino acids (LEAAs) enhance the recovery in muscles that are damaged after eccentric contractions. However, the role of LEAAs in this process remains unclear. We evaluated the content in glycogen and high energy phosphates molecules (phosphocreatine (PCr), adenosine di-phosphate (ADP) and ATP) in rats that were following electrically stimulated eccentric contractions. Muscle glycogen content decreased immediately after the contraction and remained low for the first three days after the stimulation, but increased seven days after the eccentric contraction. LEAAs administration did not change muscle glycogen content during the first three days after the contraction. Interestingly, however, it induced a further increase in muscle glycogen seven days after the stimulation. Contrarily, ATP content decreased immediately after the eccentric
TY - JOUR. T1 - Analysis of respiratory mutants reveals new aspects of the control of glycogen accumulation by the cyclin-dependent protein kinase Pho85p. AU - Wilson, Wayne A.. AU - Wang, Zhong. AU - Roach, P. J.. PY - 2002/3/27. Y1 - 2002/3/27. N2 - The PHO85 gene of Saccharomyces cerevisiae encodes a cyclin-dependent protein kinase that can interact with 10 different cyclins (Pcls). In conjunction with Pcl8p and Pcl10p, Pho85p phosphorylates and regulates glycogen synthase. Respiratory-deficient strains, such as coq3 mutants, have reduced glycogen stores and contain hyperphosphorylated and inactive glycogen synthase. We show here that pho85 coq3 mutants have dephosphorylated and active glycogen synthase yet do not maintain glycogen reserves. In contrast, deletion of PCL8 and PCL10 in the coq3 mutant background partially restores glycogen accumulation. This suggested the existence of inputs from Pho85p into glycogen storage, independent of Pcl8p and Pcl10p, and acting antagonistically.. AB - ...
TY - JOUR. T1 - 13C NMR studies of glycogen turnover in the perfused rat liver. AU - Shulman, G. I.. AU - Rothman, D. L.. AU - Chung, Youngran. AU - Rossetti, L.. AU - Petit, W. A.. AU - Barrett, E. J.. AU - Shulman, R. G.. PY - 1988. Y1 - 1988. N2 - To assess whether hepatic glycogen is actively turning over under conditions which promote net glycogen synthesis we perfused livers from 24-h fasted rats with 20 mM D-[1-13C]glucose, 10 mM L-[3-13C]alanine, 10 mM L-[3-13C]lactate, and 1 μM insulin for 90 min followed by a 75-min chase period with perfusate of the same composition containing either 13C-enriched or unlabeled substrates. The peak height of the C-1 resonance of the glucosyl subunits in glycogen was monitored, in real time, using 13C NMR techniques. During the initial 90 min the peak height of the C-1 resonance of glycogen increased at almost a constant rate reflecting a near linear increase in net glycogen synthesis, which persisted for a further 75 min if 13C-enriched substrates ...
The cDNA for mouse brain glycogen synthase has been isolated by screening a mouse cerebral cortical astrocyte lambda ZAP II cDNA library. The mouse brain glycogen synthase cDNA is 3.5 kilobases in length and encodes a protein of 737 amino acids. The coding sequence of mouse brain glycogen synthase cDNA shares approximately 87% nucleotide identity and approximately 96% amino acid identity with the muscle isozyme, while the degree of identity is lower with the liver isozyme. The regional distribution of glycogen synthase mRNA determined by in situ hybridization in the mouse brain reveals a wide distribution throughout the central nervous system with highest densities observed in the cerebellum, hippocampus and olfactory bulb. At the cellular level the expression of brain glycogen synthase mRNA is localized both in astrocytes and neurons with, however, the higher levels observed in astrocytes. Vasoactive intestinal peptide and noradrenaline, two neurotransmitters previously shown to induce a glycogen
Background: Diabetic cardiomyopathy is a distinct cardiac pathology and the underlying mechanisms are unknown. Elevated glycogen content has been observed in the diabetic human myocardium, first recorded 80 years ago, suggesting that despite impaired glucose uptake cardiomyocytes accumulate glycogen. Anecdotal evidence of glycogen accumulation in the diabetic myocardium has since been recorded in the literature but a systematic investigation of this paradoxical phenomenon has not been conducted. Glycogen storage diseases demonstrate that increased cardiac glycogen is associated with severe functional deficits, and therefore the observed glycogen excess in diabetic hearts may be an important and novel agent of pathology in diabetic cardiomyopathy. Aim: This body of work aimed to systematically investigate the role myocardial glycogen accumulation in diabetic cardiomyopathy, with a focus on glycophagy, a glycogen-specific autophagy process. Key metabolic signaling pathways (insulin, AMPK, ...
It is generally acknowledged that fasted animals recovering from physical activity of near-maximal intensity can replenish their muscle glycogen stores even in the absence of food intake. In some mammal species, such as in rats and humans, the extent of this replenishment is only partial (Hermansen and Vaage, 1977; Astrand et al., 1986; Choi et al., 1994; Nikolovski et al., 1996; Peters et al., 1996; Bangsbo et al., 1997; Ferreira et al., 2001; Fournier et al., 2002), thus suggesting that a few consecutive bouts of high-intensity exercise might eventually lead to the progressive depletion of their muscle glycogen stores. In order to test this prediction, groups of rats were subjected to a series of three bouts of high-intensity swims to exhaustion, each separated from the subsequent one by a recovery period previously shown to be long enough for muscle glycogen and lactate to return to stable levels (Ferreira et al., 2001). This study shows for the first time that repeated bouts of ...
Since its identification more than 150 years ago, there has been an extensive characterisation of glycogen metabolism and its regulatory pathways in the two main glycogen storage organs of the body, i.e. liver and muscle. In recent years, glycogen metabolism has also been demonstrated to be upregulated in many tumour types, suggesting it is an important aspect of cancer cell pathophysiology. Here, we provide an overview of glycogen metabolism and its regulation, with a focus on its role in metabolic reprogramming of cancer cells. The various methods to detect glycogen in tumours in vivo are also reviewed. Finally, we discuss the targeting of glycogen metabolism as a strategy for cancer treatment.
In obesity, insulin-stimulated glucose uptake in skeletal muscle is decreased. We investigated whether the stimulatory effect of acute exercise on glucose uptake and subsequent glycogen synthesis was normal. The study was performed on 18 healthy volu
Hepatic glycogen synthesis is impaired in insulin-dependent diabetic rats and in adrenalectomized starved rats, and although this is known to be due to defective activation of glycogen synthase by glycogen synthase phosphatase, the underlying molecular mechanism has not been delineated. Glycogen synthase phosphatase comprises the catalytic subunit of protein phosphatase 1 (PP1) complexed with the hepatic glycogen-binding subunit, termed GL. In liver extracts of insulin-dependent diabetic and adrenalectomized starved rats, the level of GL was shown by immunoblotting to be substantially reduced compared with that in control extracts, whereas the level of PP1 catalytic subunit was not affected by these treatments. Insulin administration to diabetic rats restored the level of GL and prolonged administration raised it above the control levels, whereas re-feeding partially restored the GL level in adrenalectomized starved rats. The regulation of GL protein levels by insulin and starvation/feeding was ...
Title: Glycogen and its Metabolism. VOLUME: 2 ISSUE: 2. Author(s):Peter J. Roach. Affiliation:MS405A, Medical ScienceBuilding, 635 Barnhill Drive, Indianapolis, IN 46202, USA. Keywords:glycogen, phosphorylayion, catecholamines, glycogenolysis, glycogenin, glycogen synthesis, glycogen synthase, glycogen phosphorylase, acid glucosidase. Abstract: Glycogen is a branched polymer of glucose which serves as a reservoir of glucose units. The two largest deposits in mammals are in the liver and skeletal muscle but many cells are capable synthesizing glycogen. Its accumulation and utilization are under elaborate controls involving primarily covalent phosphorylation and allosteric ligand binding. Both muscle and liver glycogen reserves are important for whole body glucose metabolism and their replenishment is linked hormonally to nutritional status. Control differs between muscle and liver in part due to the existence of different tissue-specific isoforms at key steps. Control of synthesis is shared ...
Muscle glycogen provides a readily available source of glucose-1-phosphate for glycolysis within the muscle itself. Liver glycogen functions as a reserve to maintain the blood glucose concentration in the fasting state. The liver concentration of glycogen is about 450 mmol /L glucose equivalents after a meal, falling to about 200 mmol /L after an overnight fast; after 12 to 18 hours of fasting, liver glycogen is almost totally depleted. Although muscle glycogen does not directly yield free glucose (because muscle lacks glucose-6-phosphatase), pyruvate formed by glycolysis in muscle can undergo transamination to alanine, which is exported from muscle and used for gluconeogenesis in the liver (see Figure 19-4). Glycogen storage diseases are a group of inherited disorders characterized by deficient mobilization of glycogen or deposition of abnormal forms of glycogen, leading to liver damage and muscle weakness; some glycogen storage diseases result in early death. ...
Glycogen content and contraction strongly regulate glycogen synthase (GS) activity, and the aim of the present study was to explore their effects and interaction on GS phosphorylation and kinetic properties. Glycogen content in rat epitrochlearis muscles was manipulated in vivo. After manipulation, incubated muscles with normal glycogen [NG; 210.9 ± 7.1 mmol/kg dry weight (dw)], low glycogen (LG; 108.1 ± 4.5 mmol/ kg dw), and high glycogen (HG; 482.7 ± 42.1 mmol/kg dw) were contracted or rested before the studies of GS kinetic properties and GS phosphorylation (using phospho-specific antibodies). LG decreased and HG increased GS Km for UDP-glucose (LG: 0.27 ± 0.02 , NG: 0.71 ± 0.06 , HG: 1.11 ± 0.12 mM; P , 0.001). In addition, GS fractional activity inversely correlated with glycogen content (R = -0.70; P , 0.001; n = 44). Contraction decreased Km for UDP-glucose (LG: 0.14 ± 0.01 = NG: 0.16 ± 0.01 , HG: 0.33 ± 0.03 mM; P , 0.001) and increased GS fractional activity, and these effects ...
TY - JOUR. T1 - Factors influencing pituitary glycogen metabolism and gonadotropic hormone release. I. Luteinizing hormone releasing hormone. AU - Makino, T.. AU - Demers, L. M.. AU - Greep, R. O.. PY - 1974/1/1. Y1 - 1974/1/1. N2 - The mechanism of release of luteinizing hormone (LH) and follicle stimulating hormone (FSH) from the rat anterior pituitary by LH releasing hormone (LH RH) was further evaluated by studies on pituitary glycogen metabolism and its relation to the hormone release mechanism in vitro. Pituitary glycogen content and the activity levels of its 2 major regulatory enzymes, glycogen synthetase and glycogen phosphorylase, were analyzed after exposure to different doses of synthetic LH RH in vitro. Less than 5 ng of LH RH induced within minutes a maximum glycogenolytic response with an increase in the proportion of pituitary phosphorylase in the more active a form and a decrease in pituitary glycogen. Exogenous N6,O2 dibutyryl cyclic AMP (10 millimol) with theophylline (1 ...
Transcription of metabolic genes is transiently induced during recovery from exercise in skeletal muscle of humans. To determine whether pre-exercise muscle glycogen content influences the magnitude and/or duration of this adaptive response, six male subjects performed one-legged cycling exercise to lower muscle glycogen content in one leg and then, the following day, completed 2.5 h low intensity two-legged cycling exercise. Nuclei and mRNA were isolated from biopsies obtained from the vastus lateralis muscle of the control and reduced glycogen (pre-exercise glycogen = 609 ± 47 and 337 ± 33 mmol kg-1 dry weight, respectively) legs before and after 0, 2 and 5 h of recovery. Exercise induced a significant (P 6-fold) than in the control (< 3-fold) trial. Induction of PDK4 and UCP3 mRNA in response to exercise was also signficantly higher in the low glycogen (11.4- and 3.5-fold, respectively) than in the control (5.0- and 1.7-fold, respectively) trial. These data indicate that low muscle ...
Recovery is governed by the length of time taken to fully restore muscle glycogen. Muscle glycogen is depleted after 2-3 hours of continuous exercise at 60-80% VO2max. Glycogen depletion can also occur after 15-20 min of very intense exercise at 90-130% VO2max. Low muscle glycogen levels increase the risk of injury. Restoration of muscle glycogen can take 20 hours with correct diet and supplementation. Less than an optimal diet will increase recovery time. CHO replenishment during exercise seems to be optimal at 7-8% concentration in water. However, after exercise it can be of a much higher concnetration. Implication. For intermittent high intensity sports (e.g., soccer, hockey) the ingestion of CHO throughout the game, and during any rest period will result in muscle glycogen being restored and increased sprinting ability towards the end of the game. This will not happen when only water is consumed. Return to Table of Contents for this issue. ...
