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 ...
Muscle glycogen availability can limit endurance exercise performance. We previously demonstrated 5 days of creatine (Cr) and carbohydrate (CHO) ingestion augmented post-exercise muscle glycogen storage compared to CHO feeding alone in healthy volunteers. Here, we aimed to characterise the time-cour …
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 …
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
TY - JOUR. T1 - Amino acid sequence at the site on rabbit skeletal muscle glycogen synthase phosphorylated by the endogenous glycogen synthase kinase-2 activity. AU - Rylatt, Dennis B.. AU - Cohen, Philip. PY - 1979/2/1. Y1 - 1979/2/1. UR - U2 - 10.1016/0014-5793(79)80154-4. DO - 10.1016/0014-5793(79)80154-4. M3 - Article. C2 - 107044. AN - SCOPUS:0018438921. VL - 98. SP - 71. EP - 75. JO - FEBS Letters. JF - FEBS Letters. SN - 0014-5793. IS - 1. ER - ...
Hormonal control of hepatic glycogen and blood glucose levels is one of the major homeostatic mechanisms in mammals: glycogen is synthesized when portal glucose concentration is sufficiently elevated and degraded when glucose levels are low. We have studied initial events of hepatic glycogen synthesis by injecting the synthetic glucocorticoid dexamethasone (DEX) into adrenalectomized rats fasted overnight. Hepatic glycogen levels are very low in adrenalectomized rats, and DEX causes rapid deposition of the complex carbohydrate. Investigation of the process of glycogen deposition was performed by light and electron microscopic (EM) radioautography using [3H]galactose as a glycogen precursor. Rats injected with DEX for 2-3 h and [3H]galactose one hour before being killed displayed an increasing number of intensely labeled hepatocytes. EM radioautography revealed silver grains over small (+/- 1 micron) ovoid or round areas of the cytosome that were rich in smooth endoplasmic reticulum (SER) and ...
TY - JOUR. T1 - Glycogen metabolism in a Saccharomyces cerevisiae phosphoglucose isomerase (pgi1) disruption mutant. AU - Corominas, Josep. AU - Clotet, Josep. AU - Fernández-Bañares, Isabel. AU - Boles, Eckhard. AU - Zimmmermann, Friedrich K.. AU - Guinovart, Joan J.. AU - Ariño, Joaquín. PY - 1992/9/28. Y1 - 1992/9/28. N2 - Disruption of the gene pgi1 of Saccharomyces cerevisiae, which codes for phosphoglucose isomerase, results in a dramatic increase in the amount of intracellular glycogen in early exponential cultures. The level or glucose 6-phosphate was much higher in mutant than in wild-type cells. Phosphorylase a activity and the state of activation of glycogen synthase were also investigated. Phosphorylase a activity was rather low along the culture in wild-type cells, whereas it was consistently higher in mutants. Glycogen synthase was mostly in the active form in early-medium exponential cultures in wild-type cells whereas the activation state of this enzyme in mutant cells, ...
We examined the insulin dose-response characteristics of human muscle glycogen synthase and phosphorylase activation. We also determined whether increasing the rate of glucose disposal by hyperglycemia at a fixed insulin concentration activates glycogen synthase. Physiological increments in plasma insulin but not glucose increased the fractional activity of glycogen synthase. The ED50: s for insulin stimulation of whole body and forearm glucose disposal were similar and unaffected by glycemia. Glycogen synthase activation was exponentially related to the insulin-mediated component of whole body and forearm glucose disposal at each glucose concentration. Neither insulin nor glucose changed glycogen phosphorylase activity. These results suggest that insulin but not the rate of glucose disposal per se regulates glycogen synthesis by a mechanism that involves dephosphorylation of glycogen synthase but not phosphorylase. This implies that the low glycogen synthase activities found in ...
Author(s): Roa, Jinae N; Tresguerres, Martin | Abstract: Na+/K+-ATPase (NKA)- and vacuolar H+-ATPase (VHA)-rich cells in shark gills secrete excess acid and base, respectively, to seawater to maintain blood acid-base homeostasis. Both cell types are rich in mitochondria, indicating high ATP demand; however, their metabolic fuel is unknown. Here, we report that NKA- and VHA-rich cells have large glycogen stores. Glycogen abundance in NKA-rich cells was lower in starved sharks compared with 24 h post-fed sharks, reflecting higher energy demand for acid secretion during normal activity and glycogen replenishment during the post-feeding period. Conversely, glycogen abundance in VHA-rich cells was high in starved sharks and it became depleted post-feeding. Furthermore, inactive cells with cytoplasmic VHA had large glycogen stores and active cells with basolateral VHA had depleted glycogen stores. These results indicate that glycogen is a main energy source in both NKA- and VHA-rich cells, and point to
Supercompensated brain glycogen levels may contribute to the development of hypoglycemia-associated autonomic failure (HAAF) following recurrent hypoglycemia (RH) by providing energy for the brain during subsequent periods of hypoglycemia. To assess the role of glycogen supercompensation in the generation of HAAF, we estimated the level of brain glycogen following RH and acute hypoglycemia (AH). After undergoing 3 hyperinsulinemic, euglycemic and 3 hyperinsulinemic, hypoglycemic clamps (RH) on separate occasions at least 1 month apart, five healthy volunteers received [1-C]glucose intravenously over 80+ h while maintaining euglycemia. C-glycogen levels in the occipital lobe were measured by C magnetic resonance spectroscopy at ∼8, 20, 32, 44, 56, 68 and 80 h at 4 T and glycogen levels estimated by fitting the data with a biophysical model that takes into account the tiered glycogen structure. Similarly, prior C-glycogen data obtained following a single hypoglycemic episode (AH) were fitted ...
Sarcoplasmic vesicles and ß-glycogen particles 30-40 mµ in diameter were isolated from perfused rabbit skeletal muscle by the differential precipitation-centrifugation method. This microsomal fraction was subjected to zonal centrifugation on buffered sucrose gradients, in a B XIV Anderson type rotor, for 15 hr at 45,000 rpm in order to separate the two cytoplasmic organelles. Zonal profiles of absorbance at 280 mµ, proteins, glycogen, and enzymatic activities (phosphorylase b kinase, phosphorylase b, and glycogen synthetase) were performed. Whereas the entire synthetase activity was found combined with the glycogen particles, 39% of phosphorylase and 53% of phosphorylase b kinase activities, present in the microsomal fraction, were recovered in the purified vesicular fraction (d = 1.175). This latter fraction consists of vesicles, derived from the sarcoplasmic reticulum, and of small particles 10-20 mµ in diameter attached to the outer surface of the membranes. These particles disappear ...
TY - JOUR. T1 - Complete reversal of glycogen hepatopathy with pancreas transplantation. T2 - Two cases. AU - Fridell, Jonathan A.. AU - Saxena, Romil. AU - Chalasani, Naga. AU - Goggins, William C.. AU - Powelson, John A.. AU - Cummings, Oscar. PY - 2007/1. Y1 - 2007/1. N2 - Glycogen hepatopathy is the pathological overloading of hepatocytes with glycogen that is associated with poorly controlled diabetes mellitus. Clinically, it presents with abdominal discomfort, tender hepatomegaly and elevated transaminases. In this report, we describe our experience with two cases of type I diabetes mellitus and glycogen hepatopathy. The patients underwent isolated pancreas transplantation, following which, we have been able to demonstrate complete histological resolution of glycogen hepatopathy associated with control of glucose metabolism.. AB - Glycogen hepatopathy is the pathological overloading of hepatocytes with glycogen that is associated with poorly controlled diabetes mellitus. Clinically, it ...