Protein targeting to glycogen (PTG) is a scaffolding protein that targets protein phosphatase 1α (PP1α) to glycogen, and links it to enzymes involved in glycogen synthesis and degradation. We generated mice that possess a heterozygous deletion of the PTG gene. These mice have reduced glycogen stores in adipose tissue, liver, heart, and skeletal muscle, corresponding with decreased glycogen synthase activity and glycogen synthesis rate. Although young PTG heterozygous mice initially demonstrate normal glucose tolerance, progressive glucose intolerance, hyperinsulinemia, and insulin resistance develop with aging. Insulin resistance in older PTG heterozygous mice correlates with a significant increase in muscle triglyceride content, with a corresponding attenuation of insulin receptor signaling. These data suggest that PTG plays a critical role in glycogen synthesis and is necessary to maintain the appropriate metabolic balance for the partitioning of fuel substrates between glycogen and ...
Key points Muscle glycogen (the storage form of glucose) is consumed during muscle work and the depletion of glycogen is thought to be a main contributor to muscle fatigue. In this study, we used a novel approach to first measure fatigue-induced reductions in force and tetanic Ca2+ in isolated single mouse muscle fibres following repeated contractions and subsequently quantify the subcellular distribution of glycogen in the same fibre. Using this approach, we investigated whether the decreased tetanic Ca2+ induced by repeated contractions was associated with glycogen depletion in certain subcellular regions. The results show a positive correlation between depletion of glycogen located within the myofibrils and low tetanic Ca2+ after repetitive stimulation. We conclude that subcellular glycogen depletion has a central role in the decrease in tetanic Ca2+ that occurs during repetitive contractions. In skeletal muscle fibres, glycogen has been shown to be stored at different subcellular locations: ...
Looking for glycogen synthetase? Find out information about glycogen synthetase. An enzyme that catalyzes the synthesis of the amylose chain of glycogen Explanation of glycogen synthetase
The time of ingestion of a carbohydrate supplement on muscle glycogen storage postexercise was examined. Twelve male cyclists exercised continuously for 70 min on a cycle ergometer at 68% VO2max, interrupted by six 2-min intervals at 88% VO2max, on two separate occasions. A 25% carbohydrate solution …
Exercise increases insulin sensitivity in both normal subjects and the insulin-resistant offspring of diabetic parents because of a twofold increase in insulin-stimulated glycogen synthesis in muscle, due to an increase in insulin-stimulated glucose transport-phosphorylation.
Your diet can have a major impact on your bodys ability to produce glycogen. This is especially the case if youre on a low-carb diet where youre reducing the number of carbohydrates youre consuming with each meal.. It should be noted that low-carb diets come with their own side effects, primarily because your bodys glycogen stores may not have the fuel needed to replenish properly, resulting in symptoms of mental dullness and fatigue. Over time, your body should adjust to these changes, and your glycogen stores should replenish, bringing your energy levels back up to normal.. In the same manner, you may experience a decrease in glycogen stores if you lose any amount of weight. As many people who have been on a diet may have experienced, weight loss may occur initially, but may eventually plateau and even begin increasing after a certain point.. This process occurs partially because glycogen is primarily made up of water, making up three to four times the weight of the molecule itself. ...
It is also significant that conditions 1 & 2 above caused greater glycogen to be utilized during the test run (21k) than the 3rd condition. BUT, the authors said there was no difference in the run times between groups, and the post-exercise glycogen levels between groups were similar. What does this mean? Carbo loading may increase glycogen stores, which translates to greater glycogen utilization during the run. However, this doesnt benefit performance. What is most interesting to me is that the low-CHO diet for the first 3 days had virtually no benefit over a moderate-CHO diet (in terms of glycogen storage). This could be the study that Rich was referring to when he talked about the myth of carbo-loading. It has been generally accepted that the depletion phase of 1970s-sytle carboloading is of no greater benefit than eating a moderately high CHO diet and pushing additional carbs in the 72 hours preceding depleting exercise. SO, then, Chucks assertion that restricting carbs 7-4 days ...
Assuming that your workout or race starts in the morning, the purpose of your pre-race meal is to top off liver glycogen stores, which your body has expended during your night of sleep. Muscle glycogen, the first fuel recruited when exercise commences, remains intact overnight. If you had a proper recovery meal after your last workout, youll have a full load of muscle glycogen on board, which constitutes about 80% of your total glycogen stores. If you didnt re-supply with complex carbs and protein after your last workout, theres nothing you can do about it now; in fact, youll only hurt yourself by trying. To repeat: during sleep, your liver-stored glycogen maintains proper blood glucose level; you expend nary a calorie of your muscle glycogen. You might wake up feeling hungry, and Ill discuss that issue later, but youll have a full supply of muscle-stored glycogen, your bodys first used and main energy source. Your stomach might be saying, Im hungry, but your muscles are saying, Hey, ...
Glucose and muscle glycogen (the storage form of glucose) The main source of fuel during intense weight training. Low muscle glycogen levels can limit your wor
We examined whether carbohydrate-protein ingestion influences muscle glycogen metabolism during short-term recovery from exhaustive treadmill running and subsequent exercise. Six endurance-trained individuals underwent two trials in a randomized double-blind design, each involving an initial run-to-exhaustion at 70% VO2max (Run-1) followed by 4-h recovery (REC) and subsequent run-to-exhaustion at 70% VO2max (Run-2). Carbohydrate-protein (CHO-P; 0.8 g carbohydrate·kg body mass [BM-1]·h-1 plus 0.4 g protein·kg BM-1·h-1) or isocaloric carbohydrate (CHO; 1.2 g carbohydrate·kg BM-1·h-1) beverages were ingested at 30-min intervals during recovery. Muscle biopsies were taken upon cessation of Run-1, postrecovery and fatigue in Run-2. Time-to-exhaustion in Run-1 was similar with CHO and CHO-P (81 ± 17 and 84 ± 19 min, respectively). Muscle glycogen concentrations were similar between treatments after Run-1 (99 ± 3 mmol·kg dry mass [dm-1]). During REC, muscle glycogen concentrations increased ...
I recently experienced an extreme bout of glycogen depletion. Glycogen keeps your muscles moving and brain functioning - when you run out of it you bonk or hit the wall... actually in the 1960s, it was determined that the major source of carbohydrate during exercise was the muscle glycogen stores. It was demonstrated that the capacity…
Re muscles. When exercising - and this is important - muscles cells will also take up glucose, even in the (relative - cos you always have at least some in your circulation )absence of insulin. Exercise ( via AMPK ? ) stimulates a secondary pool of GLUT4 which then go get glucose. Perhaps most importantly, this can last for betwen 24 to 36hours, and is in part why exercise is recommended for diabetics etc and also why they tell you not to let much more than a day to pass between exercising. Re HIIT. As well as promoting the above, it also very rapidly empties muscle glycogen stores. In intensive exercise, the cells cannot get sufficient fuel quickly enough from the circulation, so the muscle glycogen stores get used up rapidly and HIIT is one of the best ways of doing this. So when youve finished exercising, the muscle cells will immediately replenish this. All of which, in addition to the above, helps keep your blood glucose levels down ...
Glycogen granule definition at, a free online dictionary with pronunciation, synonyms and translation. Look it up now!
Citrulline pulls the glucose switch on your metabolic switchboard. Galactose is the better glucose - at least when it comes to pre-/intra-workout nutrition. There is no need to hurry glycogen repletion, if your next 5k is still 24h away. 4 weeks are not enough for your antioxidant defenses to recover from 3 weeks of overreaching...
Glycogenin-1 is an enzyme that is involved in the biosynthesis of glycogen. This enzyme is important for the function of self-glucosylated to form an oligosaccharide primer that serves as substrate for glycogen synthase. This is done through an inter-subunit mechanism. It also plays a role in glycogen metabolism regulation and in the maximal glycogen levels attaintment in skeletal muscle. Recombinant human glycogenin-1 was expressed in E. coli and purified by using conventional chromatography techniques. Glycogen is a multi branched polysaccharide. It is the way all the animal cells have to store glucose. In the human body, the two main tissues of glycogen accumulation are liver and skeletal muscle. The concentration of this polysaccharide is superior at the liver, but, due to the major mass of skeletal that muscle humans have, this tissue contains three quarters of the corporal glycogen. On the one hand, the function of the liver glycogen is to maintain glucose homeostasis as a way to ...
A note on carbohydrate (carbo) loading: Carbo-loading is a method some athletes use to maximize glycogen stores. The original method began 1 week prior to the event. For the first 3 days, athletes ate a very low carbohydrate diet (about 10% of total calories) and exercised intensely to deplete glycogen stores. The following 3 days the athlete ate a very high carbohydrate diet (about 90% of total calories) and reduced exercise intensity to maximize glycogen stores. Over the years this technique has been modified and the depletion phase has basically been eliminated. Now athletes usually just increase carbohydrate intake for the 3 days prior to the event (about 70% of calories) and decrease exercise intensity. Consult a physician before attempting a carbo-loading diet.. Protein. Protein is needed for muscle and tissue growth and repair. However, too much protein can cause dehydration and muscle heaviness. When muscle glycogen stores are high, protein contributes less than 5% of the energy needed ...
Constitutively active protein kinase that acts as a negative regulator in the hormonal control of glucose homeostasis, Wnt signaling and regulation of transcription factors and microtubules, by phosphorylating and inactivating glycogen synthase (GYS1 or GYS2), CTNNB1/beta-catenin, APC and AXIN1. Requires primed phosphorylation of the majority of its substrates. Contributes to insulin regulation of glycogen synthesis by phosphorylating and inhibiting GYS1 activity and hence glycogen synthesis. Regulates glycogen metabolism in liver, but not in muscle. May also mediate the development of insulin resistance by regulating activation of transcription factors. In Wnt signaling, regulates the level and transcriptional activity of nuclear CTNNB1/beta-catenin. Facilitates amyloid precursor protein (APP) processing and the generation of APP-derived amyloid plaques found in Alzheimer disease. May be involved in the regulation of replication in pancreatic beta-cells. Is necessary for the establishment of neuronal
The exact composition of Glycogen Solution is confidential. The Glycogen concentration is 20mg/mL. Glycogen Solution is a component of Gentra Puregene Kits for DNA purification. During isopropanol precipitation, Glycogen Solution acts as a nucleic acid carrier and helps to efficiently precipitate small amounts of DNA. In addition, it facilitates visualization of the DNA pellet. Glycogen Solution can be purchased separately ...
Glycogen Biosynthesis; Glycogen Breakdown Glycogen - Wikipedia Glycogen is the analogue of starch, a glucose polymer that functions as energy storage in plants. It has a structure similar to amylopectin (a component of starch),.... ...
Using mice that overexpress PTG specifically in the liver, we examined the impact of liver glycogen on food intake. The overexpression of this protein caused an increase in hepatic glycogen stores in mice. When fed an HFD, these animals decreased their food intake and had a lower body weight and decreased fat mass. Changes in key regulators of food intake in the hypothalamus support the decrease in appetite observed in these animals. Expression of POMC, an anorexigenic signal, increased, whereas that of orexigenic NPY decreased. These data support the idea that liver glycogen stores regulate food intake, thus reinforcing the glycogenostatic theory (12). However, in the present study, this effect was limited to hyperphagic conditions, such as HFD. Friedman (34) proposed that changes in glycogen stores do not necessarily signal changes in food intake; rather, the partitioning of carbohydrates in and out of glycogen affects eating behavior by altering fuel fluxes, and, by analogy to fat fuels, ...
What does it do for your muscles and burning fat?. Understanding the relationship between carbohydrates and glycogen can help you respond better to the demands of your body. Sometimes the more active we become and cleaner with our nutrition your glycogen levels can find themselves in a deficit. When your glycogen is low and needs to be replenished we can appear leaner and tighter. However, mentally we may feel foggy and tired. Have you ever notice after eating unclean food, had an all out binge and woke up the next day feeling just as tight, you swear maybe even tighter? You think your eyes are playing tricks on you. This may actually be the case! That is likely because your glycogen levels were low and eating that rich food restored them, letting the body let go of retained water and provided the illusion of swelled muscles to gain that look of tightness. You may even have heard of some fitness athletes before a shoot will plan a couple glasses of wine and a sweet treat the night before. This ...
Many organisms store energy in the form of polysaccharides, commonly homopolymers of glucose. Glycogen, the polysaccharide used by animals to store energy, is composed of alpha-1,4-glycosidic bonds with branched alpha-1,6 bonds present at about every tenth monomer. Starch, used by plant cells, is similar in structure but exists in two forms: amylose is the helical form of starch comprised only of alpha-1,4 linkages, and amylopectin has a structure like glycogen except that the branched alpha-1,6 linkages are present on only about one in 30 monomers. These polysaccharides often contain tens of thousands of monomers, and each type is synthesized in the cell and broken down when energy is needed. Glycogen metabolism is an intricate process involving many enzymes and cofactors resulting in the regular release and storage of glucose. This metabolic process is in turn broken down to glycogen degradation and synthesis. Glycogen synthesis is carried out by the enzyme glycogen synthase in which the ... is the marketplace for research antibodies. Find the right antibody for your research needs. Cardiomyopathy and exercise intolerance in muscle glycogen storage disease 0.
The aim of these experiments was to investigate the interrelationships of fat and carbohydrate (CHO) metabolism in mammalian muscle. In particular, it was hoped to clarify the mechanisms regulating the integration of the supply and utilisation of metabolic substrates in skeletal muscle. This was achieved by studying the response to a perturbation of normal metabolic processes. Administration of a low CHO diet following exereise-induced glycogen depletion resulted in a situation where the muscle and liver glycogen stores were lower than normal, and the availability of plasma FFA was greater than normal. Administration of a high CHO diet immediately following the low CHO diet resulted in the achievement of greater than normal glycogen stores and a restricted availability of FFA. Subjects were studied at rest and during exercise of different intensities at each stage of this dietary regime Measurements were made of blood metabolites and cardiovascular and respiratory parameters. Following the low ...
Where does the myth of the superiority of low intensity cardio come from? Does high intensity exercise take a toll on your antioxidant defense system? Why is burning glycogen actually nothing bad? And what
Muscles respond to changes in training stimulus; specifically, increases in total workout volume and variation in rep ranges. Progressive overload is perhaps the biggest factor that affects muscular growth - that is performing more repetitions per workout and continually using heavier weight over time.. Performing the Team MassiveJoes Extended Hypertrophy training method places an ever increasing demand on muscle tissue in the form of increasing load, volume and time-under-tension (TUT).. By utilising higher rep ranges during the frst 2 working sets, Team MassiveJoes Extended Hypertrophy acutely depletes muscle glycogen stores, which over-time results in your body actively increasing its capacity for glycogen storage in muscle tissue. As muscular glycogen storage increases so does intracellular water retention and cellular hydration, one of the most powerful anabolic triggers for increased muscle protein synthesis and sarcoplasmic muscle growth.. By targeting the moderate rep range in the 3rd ...
Glycogen synthase adds this UDP-glucose to a glycogen chain.[9] Gluconeogenesis[edit]. Glucagon is traditionally a catabolic ... Glycogen storage[edit]. During periods of high blood sugar, glucose 6-phosphate from glycolysis is diverted to the glycogen- ...
What is the function of the retrocerebral organ of rotifers (pseudocoelomate animals)? Glycogen body. The function of this ...
Glycogenesis The process by which glycogen is formed from glucose. Controlled by insulin. See also: Glycogen. Glycosuria Having ... Glycogen A substance made from multiple glucose molecules. Sometimes called 'animal starch'. It is stored in liver and muscle ... The glucose in liver glycogen is put back into the blood when required. That in muscle cells is not, as they lack the necessary ... starch and glycogen-both chains of glucose molecules).are eventually broken down to glucose during digestion. They eventually ...
... triggering a conformational shift which favors the more active glycogen phosphorylase "a" form over the less active glycogen ... 2. Glycogen metabolism". Eur J Biochem. 132 (2): 263-274. doi:10.1111/j.1432-1033.1983.tb07358.x. PMID 6301825. Ingebritsen TS ... Defects in phosphorylase kinase genes are the cause of glycogen storage disease type IX (GSD type IX) and GSD type VI (formerly ... The substrate of PhK, glycogen phosphorylase, had been isolated by Carl and Gerty Cori in the 1930s, who determined that there ...
"Mutations in the gal83 glycogen-binding domain activate the snf1/gal83 kinase pathway by a glycogen-independent mechanism". ... 6-glucosidic linkages of glycogen; and pullulanase is a starch-debranching enzyme. CBM48 binds glycogen. Carbohydrate-binding ... Armstrong, C. G.; Doherty, M. J.; Cohen, P. T. (1998). "Identification of the separate domains in the hepatic glycogen- ... Isoamylase hydrolyses 1,6-alpha-D-glucosidic branch linkages in glycogen, amylopectin and dextrin; 1,4-alpha-glucan branching ...
"PATHWAYS: GLYCOGEN & GLUCOSE". Washington University, St. Louis. "HOW CELLS COMMUNICATE DURING THE FIGHT OR FLIGHT RESPONSE". ... particularly fat and glycogen) for muscular action Dilation of blood vessels for muscles Inhibition of the lacrimal gland ( ...
doi:10.1016/s0140-6736(62)92145-1. Mahler, Robert (1969). "Glycogen storage diseases". J Clin Pathol Suppl (Assoc Clin Pathol ...
The metabolism of glycogen is controlled by activity of phosphorylase, the enzyme that breaks down glycogen, and glycogen ... Insulin causes glycogen synthesis by activating protein phosphatases and producing a decrease in the phosphorylation of these ... Newgard CB, Brady MJ, O'Doherty RM, Saltiel AR (December 2000). "Organizing glucose disposal: emerging roles of the glycogen ... These enzymes are regulated in a reciprocal fashion, with phosphorylation inhibiting glycogen synthase, but activating ...
... that helps to break down glycogen in the lysosome. It is functionally similar to glycogen debranching enzyme, but is on a ... Defects in this gene are the cause of glycogen storage disease II, also known as Pompe disease, which is an autosomal recessive ... GeneReview/NIH/UW entry on Glycogen Storage Disease Type II (Pompe Disease) Human GAA genome location and GAA gene details page ... Errors in this gene cause glycogen storage disease type II (Pompe disease). This gene encodes lysosomal alpha-glucosidase, ...
Greenberg E; Preiss J (1965). "Biosynthesis of bacterial glycogen. II. Purification and properties of the adenosine ... diphosphoglucose:glycogen transglucosylase of arthrobacter species NRRL B1973". J. Biol. Chem. 240: 2341-2348. PMID 14304835. ...
A diagnosis can be made through a muscle biopsy that shows excess glycogen accumulation. Glycogen deposits in the muscle are a ... "Glycogen Storage Disease Type VII". Genetics Home Reference. US National Library of Medicine. Toscano A, Musumeci O (October ... Unlike most other glycogen storage diseases, it directly affects glycolysis. The mutation impairs the ability of ... "Glycogen Storage Disease Type VII". Rare Disease Database. National Organization for Rare Disorders. Swoboda, Kathryn; Specht, ...
Effect of glycogen" (PDF). Biological Bulletin. 133 (2): 310-6. "Apostome". Encyclopædia Britannica. v t e. ...
Effect of glycogen" (PDF). Biological Bulletin. 133 (2): 310-6. v t e. ...
... or glycogen phosphorylase, muscle associated (PYGM) is the muscle isoform of the enzyme glycogen phosphorylase ... "Reaction participants of glycogen phosphorylase". Retrieved 2020-12-26. Mancuso M, Orsucci D, Volterrani D, ... Glycogen phosphorylase catalyses the following reaction: ((1→4)-alpha-D-glucosyl) (n) + phosphate = ((1→4)-alpha-D-glucosyl) (n ... This enzyme helps break down glycogen (a form of stored carbohydrate) into glucose-1-phosphate (not glucose), so it can be used ...
Shen L; Preiss J (1965). "Biosynthesis of bacterial glycogen. I. Purification and properties of the adenosine diphosphoglucose ...
Whelan, W. J.; Cameron, Margaret P. (16 September 2009). Control of Glycogen Metabolism. John Wiley & Sons. p. 60. ISBN ... or stored as glycogen. The lack of the sucrase-isomaltase enzyme in humans causes sucrose intolerance, but because there are ... the same bond that is found at the branch points of glycogen and amylopectin.[citation needed] Like glucose, maltose is a ...
AGL Glycogen storage disease IV; 232500; GBE1 Glycogen storage disease IXc; 613027; PHKG2 Glycogen storage disease of heart, ... PFKM Glycogen storage disease X; 261670; PGAM2 Glycogen storage disease XI; 612933; LDHA Glycogen storage disease XII; 611881; ... ENO3 Glycogen storage disease XIV; 612934; PGM1 Glycogen storage disease XV; 613507; GYG1 Glycogen storage disease type 0; ... GNMT Glycogen storage disease 0, muscle; 611556; GYS1 Glycogen storage disease Ib; 232220; SLC37A4 Glycogen storage disease Ic ...
"Glycogen Branching Enzyme Deficiency (GBED) in Horses". Glycogen Branching Enzyme Deficiency (GBED). University of Minnsesota. ... Glycogen Branching Enzyme Deficiency (GBED) is a genetic disease where the horse is lacking an enzyme necessary for storing ... and is also related to a glycogen storage disorder. While also seen in some draft horse breeds, PSSM has been traced to three ... glycogen, the horse's heart muscle and skeletal muscles cannot function, leading to rapid death. The disease occurs in foals ...
Tarui's disease, a glycogen storage disease that leads to exercise intolerance, is due to a mutation in the PFK gene that ... At the same time, it was found that PKA inhibited glycogen synthase, which was the first example of a phosphorylation event ... ". "Phosphofructokinase Deficiency Glycogen Storage Disease". Bauer, S; Kemter, K; Bacher, A; Huber, R; Fischer, M; Steinbacher ... was the first clue that phosphorylation might serve as a means of regulation in other metabolic pathways besides glycogen ...
They worked on glycogen phosphorylase; Krebs and Fischer defined a series of reactions leading to the activation/inactivation ... The shape and the function of the protein is altered enabling it to take part in converting glycogen into glucose which is used ... 1511-20, PMID 5332191 KREBS, E G; FISCHER, E H (1964), "Phosphorylase and related enzymes of Glycogen Metabolism", Vitam. Horm ...
... will hydrolytically cleave pullulan (alpha-glucan polysaccharides). Lee EY, Whelan WJ (1972). "Glycogen and starch ... Bender H, Wallenfels K (1966). "Pullulanase (an amylopectin and glycogen debranching enzyme) from Aerobacter aerogenes". ...
Cytosolic substrates of p90rsk include protein phosphatase 1; glycogen synthase kinase 3 (GSK3); L1 CAM, a neural cell adhesion ...
Mikael Häggström is a Doctor of Medicine, and the creator of WikiJournal of Medicine, as well as Radlines. He was born in Gothenburg, Sweden, and is a grandchild of Estonian historian Karin Aasma. He grew up in Uddevalla on the Swedish west coast. He decided to become a doctor while backpacking for half a year in 2005, taking the Trans-Siberian train to China and crossing the Himalayas from Tibet to Nepal. He graduated from Uppsala University, Faculty of Medicine in 2013. He did his internship in Sundsvall, and has worked 1.5 years as a physician in obstetrics and gynecology and 3 years in radiology. He is currently doing specialist training in pathology at the NU Hospital Group, Sweden. He has contributed to Wikipedia since 2006, including a multitude of medical images. He is the creator and current editor-in-chief of WikiJournal of Medicine, a new Wikipedia-integrated, peer-reviewed, open-access academic journal.[1] He is also the creator of Radlines and Patholines, containing open access ...
Well exercised muscles can not only add more size but can also develop more mitochondria, myoglobin, glycogen and a higher ... The sarcoplasm is also composed of glycogen, a polysaccharide of glucose monomers, which provides energy to the cell with ...
It appears that fructose is a better substrate for glycogen synthesis than glucose and that glycogen replenishment takes ... The synthesis of glycogen in the liver following a fructose-containing meal proceeds from gluconeogenic precursors. Fructose is ... 15% - 18% is converted to glycogen. Glucose and lactate are then used normally as energy to fuel cells all over the body. ... Once liver glycogen is replenished, the intermediates of fructose metabolism are primarily directed toward triglyceride ...
Mordoh J, Leloir LF, Krisman CR (January 1965). "In vitro Synthesis of Particulate Glycogen". Proc. Natl. Acad. Sci. U.S.A. 53 ... Parodi AJ, Krisman CR, Leloir LF, Mordoh J (September 1967). "Properties of synthetic and native liver glycogen". Arch. Biochem ...