TY - JOUR. T1 - Studies on the mechanism by which exogenous glucose is converted into liver glycogen in the rat. A direct or an indirect pathway?. AU - Newgard, C. B.. AU - Hirsch, L. J.. AU - Foster, D. W.. AU - McGarry, J. D.. PY - 1983/1/1. Y1 - 1983/1/1. N2 - To quantify the extent to which exogenous glucose is used directly or indirectly for hepatic glycogen synthesis, fasted rats were given [U-14C,3-3H]glucose intragastrically, intravenously, or as a component of a solid diet eaten ad libitum. In all cases liver glycogen was deposited at high linear rates over a 3-h period. Portal vein glucose levels seldom exceeded 8 mM. At a time when the specific activities of 3H and 14C in circulating glucose were identical with those in the administered material their values in newly synthesized glycogen were reduced by 72-88% and 50-65%, respectively. An intragastric load of unlabeled glucose sufficient to suppress completely hepatic glucose output greatly stimulated the incorporation of ...
1. During conversion of [6-3H,U-14C]glucose to glycogen in liver, loss of 6-3H can occur either by cycling via pyruvate (between glycolysis and gluconeogenesis) or by other mechanisms. We used mercaptopicolinate, an inhibitor of phosphoenolpyruvate carboxykinase, to determine the extent to which pyruvate cycling contributes to loss of 6-3H during glucose conversion to glycogen in hepatocytes. 2. Mercaptopicolinate increased the 3H/14C ratio in glycogen during incubation of rat, guinea pig, pig and human hepatocytes with [6-3H,U-14C]glucose. The increase in the 3H/14C ratio in glycogen caused by mercaptopicolinate was greater in periportal than in perivenous rat hepatocytes, indicating that cycling of glucose via pyruvate is more prominent in cells with a higher gluconeogenic relative to glycolytic capacity. 3. The effect of mercaptopicolinate on the 3H/14C ratio in glycogen was observed both in the absence and in the presence of insulin, indicating that stimulation of glycogen synthesis by ...
These are individual glycogen concentrations pre, immediately post, and two hours post 180 min of running at 64% VO2 Max. I would have paid a lot of money for them to keep these guys in the lab, feed them their normal diet, and keep taking daily biopsies to see when each group got back to baseline glycogen concentrations and how this was related to performances on subsequent wingate tests.. Unfortunately, for all of us barbell junkies these guys ran for three hours at a luke warm pace and only got knifed in the leg three times.. Yet, this is the first study to show that fat-adapted athletes had such high resting glycogen concentrations that were not significantly different than high carb athletes and that glycogen replenishment was also not significantly different between groups.. Remember, the results were all over the board in both groups, the study had a small n, and there was no real dietary control. Athletes were also traveling to the lab from all over country the days before testing. ...
Looking for online definition of glycogen infiltration in the Medical Dictionary? glycogen infiltration explanation free. What is glycogen infiltration? Meaning of glycogen infiltration medical term. What does glycogen infiltration mean?
The effect of estradiol and/or clomiphene on blood glucose, uterine and liver glycogen was studied in the rat during delayed implantation. Estrogen induced a sharp increase in uterine glycogen at 6 hours while clomiphene caused a significant increase at 24 hours. Pretreatment with clomiphene inhibited estrogen induced glycogenesis. Estrogen administration resulted in a three fold increase in liver glycogen at 6 hours while clomiphene induced a two fold increase at 24 hours. Pretreatment with clomiphene completely blocked subsequent estrogen action on the liver. The mechanism of estradiol-induced uterine and hepatic glycogenesis as well as the mode of estrogen-clomiphene interaction are discussed. ...
The exact function(s) of the GBD remains unclear, although there are several experimental findings linking AMPK with glycogen; however, these observations are currently difficult to synthesize into a single, all-encompassing hypothesis. The GBD does cause a partial localization of AMPK to glycogen particles, where one of its known downstream targets - glycogen synthase - resides (Hudson et al., 2003). There is also indirect evidence that glycogen regulates AMPK activity: in both rat (Wojtaszewski et al., 2002) and human (Wojtaszewski et al., 2003) skeletal muscle, a high content of glycogen represses activation of AMPK. This makes physiological sense because if muscle glycogen content is high it tends to be used preferentially as fuel and, although AMPK activation stimulates the usage by muscle of alternative fuels such as blood glucose and fatty acids, it is not required for glycogen breakdown or glycolysis. As yet, repression of AMPK activation by glycogen has not been reproduced in a ...
Loss-of-function gac1 mutants of Saccharomyces cerevisiae fail to accumulate normal levels of glycogen because of low glycogen synthase activity. Increased dosage of GAC1 results in increased activity of glycogen synthase and a corresponding hyperaccumulation of glycogen. The glycogen accumulation phenotype of gac1 is similar to that of glc7-1, a type 1 protein phosphatase mutant. We have partially characterized the GAC1 gene product (Gac1p) and show that levels of Gac1p increase during growth with the same kinetics as glycogen accumulation. Gac1p is phosphorylated in vivo and is hyperphosphorylated in a glc7-1 mutant. Gac1p and the type 1 protein phosphatase directly interact in vitro, as assayed by coimmunoprecipitation, and in vivo, as determined by the dihybrid assay described elsewhere (S. Fields and O.-k. Song, Nature [London] 340:245-246, 1989). The interaction between Gac1p and the glc7-1-encoded form of the type 1 protein phosphatase is defective, as assayed by either ...
Lowry Drug Anti Fatigue Caps 90 Capsules [H160252] - Reduce ammonia & reduce fatigue Scavenge excess ammonia to reduce fatigue. Prolong endurance, even in ultra workouts or races. Increase glycogen availability for energy production. Help prevent cramps. Gluten-Free and Vegan Friendly. Extra Benefits:Although Anti-Fatigue Caps is designed primarily for ammonia reduction in long distance events, the nutrients in the formula are excellent for helping counteract everyday fatigue, even chronic fatigue symptoms. Thoroughly tested over several years in the most extreme athletic endurance events, Anti-Fatigue Caps helps remove fatigue-causing, performance-robbing ammonia. During extended endurance exercise the body accumulates excess ammonia from protein metabolism, which interferes with glycogen production, disrupting energy output. Anti-Fatigue Caps is a one-of-a-kind supplement combining two well-known ammonia-scavenging nutrients. Clean up the waste products of combustion, or youll pay the price. To stay
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View Notes - 9-glycogen from STEP 1 at Montgomery College. Biochemistry of Metabolism Glycogen Metabolism Copyright 1999-2007 by Joyce J. Diwan. All rights reserved. CH2OH H OH H CH2OH H OH H OH O H
Gerty Theresa Cori (1896-1957) was awarded a quarter of the 1947 Nobel Prize in Physiology or Medicine for her discovery of how glycogen is broken down and resynthesized in the body to be either used or stored as a source of energy. Her initial research was physiological in nature, and focused on the role of epinephrine in glycogen metabolism. This led to research of a more biochemical nature, including investigations on glycogen breakdown in minced frog muscle. In 1936, she isolated glucose-1-phosphate - also called the Cori ester -- and established that it was a breakdown product of glycogen. Cori also characterized glycogen phosphorylase, the enzyme responsible for breakdown of glycogen to glucose 1-phosphate. In the 1940s, Cori began to purify and crystallize some of the enzymes that she and her husband, Carl, had earlier described, such as glycogen phosphorylase. Cori also elucidated the molecular defects underlying a number of genetically determined glycogen storage diseases.. ...