After splitting of the peridal layers to expose the gleba, enzymatic conversion of glycogen to glucose increases the internal ... doi:10.1016/S0007-1536(72)80147-5. Walker LB, Anderson E (1925). "Relation of glycogen to spore-ejection". Mycologia. 17 (4): ...
Examples are starch, cellulose, and glycogen. They are generally large and often have a complex branched connectivity. Because ...
Glycogen stores are maximal at term. Within the first hour of life, blood glucose will typically reach its lowest point and ...
Glycogen phosphorylase is found in muscle and is responsible for mobilising the energy store of glycogen to provide fuel to ... In 1972 she received some crystals of glycogen phosphorylase and this was the beginning of a major chapter in her research ... Barford, D.; Johnson, L. N. (1989). "The allosteric transition of glycogen phosphorylase". Nature. 340 (6235): 609-616. Bibcode ... and she is a depositor on 100 PDB entries including many forms of glycogen phosphorylase and of cell cycle CDK/cyclin complexes ...
Glycogen phosphorylase is one of the phosphorylase enzymes (EC Glycogen phosphorylase catalyzes the rate-limiting ... α-1,4 glycogen chain)n + Pi ⇌ (α-1,4 glycogen chain)n-1 + α-D-glucose-1-phosphate.[2] ... Glycogen phosphorylase can act only on linear chains of glycogen (α1-4 glycosidic linkage). Its work will immediately come to a ... The protonated oxygen now represents a good leaving group, and the glycogen chain is separated from the terminal glycogen in an ...
This stored form of glucose is made up of many connected glucose molecules and is called glycogen. ... Glycogen. The body breaks down most carbohydrates from the foods we eat and converts them to a type of sugar called glucose. ... This stored form of glucose is made up of many connected glucose molecules and is called glycogen. When the body needs a quick ... boost of energy or when the body isnt getting glucose from food, glycogen is broken down to release glucose into the ...
... Made by : khloud A.elbaset Under supervision of Dr./ Galila Yakout ... Glycogen Storage Disease Type 0( Glycogen Synthase Deficiency)GSD 0 is caused by a deficiency of glycogen synthase (GS), a key- ... Glycogen storage disease * 1. Glycogen storage disease Made by : khloud A.elbaset Under supervision of Dr./ Galila Yakout ... 2. Glycogen :Glycogen, an important energy source, isfound in most tissues, but is especiallyabundant in liver and muscle.In ...
The Role of Glycogen in Aerobic and Resistance Exercise. The role of glycogen (stored carbohydrate in muscle) in aerobic ... since glycogen depletion may reduce work output and duration.. References. Essen-Gustavsson, B. & Tesch, P. A. 1990. Glycogen ... Muscle glycogen concentration was 26% lower post-exercise, a rather modest decline considering the demanding exercise protocol ... This article will review two recent articles that further elucidate the role of glycogen in resistance exercise. It is hoped ...
Due to the way glycogen is synthesised, every glycogen granule has at its core a glycogenin protein. Glycogen is in muscle, ... In humans, glycogen is made and stored primarily in the cells of the liver and skeletal muscle. In the liver, glycogen can make ... Glycogen functions as one of two forms of energy reserves, glycogen being for short-term and the other form being triglyceride ... Glycogen is cleaved from the nonreducing ends of the chain by the enzyme glycogen phosphorylase to produce monomers of glucose- ...
... is an inherited disorder caused by an inability to break down a complex sugar called glycogen in liver cells. Explore symptoms ... Glycogen storage disease type VI (also known as GSDVI or Hers disease) ... Identification of a mutation in liver glycogen phosphorylase in glycogen storage disease type VI. Hum Mol Genet. 1998 May;7(5): ... PYGL gene mutations prevent liver glycogen phosphorylase from breaking down glycogen effectively. Because liver cells cannot ...
... is a condition caused by the bodys inability to form a complex sugar called glycogen, which is a major source of stored energy ... Glycogen storage disease type 0 (also known as GSD 0) ... Glycogen storage disease due to hepatic glycogen synthase ... Mutations in the GYS1 or GYS2 gene lead to a lack of functional glycogen synthase, which prevents the production of glycogen ... Both versions of glycogen synthase have the same function, to form glycogen molecules by linking together molecules of the ...
... disorders where an abnormal amount or type of glycogen is stored in the... ... Support those with GSD and raise money for research Glycogen storage disease (GSD) is a group of inherited (born with) ... Support Glycogen Storage Disease is in Americas Giving Challenge-Lets win $50,000!. Hi everyone, Our cause just entered in ... Support those with GSD and raise money for research Glycogen storage disease (GSD) is a group of inherited (born with) ...
of Glycogen. Jessen, Flemming flj at Fri Jan 10 10:08:27 EST 1997 *Previous message: test ... I am analyzing for glycogen in different tissues from fish using the traditional enzymatic method. Now I would like to know if ...
Glycogen vs Fat. *Glycogen can be rapidly mobilized in skeletal muscle *Glycogen can be utilized a fuel substrate in the ... Super glycogen saturation technique can increase amount of work by 19% *Old method involved glycogen depletion through an ... Glycogen can maintain blood glucose levels to be used by certain tissues such as the brain *Carbon atoms of fat cannot be used ... Glycogen stores significantly more limited than adipose tissue Effects on Performance. *Increased storage can double duration ...
Glycogen acanthosis definition at, a free online dictionary with pronunciation, synonyms and translation. Look ... glycogen acanthosis in Medicine Expand. glycogen acanthosis n. Elevated gray-white plaques in the distal mucosa of the ... esophagus, with epithelium thickened by the proliferation of large glycogen-filled squamous cells. ...
The importance of muscle glycogen as a metabolic substrate in sustaining prolonged exercise is well acknowledged. Being stored ... Muscle Glycogen Muscle Glycogen Content Muscle Glycogen Synthesis Endurance Exercise Performance Muscle Substrate These ... Lamer J. Insulin and the stimulation of glycogen synthesis: the road from glycogen structure to glycogen synthase to cyclic AMP ... Effect of muscle glycogen content on exercise-induced changes in muscle T2 times. J Appl Physiol 1998; 84(4): 1178-84PubMed ...
Glycogen granule definition at, a free online dictionary with pronunciation, synonyms and translation. Look it ... glycogen granule in Medicine Expand. glycogen granule n. A granule of glycogen occurring in a cell as an alpha granule or a ...
Glycogen has been linked to diverse processes, the most recent of which is its role in disease progression and ageing. ... However, excess glycogen shortens the nematode lifespan. This is because glycogen prevents thiol-oxidation which interferes ... The AMPK β‐subunit contains a glycogen‐binding domain (GBD), which, when bound by glycogen, inhibits the activity of purified ... Interestingly, the loss of glycogen synthase does not affect lifespan, indicating that glycogen storage is not required to ...
Is that ~200g of glycogen stored in the muscles to ... you still need some glycogen in the muslces. When glycogen is ... if muscle glycogen is depleted, will ingested carbohydrates be used first to replenish muscle glycogen and then to fuel other ... Or can some of this glycogen replaced by converting lactate back to glycogen, or from gluconeogenisis, etc? ... When glycogen is depleted, you hit the wall (you can still walk or jog easily, but cant run fast). Thats why you might carry ...
Glycogen is a major source of energy for muscle contraction. Its breakdown and synthesis are regulated by the contractile state ... through changes in the phosphorylation state of glycogen phosphorylase and glycogen synthase. When muscle is stimulated ... Glycogen is a major source of energy for muscle contraction. Its breakdown and synthesis are regulated by the contractile state ... L. N. Johnson, E. A. Stura, K. S. Wilson, M. S. P. Sansom and I. T. Weber, Nucleotide binding to glycogen phosphorylase b in ...
InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites. We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their individual strengths to produce a powerful integrated database and diagnostic tool.
These enzymes normally catalyze reactions that ultimately convert glycogen compounds to glucose. ... A glycogen storage disease (GSD) is the result of an enzyme defect. ... encoded search term (Type Ib Glycogen Storage Disease) and Type Ib Glycogen Storage Disease What to Read Next on Medscape. ... Detection of glycogen in a glycogen storage disease by 13C nuclear magnetic resonance. FEBS Lett. 1982 Dec 27. 150(2):489-93. [ ...
Glycogen is a polysaccharide molecule stored together with water in animal cells. Its primarily used as a source of energy, ... Glycogen is stored in muscle tissue and in the liver, with levels tending to peak immediately after a meal. In humans, the body ... Glycogen is a polysaccharide molecule stored in animal cells along with water and used as a source of energy. When broken down ... I have tried the fat burn post glycogen, but the problem lies in that the body says no. The body has nothing in the tank so ...
Source for information on Carbohydrate Stores: Muscle Glycogen, Liver Glycogen, and Glucose: World of Sports Science dictionary ... Liver Glycogen, and GlucoseThe energy required to power the human body begins with the consumption of food, and the subsequent ... extraction by the body of the carbohydrate-based sugars, known as glucose and glycogen. The manufacture, storage, and ... "Carbohydrate Stores: Muscle Glycogen, Liver Glycogen, and Glucose." World of Sports Science. . 13 Jun. 2019 , ...
The PDB archive contains information about experimentally-determined structures of proteins, nucleic acids, and complex assemblies. As a member of the wwPDB, the RCSB PDB curates and annotates PDB data according to agreed upon standards. The RCSB PDB also provides a variety of tools and resources. Users can perform simple and advanced searches based on annotations relating to sequence, structure and function. These molecules are visualized, downloaded, and analyzed by users who range from students to specialized scientists.
1) It requires a LOT of energy for your muscles to build up that brick wall again (i.e. replace and store muscle glycogen). ... Think of muscle glycogen as a BIG BRICK WALL in your muscles. ... Glycogen is the form of stored carbohydrate in your muscles.. ... When you do a muscle depletion workout, you deplete the levels of glycogen in your muscles. ... And "glycolysis" is the breakdown of glycogen.. ... "glycogen depletion" style workout.. Now Ive been working on ...
Enzyme deficiency results in glycogen accumulation in tissues. ... A glycogen storage disease (GSD) results from the absence of ... enzymes that ultimately convert glycogen compounds to glucose. ... Type VI Glycogen Storage Disease * Type IV Glycogen Storage ... encoded search term (Type III Glycogen Storage Disease) and Type III Glycogen Storage Disease What to Read Next on Medscape. ... Detection of glycogen in a glycogen storage disease by 13C nuclear magnetic resonance. FEBS Lett. 150(2):489-93. [Medline]. ...
Next Generation Science Standards and NGSS are registered trademarks of Achieve. Neither Achieve nor the lead states and partners that developed the Next Generation Science Standards were involved in the production of this product, and do not endorse it.. ...
Going for Glycogen. Glycogen is your bodys preferred energy source for exercise, as its more readily available, writes Dr. ... Whether you burn glycogen or fat doesnt matter too much from a fat-loss standpoint, writes Berardi in The Metabolism ... As a high-carb diet increases stores of glycogen, a low-carb diet will decrease them. This starts to shift your body from using ... How you eat and how you train can have a big impact on whether youre burning fat or glycogen when training. ...
Inhibition of Glycogen Synthase Kinase (GSK-3) Protects Against Oxidative Stress and Attenuates Apoptosis in Human Lens ...
This is often caused by a change in your bodys level of stored carbohydrate, known as glycogen. ... When Glycogen Drops A healthy adult can store around 400 grams of glycogen in the liver and about 100 grams in the muscle cells ... If your glycogen levels drop, you can lose half a kilogram -- over 1 pound. Additionally, every gram of glycogen carries with ... This is often caused by a change in your bodys level of stored carbohydrate, known as glycogen. Changes in glycogen are normal ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Glycogen-storage diseases comprise a group of conditions that have inherited defects in glycogen metabolism as a common ... Glycogen-storage diseases comprise a group of conditions that have inherited defects in glycogen metabolism as a common ... encoded search term (What is the role of glycogen-storage diseases in Fanconi syndrome?) and What is the role of glycogen- ... A Fanconi syndrome ensues only in those forms of the syndrome in which the deposition of glycogen in the renal tubules ...