Taken together, these results further confirmed that (-)-HCA could reduce body weight gain through promoting energy expenditure via its effect on increasing thyroid hormones levels. (-)-Hydroxycitric acid inhibits ATP-citrate lyase and increases the cellular pool of citrate, which in turn inhibits glycolysis and thus redirects the carbon sources for glycogen production within the liver or muscle (Cheng et al., 2012; Shara et al., 2003). No changes were observed on the glucose content, while 1000 mg/kg (-)HCA treatment significantly increased the hepatic glycogen and muscle glycogen contents in rats. Our results is similar to previous study results that show glycogen levels in skeletal muscle are increased after (-)-HCA supplementation in animal models (Ishihara et al., 2000) or in human (Cheng et al., 2012). Our results showed that 2000 mg/kg and 3000 mg/kg (-)-HCA treatment significantly increased insulin content in rats. Insulin can promote the storage of glucose and inhibit lipolysis and ...
Laura:. Check out this research article on marathon race pace. Essentially, we believe that marathoners race best (with exceptions, of course) when their pace is about 15 seconds faster than the first mile of their MAF test. The problem is that if you run any faster than that-that 8:15 pace you want to run in Chicago-your glycogen stores will become depleted too fast and your body wont be able to keep up that speed. Your best bet is to stay close enough to your 1st mile MAF (within 15 seconds) that your glycogen stores dont become depleted. The reason the marathon race pace is always faster than MAF is because you want to be using your muscle glycogen stores enough for them to become completely depleted by the end of the race but not before.. In other words, if your 1st mile MAF pace is say, a 9 min mile pace, it would be very very difficult (not to mention extremely stressful and unhealthy) to be able to keep a 8:15 marathon pace. But most likely, if you do try, youll find that youll hit ...
To evaluate possible mechanisms by which insulin inhibits hepatic apolipoprotein B (apoB) secretion, we incubated primary cultures of rat hepatocytes with sodium ort ho vanadate, a phosphotyrosine phosphatase inhibitor and insulin-mimetic agent. Vanadate (10 μM) and insulin (10 nM) inhibited the medium accumulation of apoB (secretion) by 21 and 37%, respectively, without increasing intracellular apoB. The effects of insulin and vanadate together were not additive. Both insulin and vanadate enhanced intracellular glycogen accumulation by 82 and 37%, respectively. Unlike insulin, vanadate, at a concentration that inhibited apoB secretion (10 μM), had no effect on intracellular lipogenesis, inhibited the secretion of newly synthesized hepatic proteins, and had a delayed onset and termination of action on inhibition of apoB secretion. At higher concentrations (40 and 80 μM), vanadate stimulated intracellular lipogenesis. In conclusion, our data indicate that vanadate mimics insulin action in ...
TY - JOUR. T1 - A conserved domain for glycogen binding in protein phosphatase-1 targeting subunits. AU - Wu, Jun. AU - Liu, Jun. AU - Thompson, Irene. AU - Oliver, Carey J.. AU - Shenolikar, Shirish. AU - Brautigan, David L.. N1 - Funding Information: The authors thank E.Y.C. Lee and John C. Lawrence, Jr. for purified proteins, Charles Richardson and David Metcalf for assistance in obtaining CD spectra, and Christine Palazzolo for assistance in preparation of the manuscript. This research was supported by Grants MCB9507357 from the National Science Foundation (to D.L.B.) and American Diabetes Association (to S.S.). Facilities provided in part by a grant from the Lucille P. Markey Charitable Trust.. PY - 1998/11/13. Y1 - 1998/11/13. N2 - The skeletal muscle glycogen-binding subunit (G(M)) of protein phosphatase-1 (PP1) is the founding member of a family of proteins that tether the PP1 catalytic subunit (PP1C) to glycogen and promote the dephosphorylation of glycogen synthase. A hydrophobic ...
In older endurance athletes, glycogen (carbohydrate) storage per unit of muscle is lower than in similarly trained younger runners while glycogen usage per unit of energy expenditure is higher during endurance exercise. However, following regular endurance training, older individuals are able to increase muscle glycogen storage and restore glycogen stores post-exercise at rates similar to younger athletes.. The recommended carbohydrate intake for athletes (see Table below) is similar to that of the general population and therefore is similar for masters athletes since carbohydrate absorption and utilisation remains intact with aging. Thus, the older athlete should consume at least 55% of daily energy intake as carbohydrate obtained from a variety of food sources and the bulk of the carbohydrate-containing foods consumed should be those rich in complex carbohydrates and with a low glycemic index (see Chapter 16 of The Masters Athlete or ). A high percentage of this ...
Defective acute regulation of hepatic glycogen synthase by glucose and insulin, caused by severe insulin deficiency, can be corrected in adult rat hepatocytes in primary culture by inclusion of insulin, triiodothyronine, and cortisol in a chemically defined serum-free culture medium over a 3-day period (Miller, T. B., Jr., Garnache, A. K., Cruz, J., McPherson, R. K., and Wolleben, C. (1986) J. Biol. Chem. 261, 785-790). Using primary cultures of hepatocytes isolated from normal and diabetic rats in the same serum-free chemically defined medium, the present study addresses the effects of cycloheximide and actinomycin D on the chronic actions of insulin, triiodothyronine, and cortisol to facilitate the direct effects of glucose on the short-term activation of glycogen synthase. The short-term presence (1 h) of the protein synthesis blockers had no effect on acute activation of glycogen synthase by glucose in primary hepatocyte cultures from normal rats. Normal cells maintained in the presence of
After your workout you want to replenish with carbohydrates, not the grain and bread variety, but a shake, smoothie, protein bar, anything that is not too heavy for the stomach. The first 30 minutes after a workout are crucial for replenishing! This is what will prepare you for the next workout later that day or tomorrows. If you wait past that time the muscle glycogen synthesis is deceased, even up to 66%. What this means is that if you wait too long on carbohydrate intake then you will reduce muscle glycogen storage and increase risk of injury. Working out is a balance of effort and fuel. If you are not refueling your body you will not be able to work out later, and you want the energy to burn the body fat. Muscles burn body fat and you need complex carbohydrates to work the muscles for future workouts. Complex carbohydrates are found in grains, fruits, vegetables, beans, and milk. My ideal recovery snack or refuel is a veggie juice or shake, something in a liquid form. Find out what is ...
We examined the effects of whey versus collagen protein on skeletal muscle cell signaling responses associated with mitochondrial biogenesis and protein synthesis in recovery from an acute training session completed with low carbohydrate availability. In a repeated-measures design (after adhering to a 36-hr exercise-dietary intervention to standardize preexercise muscle glycogen), eight males completed a 75-min nonexhaustive cycling protocol and consumed 22 g of a hydrolyzed collagen blend (COLLAGEN) or whey (WHEY) protein 45 min prior to exercise, 22 g during exercise, and 22 g immediately postexercise. Exercise decreased (p , .05) muscle glycogen content by comparable levels from pre- to postexercise in both trials (≈300-150 mmol/kg·dry weight). WHEY protein induced greater increases in plasma branched chain amino acids (p = .03) and leucine (p = .02) than COLLAGEN. Exercise induced (p , .05) similar increases in PGC-1α (fivefold) mRNA at 1.5 hr postexercise between conditions, although no ...
for the analysis of glycogen in the tissue extracts. A biopsy technique was developed to remove between 5 and 10 mg of foot tissue in Amblema plicata plicata. The survival rate did not differ between biopsied and non-biopsied mussels during a 581-d observation period, demonstrating that the biopsy technique Mill allow nonlethal evaluation of the physiological condition of individual mussels through measurement of changes in contaminant, genetic, and biochemical indicators in tissue. We also modified the standard alkaline digestion and phenol-sulfuric acid analysis of glycogen for use on the small samples of biopsied tissue and to reduce analysis time and cost. We present quality control data, including method detection limits and estimates of precision and bias. The modified analytical method is rapid and accurate and has a method detection limit of 0.014 mg glycogen. Glycogen content in the biopsied samples was well above the method detection limit; it ranged from 0.09 to 0.36 mg, indicating ...
FUNCTION: [Summary is not available for the mouse gene. This summary is for the human ortholog.] The protein encoded by this gene, liver glycogen synthase, catalyzes the rate-limiting step in the synthesis of glycogen - the transfer of a glucose molecule from UDP-glucose to a terminal branch of the glycogen molecule. Mutations in this gene cause glycogen storage disease type 0 (GSD-0) - a rare type of early childhood fasting hypoglycemia with decreased liver glycogen content. [provided by RefSeq, Dec 2009 ...
By John C. Hill, and Iñigo San Millán DOI: 10.3810/psm.2014.09.2075 Abstract: Glycogen storage is essential for exercise performance. The ability to assess…
BLOOD SUGAR CONTROL - Honey may promote better blood sugar control. Proper fueling of the liver is central to optimal glucose metabolism during sleep and exercise. Honey is the ideal liver fuel because it contains a nearly 1:1 ratio of fructose to glucose. Fructose unlocks the enzyme from the liver cells nucleus that is necessary for the incorporation of glucose into glycogen (the form in which sugar is stored in the liver and muscle cells). An adequate glycogen store in the liver is essential to supply the brain with fuel when we are sleeping and during prolonged exercise. When glycogen stores are insufficient, the brain triggers the release of stress hormones--adrenalin and cortisol--in order to convert muscle protein into glucose. Repeated metabolic stress from cortisol produced when less than optimal liver glycogen stores are available during sleep, leads over time, to impaired glucose metabolism, insulin resistance, diabetes, and increased risk for cardiovascular disease and obesity. ...
1. HuZL, ParkCA, WuXL, ReecyJM (2013) Animal QTLdb: an improved database tool for livestock animal QTL/association data dissemination in the post-genome era. Nucleic Acids Research 41: D871-D879.. 2. RenJ, MaoH, ZhangZ, XiaoS, DingN, et al. (2011) A 6-bp deletion in the TYRP1 gene causes the brown colouration phenotype in Chinese indigenous pigs. Heredity (Edinb) 106: 862-868.. 3. RubinCJ, ZodyMC, ErikssonJ, MeadowsJR, SherwoodE, et al. (2010) Whole-genome resequencing reveals loci under selection during chicken domestication. Nature 464: 587-591.. 4. RubinCJ, MegensHJ, Martinez BarrioA, MaqboolK, SayyabS, et al. (2012) Strong signatures of selection in the domestic pig genome. Proc Natl Acad Sci U S A 109: 19529-19536.. 5. AnderssonL, GeorgesM (2004) Domestic-animal genomics: deciphering the genetics of complex traits. Nat Rev Genet 5: 202-212.. 6. GeorgesM (2007) Mapping, fine Mapping, and molecular dissection of quantitative trait loci in domestic animals. Annu Rev Genomics Hum Genet 8: ...
Carbohydrate Loading. Carbohydrates are the bodys primary source of energy during high intensity exercise. Upon consumption, carbohydrates are broken down to glucose and metabolized for energy. Unused glucose is stored as glycogen in the liver and muscles. After the body has utilized carbohydrate reserves, glycogen is synthesized back into glucose to be used as the alternative source of energy. It is upon this premise that carbo-loading is practiced to improve and sustain athletic performance.. Carbo-loading is the super-compensation of glycogen stores. It is the expectation of carbo-loading that the excess glucose will be converted to glycogen and stored in the liver and muscles. This over abundance of glycogen stores will become the readily available fuel source. Benefits of Carbo-loading. Because glycogen stores are typically not abundant, energy is often halted upon utilization. Thus, an athlete is said to have hit the wall. Carbo-loading maximizes the bodys ability to store ...
Hi, My question concerns the relationship between muscle glycogen liver glycogen and ketosis. Particularly, I am wondering if there is a way to have f
TY - JOUR. T1 - 1H NMR detection of lactate and alanine in perfused rat hearts during global and low pressure ischemia. AU - Zhao, P.. AU - Storey, C. J.. AU - Babcock, E. E.. AU - Malloy, C. R.. AU - Sherry, A. D.. PY - 1995. Y1 - 1995. N2 - A spin-echo method is presented for obtaining high resolution, 13C coupled, proton spectra of lactate and alanine in intact, beating rat hearts. All hearts were depleted of glycogen prior to prolonged perfusion with either 10 mM unenriched glucose or [1-13C]glucose to restore glycogen. These two groups of hearts were then examined by 1H NMR during prolonged global (zero flow) or low pressure (low flow) ischemia. During global ischemia, lactate was derived from both glucose and glycogen, with endogenous glycogen contributing twice as much lactate as exogenous glucose. During low perfusion pressure ischemia, however, lactate was derived exclusively from exogenous glucose. The entire pool of lactate (both 12C and 13C) was visible by NMR in intact, glucose ...
BioAssay record AID 318590 submitted by ChEMBL: Elevation in glycogen level in fasting BALB/c mouse at 5.70 mg/kg, ip after 3 hrs.
Differentially expressed marker genes and glycogen levels in pectoralis major of Ross308 broilers with wooden breast syndrome indicates stress, inflammation and hypoxic conditions ...
GUERRA, Isabela; SOARES, Eliane de Abreu and BURINI, Roberto Carlos. Nutritional aspects of competitive soccer. Rev Bras Med Esporte [online]. 2001, vol.7, n.6, pp.200-206. ISSN 1517-8692. Soccer playing involves intermittent exercises the physical intensities of which depend upon the player line up in the field, the importance of the game, and competitor excellence. This review aims at describing the major metabolic impacts on these physical efforts and their nutritional implications for performance purposes. Soccer players usually spend approximately 1360 kcal each game, with a 5% decrease in the second half of the game. Glycogen reserves modulate strength and length of movements. Elite players deplete from 20% to 90% of their glycogen level during a match according to their physical conditioning, exercise intensity, environmental temperature, and pre-competition dietary intake. Body dehydration and hyperthermia accelerate glycogen depletion ...
The group directed by Prof. Guinovart is involved in several projects on glycogen metabolism and its dysfunctions in diabetes and Lafora disease. Studies on glycogen metabolism have allowed the identification of many enzymes and intermediate metabolites involved in the synthesis and degradation of this polysaccharide. However, new factors and processes that participate in glycogen regulation are constantly being discovered. Moreover, data on the mechanisms of control in distinct organs and in diverse physiological conditions are incomplete.