  • 13. Glycogen Storage Disease Type 0( Glycogen Synthase Deficiency)GSD 0 is caused by a deficiency of glycogen synthase (GS), a key-enzyme of glycogen synthesis. (
  • After a meal has been digested and glucose levels begin to fall, insulin secretion is reduced, and glycogen synthesis stops. (
  • Lamer J. Insulin and the stimulation of glycogen synthesis: the road from glycogen structure to glycogen synthase to cyclic AMP-dependant protein kinase to insulin mediators. (
  • Its breakdown and synthesis are regulated by the contractile state of the tissue as well as by the neural and hormonal control of the muscle, through changes in the phosphorylation state of glycogen phosphorylase and glycogen synthase. (
  • Impaired hepatic glycogen synthesis in glucokinase-deficient (MODY-2) subjects. (
  • The relative fluxes of the direct and indirect pathways of hepatic glycogen synthesis were also assessed using [1-13C]glucose in combination with acetaminophen to noninvasively sample the hepatic UDP-glucose pool. (
  • Finally, we show that an inability to engage in glycogen synthesis results in suppression of the enhanced survival phenotype observed in daf-2 insulin-like pathway mutants, suggesting that alterations in glycogen metabolism may serve as a basis for these mutants' resistance to hyposmotic anoxia. (
  • There are a number of inborn errors of glycogen metabolism that result from mutations in genes for virtually all of the proteins involved in glycogen synthesis, degradation, or regulation. (
  • [2] On the other hand, much less is known about the structure of glycogen synthase, the key regulatory enzyme of glycogen synthesis. (
  • Although the catalytic mechanisms used by glycogen synthase are not well known, structural similarities to glycogen phosphorylase at the catalytic and substrate binding site suggest that the mechanism for synthesis is similar in glycogen synthase and glycogen phosphorylase. (
  • However, since glycogen synthase requires an oligosaccharide primer as a glucose acceptor, it relies on glycogenin to initiate de novo glycogen synthesis. (
  • Liver glycogen serves as a storage pool to maintain the blood glucose level during fasting, whereas muscle glycogen synthesis accounts for disposal of up to 90% of ingested glucose. (
  • Glycogen branching enzyme is one of the key enzymes in the glycogen synthesis. (
  • The two families GBEs in on bacteria shows that GH13 GBE is involved in glycogen synthesis, and the real function of GH57 GBE is not clear yet. (
  • Healthy neurons do not store glycogen - the main source of energy storage for cells - while they do possess the machinery for glycogen synthesis in an inactive state. (
  • Using cellular and animal models of Huntington's disease, the researchers have shown that high level of cytotoxic mutant Huntingtin protein triggers more glycogen synthesis in neurons by activating glycogen synthase. (
  • Glycogen storage diseases are several inborn errors of metabolism that result from enzyme defects that affect the processing of glycogen synthesis or breakdown within muscles , liver , and other cell types. (
  • In skeletal muscle, contributes to insulin regulation of glycogen synthesis by phosphorylating and inhibiting GYS1 activity and hence glycogen synthesis. (
  • Regulates protein synthesis by controlling the activity of initiation factor 2B (EIF2BE/EIF2B5) in the same manner as glycogen synthase. (
  • This review gives an update on the molecular signals by which glucose transport is increased in the contracting muscle followed by a discussion of glycogen mobilization and synthesis by the action of glycogen phosphorylase and glycogen synthase, respectively. (
  • In the liver, glycogen synthesis and degradation are regulated to maintain blood-glucose levels as required to meet the needs of the organism as a whole. (
  • Glycogen synthesis is, unlike its breakdown, endergonic. (
  • This means that glycogen synthesis requires the input of energy. (
  • Energy for glycogen synthesis comes from UTP, which reacts with glucose-1-phosphate, forming UDP-glucose, in reaction catalyzed by UDP-glucose pyrophosphorylase. (
  • As glycogen synthase can only lengthen an existing chain, the protein glycogenin is needed to initiate the synthesis of glycogen. (
  • OBJECTIVE- Glucose homeostasis is achieved by triggering regulation of glycogen synthesis genes in response to insulin when mammals feed, but the underlying molecular mechanism remains largely unknown. (
  • During feeding, both mRNA and protein levels of GSK-3β decreased in Stat3 f/+ mice, which reflected the need of hepatocytes for insulin to induce glycogen synthesis. (
  • 30 seconds) is characterized by a rapid breakdown of phosphocreatine for the production and use of ATP, as well as stimulation of glycogenolysis (breakdown of glycogen) and glycolysis (breakdown of glucose), with a lesser contribution of oxidative metabolism. (
  • In this article, we review the processes of muscle glycogen and triglyceride storage and metabolism. (
  • Whether you burn glycogen or fat doesn't matter too much from a fat-loss standpoint, writes Berardi in 'The Metabolism Advantage. (
  • Glycogen-storage diseases comprise a group of conditions that have inherited defects in glycogen metabolism as a common denominator. (
  • Published in Cell Metabolism , the research (" Nuclear Glycogenolysis Modulates Histone Acetylation in Human Non-Small Cell Lung Cancers ") centers on the function of glycogen accumulation in the nucleus of a cell. (
  • Nuclear glycogen was first reported in the 1890s and its role in cellular metabolism and impact on disease has been elusive," Sun said. (
  • Glycogen is a storage molecule for fuel reserve, but this study demonstrates other functions of glycogen metabolism including epigenetics. (
  • Our team demonstrated that nuclear glycogen metabolism modulates the regulatory components of gene expression that are necessary for cancer progression. (
  • This study uncovers a previously unknown role for glycogen metabolism in the nucleus and elucidates another mechanism by which cellular metabolites control epigenetic regulation. (
  • We developed a novel nuclear-specific tracer technology coupled to high-resolution mass spectrometry to trace nuclear glycogen metabolism and discovered that it modulates histone acetylation," Sun said. (
  • These results suggest that in addition to the altered beta cell function, abnormalities in liver glycogen metabolism play an important role in the pathogenesis of hyperglycemia in patients with glucokinase-deficient maturity onset diabetes of young. (
  • Our findings demonstrate that nematode survival of a hyposmotic environment during anoxia (hyposmotic anoxia) depends on the nematode's ability to engage in glycogen metabolism. (
  • The purpose of the present study was to further define the role of cellular glycogen content in determining GS activity and determine what role, if any, AMPK plays in controlling glycogen metabolism. (
  • The major manifestations of disorders of glycogen metabolism affecting the liver are hypoglycemia and hepatomegaly. (
  • The major manifestations of disorders of glycogen metabolism affecting muscle are muscle cramps, exercise intolerance and easy fatigability, and progressive weakness. (
  • See also Glycogen Metabolism & Gluconeogenesis . (
  • Solved: 11)Glycogen Metabolism Is Regulauted By Select One. (
  • home / study / science / biology / biology questions and answers / 11)Glycogen Metabolism Is Regulauted By Select One: A Feedback Inhibition B. Hormones And Allosteric. (
  • 11)Glycogen metabolism is regulauted by Select one: A Feedback inhibition B. Hormones and alloste. (
  • Glucose allosterically regulate glycogen breakdown and epinephrine, glucagon also regulate glycogen metabolism) 12. (
  • [2] Majority of glycogen storage diseases are due to deficiency of specific enzymes involved in metabolism of glycogen either in liver or muscle or both. (
  • Regulation of glucose and glycogen metabolism during and after exercise. (
  • Glycogen degradation consists of three steps: (1) the release of glucose 1-phosphate from glycogen, (2) the remodeling of the glycogen substrate to permit further degradation, and (3) the conversion of glucose 1-phosphate into glucose 6-phosphate for further metabolism. (
  • Hepatic glycogen storage diseases (GSDs) are rare inborn errors of carbohydrate metabolism. (
  • This is an enzyme involved in breaking down glycogen, the energy storage molecule involved in animal metabolism. (
  • Glycogen storage diseases, also known as glycogenoses, are genetically linked metabolic disorders that involve the enzymes regulating glycogen metabolism. (
  • Disruption of glycogen metabolism also affects other biochemical pathways as the body seeks alternative fuel sources. (
  • The system for glycogen metabolism relies on a complex system of enzymes. (
  • Insulin acts on the hepatocytes to stimulate the action of several enzymes, including glycogen synthase. (
  • Previous resistance training research suggests that weight training is associated with a consequential depletion of muscle glycogen stores. (
  • In a therapeutic setting then, depletion of glycogen by increasing cellular levels of oxidants may produce beneficial effects in hyperglycemic patients and those with diseases related to glycogen storage. (
  • When you do a muscle depletion workout, you deplete the levels of glycogen in your muscles. (
  • In the short-term, this can lead to muscle fatigue and a drop in performance and in the long-term, chronic glycogen depletion can place extra stress on your liver, warns sports nutritionist Ben Greenfield. (
  • After the depletion of blood sugar levels, the human body needs more glycogen. (
  • Bonking is when your body draws down its glycogen stores to the point of glycogen depletion. (
  • There's also density sets, bodyweight cardio circuits, and metabolic resistance training - just 3 more methods I use in the TT Xtreme Depletion workout to exhaust your muscle glycogen and turn up the turbulence. (
  • GS becomes activated following glycogen depletion (such as occurs during exhaustive exercise) in an insulin-independent manner ( 15 ). (
  • We have recently developed a model system in vitro using cultured human muscle, in which glycogen depletion is achieved by glucose deprivation ( 18 ). (
  • Glycogen depletion in a female B6C3F1 mouse from a subchronic study. (
  • There is a notable depletion of glycogen within hepatocytes. (
  • The morphologic appearance of glycogen in hepatocytes is distinctive, allowing glycogen accumulation or depletion to be readily diagnosed in most cases. (
  • In some cases, particularly when differences in the amount of glycogen are accompanied by other cytoplasmic changes, glycogen accumulation or depletion may not be easily discerned. (
  • glycogen depletion should be diagnosed in the treated animals and given a severity grade. (
  • Consequently, interpretation of glycogen depletion should take food consumption and general animal health into consideration. (
  • Specifically, people training with carb depletion show a boost in fat metabolizing enzymes, fat utilization and muscle glycogen storage. (
  • Fatigue and Glycogen depletion aren't the same thing neccesarily. (
  • Glycogen is left with one fewer glucose molecule , and the free glucose molecule is in the form of glucose-1-phosphate . (
  • The protonated oxygen now represents a good leaving group , and the glycogen chain is separated from the terminal glycogen in an S N 1 fashion, resulting in the formation of a glucose molecule with a secondary carbocation at the 1 position. (
  • Finally, the deprotonated inorganic phosphate acts as a nucleophile and bonds with the carbocation, resulting in the formation of glucose-1-phosphate and a glycogen chain shortened by one glucose molecule. (
  • Deficiency of GBE results in the formation of an amylopectin-like compact glycogen molecule with fewer branching points and longer outer chains. (
  • Glycogen is a branched biopolymer consisting of linear chains of glucose residues with an average chain length of approximately 8-12 glucose units and 2,000-60,000 residues per one molecule of glycogen Glucose units are linked together linearly by α(1→4) glycosidic bonds from one glucose to the next. (
  • Glycogen is a non-osmotic molecule, so it can be used as a solution to storing glucose in the cell without disrupting osmotic pressure. (
  • Glycogen is a polysaccharide molecule stored in animal cells along with water and used as a source of energy. (
  • Glycogen is known as a carbohydrate energy storage molecule for cells. (
  • Non-small cell lung cancers suppress nuclear glycogen breakdown by decreasing the amount of a key signaling molecule called malin to drive cancer progression. (
  • Glycogen is the primary short term energy storage molecule in animals. (
  • In other words, glycogen is a molecule constituted of numerous glucose molecules. (
  • Glycogen phosphorylase (GP) catalyzes the hydrolysis of glycogen to generate glucose-1-phosphate and shortened glycogen molecule and is considered the rate limiting step in the degradation of glycogen [1] . (
  • Glycogen is the molecule that functions as the secondary long-term energy storage in animal and fungal cells. (
  • 6) transglycosylase, catalyzes the transfer of a terminal fragment of 6-7 glucose residues from a nonreducing end to the C-6 hydroxyl group of a glucose residue deeper into the interior of the glycogen molecule. (
  • In humans, glycogen is made and stored primarily in the cells of the liver and skeletal muscle. (
  • In skeletal muscle, glycogen is found in a low concentration (1-2% of the muscle mass) and the skeletal muscle of an adult weighing 70 kg stores roughly 400 grams of glycogen. (
  • in fasting individuals, blood glucose is maintained constant at this level at the expense of glycogen stores in the liver and skeletal muscle. (
  • During cardiac muscle contractions or rapid or sustained movement of skeletal muscle, glycogen stored in muscle cells is broken down to supply the cells with energy. (
  • The liver is capable of containing up to 10% of its volume in glycogen, in contrast to the 1% storage by volume carried on in the skeletal muscles. (