TY - JOUR. T1 - The hormonal control of glycogen metabolism. T2 - The amino acid sequence at the phosphorylation site of protein phosphatase inhibitor-1. AU - Cohen, Philip. AU - Rylatt, Dennis B.. AU - Nimmo, Gillian A.. PY - 1977/4/15. Y1 - 1977/4/15. UR - U2 - 10.1016/0014-5793(77)80147-6. DO - 10.1016/0014-5793(77)80147-6. M3 - Article. C2 - 193727. AN - SCOPUS:0017407844. VL - 76. SP - 182. EP - 186. JO - FEBS Letters. JF - FEBS Letters. SN - 0014-5793. IS - 2. ER - ...
The Metabolic Disorders Drugs market continues to grow steadily, immune to recessions and economic setbacks, thanks to changing lifestyles and the increasing number of working individuals in society. With constant and frequent innovations, the Metabolic Disorders Drugs market share is expected to continue on a growth trajectory for the next 5 years. A well-equipped market report can help those involved in the business tide over major hurdles in the business and achieve sustainable growth.. A rise in consumer disposable income along with improved living standards, particularly in developing countries is expected to fuel the Metabolic Disorders Drugs market demand. Developed countries are also expected to witness growth in the Glycogen Metabolism Disease Drug, Lipid Metabolism Disease Drug, Amino Acid Metabolism Drug, Other segments over the foreseeable future. This growth may be primarily attributed to high R&D developments and the introduction of advanced and innovative products.. Keep up with ...
We constantly tell bodybuilders about the muscle-building benefits of protein. It plays a direct role in muscle development by providing the body with amino acids. However, looking at the larger picture, muscle growth is not solely dependent on protein consumption. Carbohydrate consumption also plays an active role. In fact, the amount of carbohydrates stored inside muscles - called muscle glycogen - can determine whether or not muscles remain in an anabolic, or muscle-building, state. How vital are well-stocked glycogen stores? Protein intake above and beyond what reputable nutritionists say is enough wont boost muscle mass if glycogen stores are too low. On the other hand, if glycogen stores are full, chances of faster recovery and improved growth markedly increase.. So, why not simply load up on carbs in hopes of getting huge? Because consuming too many carbs creates the potential of increasing bodyfat. Taking steps to ensure that carbs are stored in muscles rather than as fat is half the ...
If you deplete your glycogen stores during your climbing session, it doesnt have to mean that you have to practice bad technique in the process. Neither does it have to mean that youre putting yourself at high risk for injury. My approach in gym training is to start with routes I can complete easily as a sort of warm-up, work up to more difficult ones until I peak at the most difficult routes I want to try to send until Im clearly depleted, then finally resort back to climbing the easy routes again whose sequences I have well established until Im physically drained. So, Id end with routes involving technique I dont have to put much effort into. I have those engrams so well established that I will still practice good technique on them, and I simultaneously continue to challenge myself to focus on the right things (center of gravity in relation to base of support, driving up with the legs while maintaining optimum posture for the moves, etc ...
During long periods of starvation, after the liver and muscle glycogen stores have been depleted, the body must rely on lipolysis, the breakdown of triglycerides stored in adipose tissue, for energy production. Triglycerides are composed of a 3 carbon glycerol backbone with 3 chains of fatty acids attached, one to each carbon. During lipolysis, hormone…
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Wikimedia Commons has media related to Glycogen. "Glycogen storage disease". McArdle's Diseases. Glycogen at the US National ... 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- ...
... breaks up glycogen into glucose subunits (see also figure below): (α-1,4 glycogen chain)n + Pi ⇌ (α-1,4 ... Glycogen phosphorylase kinase activates glycogen phosphorylase in the same manner mentioned previously. Glycogen phosphorylase ... Evidence that dephosphorylation of glycogen phosphorylase and glycogen synthase in the glycogen and microsomal fractions of rat ... Glycogen phosphorylase can act only on linear chains of glycogen (α1-4 glycosidic linkage). Its work will immediately come to a ...
... but it does not seem to be related to the normal function of glycogen in animals, which is the storage of energy. Glycogen ... A glycogen body is an oval structure in the spinal cord of birds that is made of specialized cells that contain large amounts ... Imagawa, T; Shogaki, K; Uehara, M (October 2006). "Interaction between glycogen body cell and neuron: examination in co-culture ... of glycogen. Housed within the synsacrum, the function of this structure is not known, ...
The control of glycogen synthase is a key step in regulating glycogen metabolism and glucose storage. Glycogen synthase is ... Liver glycogen serves as a storage pool to maintain the blood glucose level during fasting, whereas muscle glycogen synthesis ... This suggests that glycogen synthase plays an important biological role in regulating glycogen/glucose levels and is activated ... However, muscle-specific glycogen synthase activation may lead to excessive accumulation of glycogen, leading to damage in the ...
eMedicine Specialties > Glycogen-Storage Disease Type I Author: Karl S Roth. Updated: Aug 31, 2009 "Glycogen Storage Disease ... GLYCOGEN STORAGE DISEASE IXa1; GSD9A1 OMIM - Online Mendelian Inheritance in Man Definition: glycogen storage disease type VIII ... GSD type 0: Although glycogen synthase deficiency does not result in storage of extra glycogen in the liver, it is often ... is a metabolic disorder caused by an enzyme deficiency affecting glycogen synthesis, glycogen breakdown, or glucose breakdown, ...
When glycogen breakdown is compromised by mutations in the glycogen debranching enzyme, metabolic diseases such as Glycogen ... GeneReviews/NCBI/NIH/UW entry on Glycogen Storage Disease Type III OMIM entries on Glycogen Storage Disease Type III Glycogen+ ... In GSD III glycogen breakdown is incomplete and there is accumulation of abnormal glycogen with short outer branches. Most ... Glycogen debranching enzymes assist phosphorylase, the primary enzyme involved in glycogen breakdown, in the mobilization of ...
... the extended glycogen polymer is branched by glycogen branching enzyme to provide glycogen breakdown enzymes, such as glycogen ... Glycogen branching enzyme is an enzyme that adds branches to the growing glycogen molecule during the synthesis of glycogen, a ... Importantly, glycogen synthase can only catalyze the synthesis of α-1,4-glycosidic linkages. Since glycogen is a readily ... highly branched glycogen molecule. Mutations in this gene are associated with glycogen storage disease type IV (also known as ...
... glycogen synthetase phosphatase, glycogen synthase phosphatase, glycogen synthase D phosphatase, Mg2+ dependent glycogen ... UDP-glycogen glucosyltransferase phosphatase, UDPglucose-glycogen glucosyltransferase phosphatase, glycogen glucosyltransferase ... The enzyme [glycogen-synthase-D] phosphatase ({EC catalyzes the reaction [glycogen-synthase D] + H2O ⇌ {\displaystyle ... The systematic name is [UDP-glucose:glycogen 4-α-D-glucosyltransferase-D] phosphohydrolase. Other names in common use include ...
The human form of the disease is known as glycogen storage disease type IV. Glycogen is a molecular polymer of glucose used to ... Glycogen-branching enzyme deficiency (GBED) is an inheritable glycogen storage disease affecting American Quarter Horses and ... This bond may be broken by amylase when the body wishes to break down glycogen into glucose for energy. Glycogen branching ... This causes low levels of muscle glycogen that is very resistant to amylase. Lacking proper glycogen storage, the horse's brain ...
... (abbreviation: GPBB) is an isoenzyme of glycogen phosphorylase. This isoform of the enzyme ... 2005). "Glycogen phosphorylase BB in acute coronary syndromes". Clin. Chem. Lab. Med. 43 (12): 1351-8. doi:10.1515/CCLM. ... Other enzymes related to glycogen phosphorylase are abbreviated as GPLL (liver) and GPMM (muscle). Apple FS, Wu AH, Mair J, et ...
GeneReview/NIH/UW entry on Glycogen Storage Disease Type I Media related to Glycogen storage disease type I at Wikimedia ... Glycogen Storage Disease Ic - 232240 PARKER, PAUL (1981). "Regression of hepatic adenomas in type Ia glycogen storage disease ... and to add the G6P molecules to the ends of chains of glycogen (glycogen synthesis). Excess G6P is also shunted into production ... leading to an accumulation of stored glycogen in the liver. Hepatomegaly from the accumulation of stored glycogen in the liver ...
"glycogen storage disease type III". Genetics Home Reference. Retrieved 2016-08-07. "Glycogen storage disease type 3 , Genetic ... Without glycogen debranching enzymes to further convert these branched glycogen polymers to glucose, limit dextrinosis ... Scholia has a topic profile for Glycogen storage disease type III. Media related to Glycogen storage disease type III at ... The gene is responsible for creating glycogen debranching enzyme, which in turn helps in glycogen decomposition. In terms of ...
... , (GSK-3 beta), is an enzyme that in humans is encoded by the GSK3B gene. In mice, the enzyme is ... "Entrez Gene: GSK3B glycogen synthase kinase 3 beta". Iwahashi K, Nishizawa D, Narita S, Numajiri M, Murayama O, Yoshihara E, et ... Glycogen synthase kinase-3 (GSK-3) is a proline-directed serine-threonine kinase that was initially identified as a ... Hoeflich KP, Luo J, Rubie EA, Tsao MS, Jin O, Woodgett JR (July 2000). "Requirement for glycogen synthase kinase-3beta in cell ...
... (GSD VI) is a type of glycogen storage disease caused by a deficiency in liver glycogen ... "Glycogen storage disease type VI". GeneReview/NIH/UW entry on Glycogen Storage Disease Type VI Media related to Glycogen ... Glycogen storage disease due to liver glycogen phosphorylase deficiency". Retrieved 11 April 2019. Glycogen- ... Because glycogen is only broken down when stored energy needs to be used, eating frequent meals can prevent the need to break ...
... (GSD5, GSD-V), also known as McArdle's disease, is a metabolic disorder, more specifically a ... "Reaction participants of glycogen phosphorylase". Retrieved 2020-12-26. NCBI Gene ID 5837: PYGM phosphorylase ... Its incidence is reported as one in 100,000, roughly the same as glycogen storage disease type I. The disease was first ... "PYGM - Glycogen phosphorylase, muscle form - Homo sapiens (Human) - PYGM gene & protein". Retrieved 2018-08-31 ...
Glycogen storage disease due to liver glycogen synthase deficiency Glycogen storage disease due to muscle and heart glycogen ... "Glycogen-Storage Disease Type 0" "Orphanet: Glycogen storage disease due to hepatic glycogen synthase deficiency". www.orpha. ... Glycogen storage disease type 0 is a disease characterized by a deficiency in the glycogen synthase enzyme (GSY). Although ... Glycogen synthetase catalyzes the rate-limiting reaction for glycogen synthesis in the liver by transferring glucose units from ...
... (GSD IV), or Andersen's Disease, is a form of glycogen storage disease, which is caused by an ... Therefore, glycogen is not made properly and abnormal glycogen molecules accumulate in cells; most severely in cardiac and ... It is a result of the absence of the glycogen branching enzyme, which is critical in the production of glycogen. This leads to ... "Deficiency of glycogen branching enzyme (GBE) activity causes glycogen storage disease type IV (GSD IV), an autosomal recessive ...
"Type II Glycogen Storage Disease". The Association for Glycogen Storage Disease. Archived from the original on 23 June 2012. ... It is the only glycogen storage disease with a defect in lysosomal metabolism, and the first glycogen storage disease to be ... of cellular glycogen. The deficiency of this enzyme results in the accumulation of structurally normal glycogen in lysosomes ... Genetics of Glycogen-Storage Disease Type II (Pompe Disease) at eMedicine Van der Ploeg AT, Kroos MA, Willemsen R, Brons NH, ...
... is a hereditary deficiency of glycogen phosphorylase kinase B that affects the liver and ... glycogen storage disease IXa1 and glycogen storage disease IXa2 that affect the liver of an individual. Mutations in PHKA2 have ... Glycogen storage disease type IX can be inherited via: X-linked recessive inheritance due to mutations at either PHKA1 or the ... The diagnosis of glycogen storage disease IX consists of the following: Complete blood count Urinalysis Histological study of ...
Glycogen body. The function of this structure in the spinal cord of birds is not known. Arthropod head problem. A long-standing ...
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 in 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 (Articles with short ...
... 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 ...
These enzymes normally catalyze reactions that ultimately convert glycogen compounds to glucose. ... A glycogen storage disease (GSD) is the result of an enzyme defect. ... Type VI Glycogen Storage Disease * Genetics of Tarui Disease (Glycogen-Storage Disease Type VII or Phosphofructokinase ... encoded search term (Type VII Glycogen Storage Disease) and Type VII Glycogen Storage Disease What to Read Next on Medscape ...
Fundraise or donate to Association for Glycogen Storage Disease (UK) Ltd with JustGiving, the worlds leading online fundraising ... About Association for Glycogen Storage Disease (UK) Ltd. Supports people with glycogen storage diseases, very rare genetic ... Association for Glycogen Storage Disease (UK) Ltd. We support children and adults with GSD to improve their chances of a good ...
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 VI Glycogen Storage Disease) and Type VI Glycogen Storage Disease What to Read Next on Medscape ... Identification of a mutation in liver glycogen phosphorylase in glycogen storage disease type VI. Hum Mol Genet. 1998 May. 7 (5 ...
Muscle biopsies for glycogen determination were taken before and after exercise, and every second hour during recove … ... and various amounts of glucose on muscle glycogen synthesis during the first 6 h after exhaustive bicycle exercise was studied ... Effect of different post-exercise sugar diets on the rate of muscle glycogen synthesis Med Sci Sports Exerc. 1987 Oct;19(5):491 ... Muscle biopsies for glycogen determination were taken before and after exercise, and every second hour during recovery. Blood ...
Timeline for Protein Glycogen phosphorylase from c.87.1.4: Oligosaccharide phosphorylase: *Protein Glycogen phosphorylase from ... Protein Glycogen phosphorylase from c.87.1.4: Oligosaccharide phosphorylase appears in SCOP 1.75. *Protein Glycogen ... Lineage for Protein: Glycogen phosphorylase. *Root: SCOPe 2.01 *. Class c: Alpha and beta proteins (a/b) [51349] (147 folds). ... Fold c.87: UDP-Glycosyltransferase/glycogen phosphorylase [53755] (1 superfamily). consists of two non-similar domains with 3 ...