  • However, it is uncertain whether exhaustive exercise induces glycogen supercompensation in the brain as in skeletal muscle. (
  • To explore this question, we exercised adult male rats to exhaustion at moderate intensity (20 m min(-1)) by treadmill, and quantified glycogen levels in several brain loci and skeletal muscles using a high-power (10 kW) microwave irradiation method as a gold standard. (
  • Skeletal muscle glycogen was depleted by 82-90% with exhaustive exercise, and supercompensated by 43-46% at 24 h after exercise. (
  • These results support the hypothesis that, like the effect in skeletal muscles, glycogen supercompensation also occurs in the brain following exhaustive exercise, and the extent of supercompensation is dependent on that of glycogen decrease during exercise across brain regions. (
  • To investigate the role of glycogen synthase in controlling glycogen accumulation, we generated three lines of transgenic mice in which the enzyme was overexpressed in skeletal muscle by using promoter-enhancer elements derived from the mouse muscle creatine kinase gene. (
  • The observation that increasing glycogen synthase enhances glycogen accumulation supports the conclusion that the activation of glycogen synthase, as well as glucose transport, contributes to the accumulation of glycogen in response to insulin in skeletal muscle. (
  • consequently, excessive glycogen deposits can damage the liver, heart and skeletal muscle. (
  • Carbohydrates are a very limited source of energy accounting for only about 1-2% of total bodily energy stores.3 Furthermore, about 80% of total carbohydrate is stored in skeletal muscle, about 14% is stored in the liver and about 6% in the blood in the form of glucose.4 This would represent about 300-400g of glycogen stored in muscle and about 70-100g stored in the liver. (
  • Within skeletal muscle and liver glucose is stored as glycogen. (
  • Glycogen phosphorylase catalyzes the rate-limiting step in glycogenolysis in animals by releasing glucose-1-phosphate from the terminal alpha-1,4-glycosidic bond. (
  • In response to insulin levels being below normal (when blood levels of glucose begin to fall below the normal range), glucagon is secreted in increasing amounts and stimulates both glycogenolysis (the breakdown of glycogen) and gluconeogenesis (the production of glucose from other sources). (
  • As a result, the phosphorylation state of glycogen phosphorylase is increased and glycogenolysis is accelerated to provide the ATP required to sustain muscle contraction. (
  • We demonstrate that the decreased abundance of malin, an E3 ubiquitin ligase, impaired nuclear glycogenolysis by preventing the nuclear translocation of glycogen phosphorylase and causing nuclear glycogen accumulation. (
  • In these patients, the breakdown of glycogen (glycogenolysis) is defective. (
  • When glycogen is broken down through a process called glycogenolysis, it is broken to make glucose which is then used by the human body or other organisms as energy. (
  • The breaking down of glycogen into glucose is called glycogenolysis. (
  • The last step in glycogenolysis, the breaking down of glycogen to glucose, is the transformation of glucose-6-phosphate to glucose. (
  • Chen Y. Glycogen Storage Diseases. (
  • Gene therapy for type I glycogen storage diseases. (
  • Fernandes J, Smit G. The Glycogen-Storage Diseases. (
  • Nutrition therapy for hepatic glycogen storage diseases. (
  • Some people have conditions known as glycogen storage diseases. (
  • What is the role of glycogen-storage diseases in Fanconi syndrome? (
  • Glycogen storage diseases (GSDs) are a group of inherited genetic disorders. (
  • GSD-IX is part of a larger group of disorders in which the body cannot metabolize glycogen into glucose (glycogen storage diseases). (
  • Abnormal ability to utilize glycogen is found in diabetes and in several genetic glycogen storage diseases. (
  • Those disorders that result in abnormal storage of glycogen are known as glycogen storage diseases (GSDs). (
  • At the University of Florida, which is the largest clinical and research facility in the world for the study of hepatic glycogen storage diseases, Weinstein and his team of researchers began to use gene therapy to see if they could devise a cure. (
  • GSD type 1a accounts for about 25 percent of cases of glycogen storage diseases among people of European ancestry. (
  • Akman HO, Oldfors A, DiMauro S. Glycogen storage diseases of muscle. (
  • They observed that increased level of glycogen synthase protects neurons from the cytotoxicity of the mutant Huntingtin protein.For long, scientists have been trying to find specific role of glycogen in neurons, especially in brain diseases like Huntington's, Lafora, Alzheimer's etc. with some believing it be neurotoxic. (
  • It is an important finding on protective role of glycogen synthase in neurodegenerative diseases which may have translational relevance," commented Professor Sathees C Raghavan from Indian Institute of Science, who is not connected with this study. (
  • A total of fourteen glycogen storage diseases have been described which differ from each other on the basis of genotypic and phenotypic heterogenity. (
  • Most of the glycogen storage diseases follow an autosomal recessive mode of inheritence. (
  • There are a wide variety of clinical manifestations of glycogen storage diseases. (
  • After which, muscle glycogen can be resynthesized near pre-exercise levels within 24 hours, equivalently with either carbohydrates form. (
  • The role of dietary carbohydrates in muscle glycogen resynthesis after strenuous running. (
  • Also, if muscle glycogen is depleted, will ingested carbohydrates be used first to replenish muscle glycogen and then to fuel other daily functions, or are they used the other way around? (
  • Glycogen is essentially stored carbohydrates, so once the body depletes these reserves, than the body switches to burning stored fat. (
  • Complex carbohydrates are composed of complex sugars known as polysaccharides, of which glycogen is the most prominent example. (
  • When the intake of carbohydrates exceeds that which can be stored and converted to energy as glycogen or glucose, the body will store the excess carbohydrates as fat, often leading to weight gain. (
  • When you start to diet and cut calories and carbohydrates, your body has to dig into its glycogen reserves, causing them to be used for energy, notes dietitian Zoe Hellman. (
  • Those who have diets rich in carbohydrates have more glycogen during exercise for energy, and they replenish their stores of glycogen after exercise more easily. (
  • I should also remind you that muscle glycogen is simply what we nerd-lingers call the carbohydrates that are stored in your muscles. (
  • The human diet contains 3 macronutrients that can be stored by the body as energy: carbohydrates (as the natural carbohydrate polymer glycogen, in mainly the liver and muscle), protein (as muscle, the natural protein source of the body) and fat (in organs and fat tissue). (
  • Glycogen is a sugar but in a polysaccharide form and is made up of many carbohydrates compared to that of glucose. (
  • Unfortunately, there are many recreational and competitive athletes who either are not aware of the importance of carbohydrates and glycogen storages for proper training and performance, or who just simply and deliberately restrict carbohydrates from their diet because some training buddy told them to, or they read it somewhere in the internet. (
  • Glycogen is the storage form of glucose and carbohydrates (CHO) in animals and humans. (
  • This combination restores the glycogen store faster than just carbohydrates. (
  • Consequently, patients with GS deficiency have decreased liver glycogen concentration, resulting in fasting hypoglycemia. (
  • Because liver cells cannot break down glycogen into glucose, individuals with GSDVI can have hypoglycemia and may use fats for energy, resulting in ketosis. (
  • Orho M, Bosshard NU, Buist NR. Mutations in the liver glycogen synthase gene in children with hypoglycemia due to glycogen storage disease type 0. (
  • When the pancreas determines that blood glucose levels are too low, causing a condition known as hypoglycemia, the pancreas produces a hormone, glucagen, to stimulate a release of stored glycogen from the liver, in the form of glucose, into the blood to restore balance. (
  • Compelling evidence indicates that astrocyte glycogen breaks down during hypoglycemia to lactate that is transferred to adjacent neurons or axons where it is used aerobically as fuel. (
  • Liver glycogen is important for the counterregulation of hypoglycemia and is reduced in individuals with type 1 diabetes (T1D). (
  • Compared with control treatment, fructose infusion caused a large increase in liver glycogen that markedly elevated the response of epinephrine and glucagon to a given hypoglycemia and increased net hepatic glucose output (NHGO). (
  • When hepatic glycogen content was lowered, glucagon and NHGO responses to insulin-induced hypoglycemia were reduced. (
  • It remains to be determined whether the risk of iatrogenic hypoglycemia in T1D humans could be lessened by targeting metabolic pathway(s) associated with hepatic glycogen repletion. (
  • More important, targeted newborn screening in this population may detect disease early, potentially reducing the impact of newborn hypoglycemia and glycogen accumulation. (
  • 11. Glycogen Storage Disease Type IV (Branching Enzyme Deficiency):Andersen Disease, is an autosomal recessive disorder due to a deficiency of glycogen branching enzyme (GBE). (
  • Enzyme deficiency results in glycogen accumulation in tissues. (
  • Disease results from a pan-deficiency of the enzyme (GSD IIIa) or muscle-specific retention of glycogen debranching enzyme (GSD IIIb). (
  • Fanconi-Bickel syndrome can be confused with type I glycogen storage disease, which is caused by a deficiency in glucose-6-phosphatase activity. (
  • One patient with amylo-1,4→1,6-transglucosidase deficiency (Type IV) was found to have a normal concentration of glycogen in the erythrocytes but the glycogen from the cellular elements of the blood was shown to be abnormal, being amylopectin-like in structure. (
  • Glycogen storage disease type IX (GSD-IX) is a group of at least four disorders characterized by a deficiency of the enzyme phosphorylase kinase. (
  • Glycogen storage disease type V is a metabolic disorder , more specifically a glycogen storage disease , caused by a deficiency of myophosphorylase. (
  • Glycogen storage disease has been divided into at least 10 different types based on the deficiency of a particular enzyme which controls blood sugar levels. (
  • Type I glycogen storage disease is a deficiency of the enzyme glucose-6-phosphatase which helps in maintaining a normal blood glucose level (sugar concentration) during fasting. (
  • [1] Glucose-6-phosphatase deficiency found in glycogen storage disease type I is identified as first specific enzymopathy in a hereditary disorder . (
  • As a high-carb diet increases stores of glycogen, a low-carb diet will decrease them. (
  • Additionally, every gram of glycogen carries with it 3 grams of water, meaning that if you deplete your regular stores of glycogen, this can show up as a 2 kilogram loss on the scale. (
  • Exercise can therefore be a useful way to reduce blood glucose levels and can be particularly useful in people with type 2 diabetes Following exercise, the muscles will try to replenish their stores of glycogen and will therefore take in available glucose from the blood to do so, helping to lower blood glucose over this period. (
  • The energy required to power the human body begins with the consumption of food, and the subsequent extraction by the body of the carbohydrate-based sugars, known as glucose and glycogen. (
  • Without glucose and glycogen to serve as energy, a person will experience extreme fatigue. (
  • Studies in Caenorhabditis elegans have revealed that high sugar diets which mediate the accumulation of glycogen, results in two conflicting effects. (
  • The accumulation of glycogen in certain organs and tissues, especially the liver, kidneys, and small intestines, impairs their ability to function normally. (
  • However, muscle-specific glycogen synthase activation may lead to excessive accumulation of glycogen, leading to damage in the heart and central nervous system following ischemic insults. (
  • The amount of glycogen stored in the body-particularly within the muscles and liver-mostly depends on physical training, basal metabolic rate, and eating habits. (
  • Is that ~200g of glycogen stored in the muscles to be used for exercise, or is it stored in the liver and used to fuel the brain and "day-to-day" functions? (
  • As you suspect, the glycogen stored in the muscles (provided you aren't taking in other glucose) is used along with fats to fuel physical activity throughout the day like your work out, your daily walk to the train, walk to the fridge, etc. (
  • The glycogen in the liver, while it can contribute circulating glucose to working muscles, generally serves up energy (reconverted glucose) to other parts of the body - the brain for example - as it sees fit. (
  • Yes, some will go to muscles recovering from a Primal-style brief-but-intense effort , but the rest stays in the liver and provides glycogen/glucose for the brain and red blood cells, etc. (
  • Once stored in the muscles, glycogen cannot be released into the bloodstream, but will be utilized as fuel to produce ATP by the muscle itself. (
  • Glycogen is the form of stored carbohydrate in your muscles. (
  • Think of muscle glycogen as a BIG BRICK WALL in your muscles. (
  • 1) It requires a LOT of energy for your muscles to build up that brick wall again (i.e. replace and store muscle glycogen). (
  • Carbs come from the carbs you eat, which travel around your blood as glucose, as well as carbs stored in your liver and muscles, known as glycogen. (
  • Running for Fitness explains that energy from glycogen stored in muscles lasts for about an hour of exercise. (
  • The best type of glycogen for athletes is starch, a complex carbohydrate that is easily broken down and stored in muscles and the liver. (
  • In these muscles, glycogen synthase activity was increased by as much as 10-fold, with concomitant increases (up to 5-fold) in the glycogen content. (