The benefits of training when glycogen stores are low ... The benefits of training when glycogen stores are low * Share ... If you think glycogen is the stored form of carbohydrate we use to produce the energy required for cycling, you would be ... After your glycogen is sufficiently depleted, switch to intervals of five minutes hard exercise with a minute of rest in between ... How low-level glycogen training affects performance. Generally, athletes of all levels are told to have a carbohydrate-rich ...
... a glycogen synthase inhibitor, a glycogen degradation molecule, an anti-sense oligonucleotide that down-regulates glycogen ... administering to a subject in need thereof an effective amount of a compound selected from the group consisting of a glycogen ... synthesis, and combinations thereof, where the cancer includes elevated levels of glycogen. ... 229920002527 Glycogen Polymers 0.000 title claims abstract description 286 * 229940096919 Glycogen Drugs 0.000 title claims ...
... as are compositions for use in treatment of glycogen storage disease type II. ... Methods of treating glycogen storage disease type H, by administering acid a-glucosidase, are described, ... EN) Methods of treating glycogen storage disease type H, by administering acid a-glucosidase, are described, as are ...
The UConn Foundation Glycogen Storage Disease Program Fund . Supporting the University of Conneticut. ... Glycogen Storage Disease Program Fund. The Glycogen Storage Disease Program Fund at UConn was created to support GSD research ...
Ask the Dietitian® is a website with weight, calorie, meal planning calculator tools and frequently asked questions (FAQs) on over 100 nutrition topics. Ask the Dietitian® has been online since July 1995 providing research based nutrition advice for consumers.. ...
Glycogen Storage Diseases - Etiology, pathophysiology, symptoms, signs, diagnosis & prognosis from the Merck Manuals - Medical ... For a more complete listing of glycogen storage diseases, see table Glycogen Storage Diseases and Disorders of Gluconeogenesis ... Diagnosis of glycogen storage diseases is suspected by history, examination, and detection of glycogen and intermediate ... Inheritance for glycogen storage diseases (GSDs) is autosomal recessive Autosomal Recessive Genetic disorders determined by a ...
Dietary whey protein increases liver and skeletal muscle glycogen levels in exercise-trained rats - Volume 93 Issue 4 ... Dietary Whey Protein Hydrolysates Increase Skeletal Muscle Glycogen Levels via Activation of Glycogen Synthase in Mice. Journal ... Ivy, JL & Kuo, CH (1998) Regulation of GLUT4 protein and glycogen synthase during muscle glycogen synthesis after exercise. ... Danforth, WH (1965) Glycogen synthetase activity in skeletal muscle. Interconversion of two forms and control of glycogen ...
View Rat Genome Database annotations to negative regulation of glycogen biosynthetic process ... An association has been curated linking Mir15b and negative regulation of glycogen biosynthetic process in Rattus norvegicus. * ... 8 RGD objects have been annotated to negative regulation of glycogen biosynthetic process (GO:0045719). ...
The structure of glycogen is similar to that of Amylopectin. The only exception being that glycogen is very highly branched. In ... This is the reason glycogen behaves differently to Amylopectin. This is the reason a glycogen molecule has a very high ... Q: The solution of iodine in KI is used to detect a solution of starch and glycogen, as it gives:. *blue colour with starch and ... Glycogen is also a Glucon i.e. it is made up exclusively of D-glucose units. It is a reserved carbohydrate source for animals ...
Early release of glycogen phosphorylase in patients with unstable angina and transient ST-T alterations. ... Early release of glycogen phosphorylase in patients with unstable angina and transient ST-T alterations. ...
Glycogen vs Starch Glycogen and Starch are two main sources of glucose that gives human body the energy needed in order to ... Glycogen. Glycogen, also known as animal starch, is a source of energy that can be found in animals only. Glycogen consists of ... Home / Health / Medicine / Nutrients & Drugs / Difference Between Glycogen and Starch. Difference Between Glycogen and Starch. ... Difference between Glycogen and Starch. Glycogen and starch are a good source of energy aside from the energy that the human ...
Glycogen storage diseases: hematological aspects*What every physician needs to know:*Are you sure your patient has a glycogen ... Glycogen storage diseases: hematological aspects. What every physician needs to know:. The glycogen storage diseases (GSDs) are ... The liver and muscles are most affected by disorders of glycogen metabolism. In the liver, glycogen is the storage form of ... "DDAVP infusion in five patients with type Ia glycogen storage disease type Ib. Results of the European study on glycogen ...
More videos of Glycogen, is, linked, to, heat, generation, in, fat, cells, finds, study are available. Watch and share videos ... Watch Glycogen is linked to heat generation in fat cells finds study video online on Rediff Videos. ... Tags : Glycogen,is,linked,to,heat,generation,in,fat,cells,finds,study ... Glycogen is linked to heat generation in fat cells finds study Show more ...
Training with low glycogen for a long run for example may give adaptations that are good for a marathon runner, but perhaps not ... In their study glycogen content, fat oxidation, and CS and HAD enzyme activity were higher in the twice every other day group, ... Evidence for Doubling, training in glycogen depleted state By stevemagness , November 9, 2009 , 5 ... If you take fuel, your able to have a better quality workout, but you are not able to push into those levels of glycogen ...
CheckOrphan is a non-profit organization located in Basel, Switzerland and Santa Cruz, California that is dedicated to rare, orphan and neglected diseases. CheckOrphan offers users an interactive and dynamic platform for all these diseases. This strategy allows visitors to be updated daily on all the latest news and interact with people internationally. This is essential, because due to the nature of these diseases, there is not a large concentration of individuals within any given proximity ...
Since the mid-1990s there has been a near exponential rise in the level of glycogen synthase kinase-3 (GSK-3) related research ... Development of Glycogen synthase kinase-3 (GSK-3) inhibitors by GlaxoSmithKline and by Johnson & Johnson (Target of the Month, ... Since the mid-1990s there has been a near exponential rise in the level of glycogen synthase kinase-3 (GSK-3) related research ... Proof of concept studies have accumulated supporting the targeting of glycogen synthase kinase-3 (GSK-3) for the treatment of ...
Preparation of pyrroledione derivatives as inhibitors of glycogen synthase kinase-3.. M.P. Coghlan (Inventor), A.E. Fenwick ( ... Preparation of pyrroledione derivatives as inhibitors of glycogen synthase kinase-3. / Coghlan, M.P. (Inventor); Fenwick, A.E ... Preparation of pyrroledione derivatives as inhibitors of glycogen synthase kinase-3. WO 2000021927 A2. 2000 Apr. ... title = "Preparation of pyrroledione derivatives as inhibitors of glycogen synthase kinase-3.", ...
Glycogen branches out: New perspectives on the role of glycogen metabolism in the integration of metabolic pathways. Am J ... Effects after 4-weeks treatment (SC, DHEA and WWBV+DHEA) on (a) hepatic glycogen and (b) muscle glycogen levels at rest. Data ... SC group and DHEA group showed no significant difference in liver glycogen levels. The glycogen content of muscle tissues in ... Effect of DHEA Supplementation Combined with WWBV Training on Hepatic and Muscle Glycogen Level. Glycogen is the predominant ...
The glycogen cost of AF match play may be greater than in soccer and rugby, and CHO feeding may also spare muscle glycogen use ... Further studies using larger sample sizes are now required to quantify the interindividual variability of glycogen cost of ... Muscle glycogen decreased by 66% in player A (pre: 656 mmol/kg dry weight [dw], post: 223 mmol/kg dw) and 24% in player B (pre ... match play by quantifying muscle glycogen utilization during an in-season AF match. Methods: After a 24-h CHO-loading protocol ...