  • Levels of glycogen phosphorylase in these muscles increased (up to 3-fold), whereas the amount of the insulin-sensitive glucose transporter 4 either remained unchanged or decreased. (
  • Symptoms and signs of GSD-III, at least during the first 4 to 6 years of life, may be indistinguishable from GSD type I. The amount of glycogen in the liver and muscles is abnormally high, the liver is enlarged, and the abdomen protrudes. (
  • When there is excess glycogen, it is stored in the body, primarily in the liver and muscles and, when the body needs more energy, is eventually converted into glucose. (
  • Because individuals with GSD-IX cannot properly break down glycogen, excess amounts accumulate in the liver, muscles, or both. (
  • The inability to break down glycogen into glucose results in an energy shortage within the muscle, resulting in muscle pain and cramping , and sometimes causing serious injury to the muscles. (
  • Muscles also have big reserves of a complex carbohydrate called glycogen . (
  • As a result, their muscles do not receive the fuel they need to grow and glycogen builds up in their liver and other organs. (
  • Glycogen is normally stored in either the muscles or the liver. (
  • Since glucose is one of the main components of creating energy (ATP) for the body including muscles, the glycogen stored in muscles help with the providing the necessary energy to keep the muscles moving. (
  • Therefore, the glycogen stored in muscle is meant to be used for the muscle, and also helps when muscles are in need of glucose to function they can utilize the nearest stores of it. (
  • Glycogen is an important source of energy that is stored in all tissues, especially in the muscles and liver. (
  • As a result, the body cannot break down glycogen in the muscles. (
  • Glycogen is mainly stored in the liver and the muscles and provides the body with a readily available source of energy if blood glucose levels decrease. (
  • In a healthy body, the pancreas will respond to higher levels of blood glucose , such as in response to eating, by releasing insulin which will lower blood glucose levels by prompting the liver and muscles to take up glucose from the blood and store it as glycogen. (
  • Glycogen plays an important role in keeping our muscles fuelled for exercise. (
  • When we exercise, our muscles will take advantage of their stored glycogen. (
  • Glucose in our blood and glycogen stored in the liver can also be used to keep our muscles fuelled. (
  • Once we complete our exercise session, our muscles will replenish their glycogen stores. (
  • Muscles that are well stocked with glycogen can simply outwork the competition. (
  • In a process analogous to putting money in the bank, the body bundles up the extra glucose and stores it as glycogen in the liver and muscles. (
  • Since glycogen storage occurs mainly in muscles and the liver, those sites display the most prominent symptoms. (
  • It was felt the energy production of the isokinetic exercise was predominantly due to the breakdown of creatine phosphate while the utilization of glycogen was much more apparent in the longer lasting squat exercise regime. (
  • however, the breakdown of muscle glycogen impedes muscle glucose uptake from the blood, thereby increasing the amount of blood glucose available for use in other tissues. (
  • Glycogen phosphorylase is the primary enzyme of glycogen breakdown. (
  • Ketones are molecules produced during the breakdown of fats, which occurs when stored sugars (such as glycogen) are unavailable. (
  • When you have reached maximum glycogen breakdown, your body can actually burn up to 300% more fat according to different studies. (
  • And "glycolysis" is the breakdown of glycogen. (
  • The chemical reactions and pathways resulting in the breakdown of glycogen, a polydisperse, highly branched glucan composed of chains of D-glucose residues. (
  • While nuclear glycogen accumulation has been reported in multiple cancers, this study demonstrates that glycogen is synthesized and broken down in the nucleus, that nuclear breakdown provides the fuel for histone modifications, and that these modifications allow cells to become cancerous. (
  • We examined their effect on liver glycogen breakdown in humans. (
  • Net rates of glycogen breakdown were calculated from the decrease of liver glycogen within 9 h using 13C nuclear magnetic resonance spectroscopy. (
  • An increase of non-esterifled fatty acid leads to a pronounced inhibition of net hepatic glycogen breakdown and increases gluconeogenesis whereas glucose production does not differ from the control condition. (
  • However, in the absence of prior glycogen breakdown, glucose treatment failed to activate GS above control values, indicating the crucial role of glycogen content. (
  • Glycogen storage disease type VI (also known as GSDVI or Hers disease) is an inherited disorder caused by an inability to break down a complex sugar called glycogen in liver cells. (
  • Glycogen storage disease type 0 (also known as GSD 0) is a condition caused by the body's inability to form a complex sugar called glycogen, which is a major source of stored energy in the body. (
  • GSD is an inherited disorder caused by the buildup of a complex sugar called glycogen in the body's cells. (
  • The role of glycogen (stored carbohydrate in muscle) in aerobic exercise has been clearly shown to be associated with increased work output and duration (Haff et al. (
  • As such, to ensure optimal exercise performance, endurance athletes are encouraged to maximise the availability of muscle glycogen through the ingestion of a high carbohydrate (CHO) diet prior to competition. (
  • With an enzyme defect, carbohydrate metabolic pathways are blocked and excess glycogen accumulates in affected tissues. (
  • Carbohydrate storage is the limiting factor in athletic performance, according to Iowa State University, as when it runs out, you no longer burn glycogen, which can lead to a decrease in performance. (
  • This is often caused by a change in your body's level of stored carbohydrate, known as glycogen. (
  • The carbohydrate is broken down and converted to a substance called glycogen, ready to be stored in the liver or the muscle cells to be used at a later date. (
  • The routine that you mention, restricting carbs 7-4 days before the event and then going on a carbohydrate rich diet does, in fact raise levels of stored glycogen. (
  • For that reason, some researchers have suggested that the routine be modified by eliminating the glycogen depleting run and the low carbohydrate diet portion. (
  • SO, then, Chuck's assertion that "restricting carbs 7-4 days before the event and then going on a carbohydrate rich diet does, in fact raise levels of storged glycogen" doesn't really hold. (
  • Concur fully with Chuck Z, my post acknowledged a "normal" high carbohydrate diet and postulated that shifting to a relatively high protein diet (remember my baked potato and the bread with the peanut butter) would be unlikely to significantly impair glycogen stores. (
  • Glycogen is formed in periods of dietary carbohydrate loading and broken down when glucose demand is high or dietary availability is low ( figure 1 ). (
  • Thus it is crucial to have a good glycogen stores as well as to have the proper carbohydrate intake during exercises lasting more than 2 hours. (
  • Therefore, for exercise lasting longer than 1:45-2 hours, proper carbohydrate and glycogen content are crucial. (
  • Utilization of carbohydrate in the form of intramuscular glycogen stores and glucose delivered from plasma becomes an increasingly important energy substrate to the working muscle with increasing exercise intensity. (
  • Erythrocyte glycogen from normal patients and from those with glycogenosis has been isolated and characterized by beta-amylase degradation and the iodine spectrum. (
  • This protein is involved in the pathway glycogen degradation, which is part of Glycan degradation. (
  • View all proteins of this organism that are known to be involved in the pathway glycogen degradation and in Glycan degradation . (
  • Much research has been done on glycogen degradation through studying the structure and function of glycogen phosphorylase, the key regulatory enzyme of glycogen degradation. (
  • Glc4 is a degradation product of glycogen and (other) branched chain starches, such as amylopectin, formed by the glycolytic activity of salivary and pancreatic α-amylases and neutral α-1,4-glucosidase activities. (
  • Glycogen phosphorylase is one of the phosphorylase enzymes ( EC ). (
  • A glycogen storage disease (GSD) results from the absence of enzymes that ultimately convert glycogen compounds to glucose. (
  • Normally, enzymes help convert glucose into glycogen for storage. (
  • Other enzymes convert the glycogen back to glucose when energy is needed. (
  • Children with GSD lack one of the enzymes responsible for making glycogen or converting glycogen to glucose. (
  • This structural property, among others, is shared with related enzymes, such as glycogen phosphorylase and other glycosyltransferases of the GT-B superfamily. (
  • The glycogen branching enzymes were classified into GH13 and GH57 families. (
  • Glycogen phosphorylase is different from other enzymes that require the cofactor PLP because instead of utilizing the pyrimidine ring, phosphorylase uses the phosphate group [6] . (
  • These enzymes are responsible for creating glycogen from glucose, transporting the glycogen to and from storage areas within cells, and extracting glucose from the glycogen as needed. (
  • Glycogen is a multibranched polysaccharide of glucose that serves as a form of energy storage in animals, fungi, and bacteria. (
  • Thermo Scientific Glycogen is a highly purified polysaccharide derived from oysters. (
  • The second domain has the polysaccharide binding domain where phosphorylase is able to attach to the glycogen substrate [5] . (
  • Glycogen is a multibranched polysaccharide o glucose that serves as a form o energy storage in ainimals [2] an fungi . (
  • The importance of muscle glycogen as a metabolic substrate in sustaining prolonged exercise is well acknowledged. (
  • Das AM, Lücke T, Meyer U, Hartmann H, Illsinger S. Glycogen storage disease type 1: impact of medium-chain triglycerides on metabolic control and growth. (
  • Schwahn B, Rauch F, Wendel U, Schönau E. Low bone mass in glycogen storage disease type 1 is associated with reduced muscle force and poor metabolic control. (
  • As the largest organ in the body, the liver performs a number of purifying and metabolic functions within the body, one of which is to store glucose in its glycogen form. (
  • In this study, we utilized pure nuclei preparations and stable isotope tracers to define the origin and metabolic fate of nuclear glycogen. (
  • These emerging principles about the roles of astrocyte glycogen contradict the long held belief that this metabolic pool has little or no functional significance. (
  • Small amounts of glycogen are also found in other tissues and cells, including the kidneys, red blood cells, white blood cells, and glial cells in the brain. (
  • I am analyzing for glycogen in different tissues from fish using the traditional enzymatic method. (
  • E. G. Krebs and E. H. Fischer, Molecular properties and transformations of glycogen phosphorylase in animal tissues. (
  • This results in a buildup of abnormal amounts or types of glycogen in tissues. (
  • The abnormal glycogen builds up in the liver and/or muscle tissues. (
  • The main role of glycogen in the liver is to store glucose for release to tissues that are unable to synthesize significant amounts during fasting. (
  • These deficiencies commonly result in excess of glycogen which deposits in several tissues in the body. (
  • The fact that the function of two key targets of insulin action, glycogen synthase and insulin receptor substrate-1 (IRS-1), are suppressed by GSK-3β ( 4 - 6 ) and the fact that GSK-3β activity is higher in diabetic tissues ( 7 ) make it a promising drug discovery target for insulin resistance and type 2 diabetes. (
  • muscle glycogen phosphorylase is present to degrade glycogen to forms of energy by means of glycolysis during muscle contractions and liver glycogen is present to regulate the blood glucose levels within the blood [2] [3] . (
  • The PYGL gene provides instructions for making an enzyme called liver glycogen phosphorylase. (
  • These genes provide instructions for making different versions of an enzyme called glycogen synthase. (
  • This process is completed through the use of an enzyme called the glycogen phosphorylase. (
  • There is another enzyme called the "debranching enzyme" which can completely degrade these parts of glycogen molecules. (
  • GSD V is caused by a flaw in the gene that makes an enzyme called glycogen phosphorylase. (
  • In this machinery,an enzyme called glycogen synthasecatalyses the formation of glycogen. (
  • Glycogen, as you remember, is stored glucose and is the body's first-line energy stockpile of fuel for harder physical efforts and keeping specific systems (brain, red blood cells, kidney cells) running efficiently all day. (
  • Glycogen is your body's preferred energy source for exercise, as it's more readily available, writes Dr. John Berardi in 'The Essentials of Sport and Exercise Nutrition. (
  • Glycogen serves as the primary fuel reserve for the body's energy needs. (
  • For the next 8-12 hours, glucose derived from liver glycogen is the primary source of blood glucose used by the rest of the body for fuel. (
  • The process by which liver glycogen is converted into blood glucose is related to the actions of the pancreas, which monitors blood glucose levels. (
  • Later, as the blood glucose levels begin to dip, the body makes a withdrawal from its glycogen savings. (
  • Its work will immediately come to a halt four residues away from α1-6 branch (which are exceedingly common in glycogen). (
  • A. Koide, K. Titani, L. H. Ericson, S. Kumar, H. Neurath and K. A. Walsh, Sequence of the aminoterminal 349 residues of rabbit muscle glycogen phosphorylase including sites of covalent and allosteric control. (
  • M. M. Hoerl, K. Feldmann, K. D. Schnackers and E. J. M. Helmreich, Ionization of pyridoxal-5-P and the interactions of AMPS and thiophosphoseryl residues in native and succinilated ~bbit muscle glycogen phosphorylase b and a inferred from P NMR spectra. (
  • Similar to the glycogen synthase, the phosphorylase cannot remove glucose 4 residues from the end of one chain or branch. (
  • Glycogen is a very large, branched polymer of glucose residues. (
  • Therefore, the liver has a higher amount of glycogen per unit mass of tissue. (
  • However, the total mass of the muscle in the body is greater than that of the liver, and so the total amount of glycogen will exceed that of the total amount of glycogen in the liver. (
  • The structure and function of glycogen phosphorylase is complex, though the function of the enzyme is due to the structure. (
  • Our work establishes neuroprotective role of glycogen synthase in Huntington's disease models and thus discovers a previously unknown function of glycogen synthase in neuronal physiology", he added. (
  • R. J. Fletterick, J. Sygusch, M. Semple and N. B. Madsen,Structure of glycogen phosphorylase a at 3.0 A° resolution and its ligand binding sites at 6 A°. J. Biol. (
  • S. Sprang and R. J. Fletterick, The structure of glycogen phosphorylase a at 2.5 A°resolution. (
  • The crystal structure of glycogen synthase from Agrobacterium tumefaciens , however, has been determined at 2.3 A resolution. (
  • Glycogen phosphorylase is also studied as a model protein regulated by both reversible phosphorylation and allosteric effects. (
  • The glycogen phosphorylase monomer is a large protein, composed of 842 amino acids with a mass of 97.434 kDa in muscle cells. (
  • Due to the way glycogen is synthesised, every glycogen granule has at its core a glycogenin protein. (
  • This lack of easy access of the catalytic site to the surface is significant in that it makes the protein activity highly susceptible to regulation, as small allosteric effects could greatly increase the relative access of glycogen to the site. (
  • Glycogen Synthase Kinase 3 (GSK-‑3) is a serine/threonine protein kinase and one of several protein kinases, which phosphorylate glycogen synthase. (
  • We report here use of human myoblasts in culture to study the relationships between cellular glycogen concentrations and the activities of glycogen synthase (GS) and AMP-activated protein kinase (AMPK). (
  • however, some level of regulation may control glycogen-targeted protein phosphatases ( 10 ). (
  • Glycogen measured in tissue lysates showing quantity (�g) per mg of extracted protein. (
  • Glycogen synthase can be classified in two general protein families. (
  • However, since glycogen synthase can only add glucose molecules, there is a protein by the name of glycogenin which acts like a primer and initially starts the reaction to form glycogen. (
  • Proteoglycans = polymer combination of glycogen and protein. (
  • Schematic twa-dimensional cross-sectional view o glycogen: A core protein o glycogenin is surroondit bi branches o glucose units. (
  • Physiologically, insulin signals through a pathway involving protein kinases including, but not limited to, phosphatidylinositol 3-kinase, AKT or protein kinase B (PKB), and glycogen synthase kinase (GSK)-3β (the phosphatidylinositol 3-kinase/Akt/GSK-3β pathway) ( 1 ). (
  • Carbo loading" may increase glycogen stores, which translates to greater glycogen utilization during the run. (
  • The primary aim here was to test the hypothesis that fasted state endurance training would yield greater improvements in fuel utilization and boost muscle glycogen storage efficiency. (
  • After the study, the researchers summed up the improvements in a few relevant variables related to performance, muscle glycogen and fuel utilization. (
  • How Long Does It Take to Deplete Glycogen Stores? (
  • It takes about 90 minutes of low-intensity exercise to deplete glycogen stores, according to Iowa State University. (
  • Iowa State University points out that the amount of time it takes to deplete glycogen stores depends on the intensity of the exercising. (
  • I want to give you 3 instant exercise changes that allow you to have better workouts and deplete more muscle glycogen. (
  • When you deplete glycogen during resistance training, you build up the lactic acid levels in your blood. (
  • If we can crank out a few more reps in each set, then we can deplete more muscle glycogen. (
  • Each subsequent pushup is an easier version and allows you to do more reps, and deplete more glycogen. (
  • Rock Climbing Forums: Climbing Information: Technique & Training: Glycogen Stores: To Deplete or Not? (
  • Glycogen Stores: To Deplete or Not? (
  • I have read that you should not deplete your glycogen stores completely in a climbing session. (
  • If you deplete your glycogen stores during your climbing session, it doesn't have to mean that you have to practice bad technique in the process. (
  • If an increase in power endurance is a priority, is it a good idea to deplete muscle glycogen stores as much as possible during an indoor climbing session? (
  • If you deplete the Glycogen your body canabalises proteins (muscle) for the energy. (
  • Interestingly, the loss of glycogen synthase does not affect lifespan, indicating that glycogen storage is not required to protect against excess glucose intake. (
  • In a recent study of transgenic mice, an overexpression of glycogen synthase [8] and an overexpression of phosphatase [9] both resulted in excess glycogen storage levels. (
  • As a result, the liver is clogged with excess glycogen and becomes enlarged and fatty. (
  • This stored form of glucose is made up of many connected glucose molecules and is called glycogen. (
  • Glycogen is the storage form of glucose in our bodies. (
  • Glycogen is the stored form of glucose and serves as a buffer for glucose needs. (
  • Glycogen is a stored form of glucose. (
  • The role of glycogen synthase kinase 3 beta in the transformation of epidermal cells. (
  • Correction of glycogen storage disease type 1a in a mouse model by gene therapy. (
  • Glycogen storage disease type 1A ( GSD type 1a ) is a very rare disorder also known as von Gierke's disease . (
  • Vitamin E supplementation improves neutropenia and reduces the frequency of infections in patients with glycogen storage disease type 1b. (
  • The erythrocyte glycogen concentration has been determined in 63 normal persons and 18 patients with glycogen storage disease. (
  • Liver transplantation has also become an effective therapy for some patients with glycogen storage disease. (
  • The action of glycogen phosphorylase provides fuel for muscle contraction. (
  • PYGL gene mutations prevent liver glycogen phosphorylase from breaking down glycogen effectively. (
  • Mutations in the liver glycogen phosphorylase gene (PYGL) underlying glycogenosis type VI. (
  • Mutations in the GYS1 or GYS2 gene lead to a lack of functional glycogen synthase, which prevents the production of glycogen from glucose. (
  • The putative glucose 6-phosphate translocase gene is mutated in essentially all cases of glycogen storage disease type I non-a. (
  • Hou DC, Kure S, Suzuki Y. Glycogen storage disease type Ib: structural and mutational analysis of the microsomal glucose-6-phosphate transporter gene. (
  • The paper identifies a mutation in the gene encoding the glycogen debranching enzyme (AGL), which had previously been undetected in a decade of investigation by the same authors. (
  • Glycogen is the analogue of starch, a glucose polymer that functions as energy storage in plants. (
  • Glucose is converted into its storage form, glycogen, which is a long string of single sugars stored as a starch, a complex sugar. (
  • why is it advantageous for starch n glycogen to be large but not soluble? (
  • Glycogen is the analogue of starch, a less branched glucose polymer in plants, and is commonly referred to as animal starch, having a similar structure to amylopectin. (
  • AMP allosteric site (yellow), phosphorylated Ser14 (orange), glycogen binding site (blue), catalytic site (red). (
  • The glycogen phosphorylase dimer has many regions of biological significance, including catalytic sites, glycogen binding sites, allosteric sites, and a reversibly phosphorylated serine residue. (
  • The allosteric site of AMP binding on muscle isoforms of glycogen phosphorylase are close to the subunit interface just like Ser14. (
  • Enzyme activity is sensitive to allosteric regulation by a number of metabolites ( 2 ), is subject to reversible phosphorylation, which inactivates the enzyme, ( 3 ) and is regulated by feedback inhibition by glycogen ( 4 - 6 ) via an unknown mechanism. (
  • Glucose-6-phosphate allosteric activating action allows glycogen synthase to operate as a glucose-6-phosphate sensor. (
  • The binding sites in glycogen phosphorylase include: a catalytic, inhibiting, AMP, glycogen and new allosteric site [1] . (
  • The glycogen binding site is located more than 30Å from the catalytic and allosteric sites. (
  • When the body needs a quick boost of energy or when the body isn't getting glucose from food, glycogen is broken down to release glucose into the bloodstream to be used as fuel for the cells. (
  • In muscle, glycogen provides energy formuscle contraction.the need to store or releaseglucose is primarily signaledby the hormones insulin and glucagon. (
  • This led the authors to conclude that energy sources in addition to muscle glycogen support heavy resistance training. (
  • Glycogen functions as one of two forms of energy reserves, glycogen being for short-term and the other form being triglyceride stores in adipose tissue (i.e., body fat) for long-term storage. (
  • Glycogen forms an energy reserve that can be quickly mobilized to meet a sudden need for glucose, but one that is less compact than the energy reserves of triglycerides (lipids). (
  • When it is needed for energy, glycogen is broken down and converted again to glucose. (
  • As a result, these cells do not have glycogen as a source of stored energy to draw upon following physical activity or fasting. (
  • Under these conditions, IMTG may offer a similar availability of energy as glycogen in the endurance-trained athlete. (
  • Glycogen is a major source of energy for muscle contraction. (
  • The liver both releases glycogen when it is needed for energy production, as well as regulates the amount of glucose present in the blood, critical to health (known as the blood sugar level). (
  • This means that glycogen is a better source of energy when training for athletic performance. (
  • At low intensities your body will turn to fat for energy, but as you start to train harder, it will switch to burning more glycogen, notes Dr. Edward Coyle of the Gatorade Sports Science Institute. (
  • When training for athletic performance, however, you should ideally be looking to use glycogen as your main energy source. (
  • Its presence was first described in the nucleus in the 1890s, but no functional role had been described for nuclear glycogen, unlike glycogen stored by the liver or muscle tissue, which is used as a form of energy in various parts of the body. (
  • Then, the body draws energy from the glycogen stored in the liver, called blood sugar. (
  • Likewise, during periods of intense neural activity when energy demand exceeds glucose supply, astrocyte glycogen is degraded to lactate, a portion of which is transferred to axons for fuel. (
  • Brain glycogen localized in astrocytes, a critical energy source for neurons, decreases during prolonged exhaustive exercise with hypoglycaemia. (
  • There are at least 13 glycogen storage disease (GSD) subtypes, in which the energy stored as glycogen cannot be adequately produced or broken down. (
  • Glycogen serves as the primary source of energy for high-intensity muscle activity by providing substrates for the generation of adenosine triphosphate (ATP). (
  • The role of muscle glycogen is as a reserve to provide energy during bursts of activity. (
  • However, glycogen is different because it is a storage form of energy. (
  • Glycogen is the major carbon and energy reserve polymer in microorganisms and animals. (
  • One form of stored energy is fat and glycogen is another. (
  • While glycogen-depleted runs may allow you to rely more on fat for energy, this does not equate to better performance. (
  • This will increase stored glycogen and teach your body to better utilize stored energy, including fat, but because your glycogen stores should be fairly well replenished after a night of sleep, you are not truly glycogen depleted. (
  • Glucose molecules are added to the chains of glycogen as long as both insulin and glucose remain plentiful. (
  • Both versions of glycogen synthase have the same function, to form glycogen molecules by linking together molecules of the simple sugar glucose, although they perform this function in different regions of the body. (
  • Glycogen is a highly branched polymer of glucose molecules, connected with an alpha-1,4 linkage, branching via an alpha-1,6 linkage. (
  • Glycogen is a chain of glucose molecules. (
  • Furthermore, glycogen is made up of many of these chains of glucose, where some glycogen molecules can contain up to some sources say 120,000 units of glucose while some sources say a range of 1,700 to 600,000. (
  • Typically, up to about 10% of the mass of the liver can be composed of glycogen molecules. (
  • Being stored in proximity to the site of contraction and able to sustain high rates of adenosine diphosphate (ADP) phosphorylation, glycogen is viewed as the primary fuel for the maintenance of exercise of a moderate to intense nature. (
  • can be accessed once the Ser-14 residue has been phosphorylated and conformational changes in glycogen phosphorylation have been observed [5] [6] . (
  • Two proline-directed kinases, glycogen synthase kinase-3 (GSK-3) and cyclin-dependent kinase-5 are thought to be key factors in abnormal tau phosphorylation (reviewed in refs. (
  • They also follow a high carb diet to maximize muscle glycogen storage. (
  • Here, we examined the effect of varying hepatic glycogen content on the counterregulatory response to low blood sugar in dogs. (
  • Isometric exercise has been shown to be impaired by reducing glycogen content while no change has been seen in isokinetic exercise. (