Thus, the objectives of this study were to determine the effects of diet and electrical stimulation on postmortem glycogen ... Postmortem muscle color is associated with energy content of the diet, antemortem muscle glycogen content, postmortem muscle pH ... and increased rate of pH and glycogen decline. ... Beef Ribeye Muscle Glycogen and Color Response as Affected by ... Thus, the objectives of this study were to determine the effects of diet and electrical stimulation on postmortem glycogen ...
Background Glycogen phosphorylase (GP) removes and converts one glucose molecule from glycogen to glucose-1-phosphate. ... Biological Function Glycogen phosphorylase that regulates glycogen mobilization (PubMed:27402852). Phosphorylase is an ... Product Name Anti-Glycogen Phosphorylase, brain, Antibody (13806). Description Anti-Glycogen Phosphorylase, brain Rabbit ... Anti-Glycogen Phosphorylase, brain, Antibody quantity. Add to cart. SKU: 13806 Categories: Antibody Products, Enzymes and ...
Glycogen synthase kinase 3 (GSK3) is a serine/threonine kinase that plays a part in a number of physiological processes ranging ... Glycogen synthase kinase 3 (GSK3) is a serine/threonine kinase that plays a part in a number of physiological processes ranging ... Glycogen synthase kinase-3 signaling in Alzheimers disease : regulation of beta-amyloid precursor protein processing and ... Glycogen synthase kinase-3 signaling in Alzheimers disease : regulation of beta-amyloid precursor protein processing and ...
glycogen. The Importance of Glycogen. By santacruzcore on October 10, 2018. in Fitness, Fitness, Health and Fitness, Nutrition ...
  • The PYGL gene provides instructions for making an enzyme called liver glycogen phosphorylase. (
  • PYGL gene mutations prevent liver glycogen phosphorylase from breaking down glycogen effectively. (
  • Mutations in the liver glycogen phosphorylase gene (PYGL) underlying glycogenosis type VI. (
  • Identification of a mutation in liver glycogen phosphorylase in glycogen storage disease type VI. (
  • A novel mutation (G233D) in the glycogen phosphorylase gene in a patient with hepatic glycogen storage disease and residual enzyme activity. (
  • Liver glycogen storage diseases due to phosphorylase system deficiencies: diagnosis thanks to non invasive blood enzymatic and molecular studies. (
  • Early release of glycogen phosphorylase in patients with unstable angina and transient ST-T alterations. (
  • Biological Function Glycogen phosphorylase that regulates glycogen mobilization (PubMed:27402852). (
  • Background Glycogen phosphorylase (GP) removes and converts one glucose molecule from glycogen to glucose-1-phosphate. (
  • Reacts with human Glycogen Phosphorylase, muscle. (
  • Glycogen Phosphorylase, Muscle Form" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (
  • An isoenzyme of GLYCOGEN PHOSPHORYLASE that catalyzes the degradation of GLYCOGEN in muscle. (
  • This graph shows the total number of publications written about "Glycogen Phosphorylase, Muscle Form" by people in UAMS Profiles by year, and whether "Glycogen Phosphorylase, Muscle Form" was a major or minor topic of these publications. (
  • Below are the most recent publications written about "Glycogen Phosphorylase, Muscle Form" by people in Profiles over the past ten years. (
  • The structure of glycogen is similar to that of Amylopectin. (
  • The ability to bind and cleave gflucose to and from glycogen depends on the branched structure of glycogen. (
  • The function of GBE is altered by a mutation, that leads to a change in the structure of glycogen and inhibits its degradation. (
  • The glycogen storage diseases (GSDs) are a group of inherited inborn errors of metabolism resulting from mutations in the genes responsible for the proteins (enzymes) involved with glycogen synthesis, degradation, and regulation. (
  • Accumulation of glycogen in the liver, skeletal muscle, or myocardium can impair the function of these sites, and deficiencies of these enzymes in red blood cells can lead to hemolysis. (
  • However, the twice every other day group increased glycogen content,fat oxidation and enzymes related to substrate use. (
  • This glucagon stimulates the enzymes needed to perform glycogenolysis, which is basically the breakdown of glycogen. (
  • Glycogen storage disorders (GSDs) are a group of inborn metabolic errors caused by various genetic defects in glycogenolytic/synthetic enzymes or protein mutations that regulate glycogen metabolism, accompanied by abnormalities in glycogen store or use [ 1 ]. (
  • Glycogen synthase kinase-3 in insulin and Wnt signalling: a double-edged sword? (
  • We investigated the effect of chromium on glycogen synthesis and insulin signaling in humans. (
  • Ignition was designed to address the most overlooked component of proper post workout nutrition- replenishing your glycogen stores and spiking your insulin for maximum protein and nutrient assimilation. (
  • In addition to a whey isolate, you should always consume a fast absorbing carbohydrate that spikes your insulin levels to replenish glycogen stores and take full advantage of the proteins you are taking. (
  • It literally will ignite muscle growth by replenishing your glycogen stores immediately and spiking your insulin levels to allow maximum protein assimilation. (
  • We also observed that whey protein regulated glycogen metabolism in these two tissues by different mechanisms. (
  • Burcelin , R , del , Carmen , Munoz , M , Guillam , MT & Thorens , B ( 2000 ) Liver hyperplasia and paradoxical regulation of glycogen metabolism and glucose-sensitive gene expression in GLUT2-null hepatocytes. (
  • When impaired hepatic glycogen metabolism is present, patients have fasting hypoglycemia, ketosis and potentially progressive liver damage. (
  • Glycogen synthase kinase 3 (GSK3) is a serine/threonine kinase that plays a part in a number of physiological processes ranging from glycogen metabolism to gene transcription. (
  • If you take fuel, your able to have a better quality workout, but you are not able to push into those levels of glycogen depletion to force fuel source adaptations. (
  • Thus, the objectives of this study were to determine the effects of diet and electrical stimulation on postmortem glycogen depletion, muscle color, and sensory properties of bull longissimus dorsi muscle. (
  • There was a significant depletion in glycogen immediately after exercise, an increase at 2 h, and a further increase above rest at 24 h (P (
  • The effect of repeated ingestions of fructose, sucrose, and various amounts of glucose on muscle glycogen synthesis during the first 6 h after exhaustive bicycle exercise was studied. (
  • When 0.35 (low glucose: N = 5), 0.70 (medium glucose: N = 5), or 1.40 (high glucose: N = 5) body weight of glucose were given orally at 0, 2, and 4 h after exercise, the rates of glycogen synthesis were (mean +/- SE) 2.1 +/- 0.5, 5.8 +/- 1.0, and 5.7 +/- 0.9, respectively. (
  • Effects of chromium supplementation on glycogen synthesis after high-i" by Jeff S Volek, Ricardo Silvestre et al. (
  • The rate of glycogen synthesis during the 2 h after exercise was not different between groups (Cr: 25.8 +/- 8.0 and Pl: 17.1 +/- 4.7 (
  • Conclusions: Chromium supplementation did not augment glycogen synthesis during recovery from high-intensity exercise and high-carbohydrate feeding, although there was a trend for lower PI 3-kinase activity. (
  • Glycogen starts to accumulate in the fetal cells about 26 weeks into gestation and helps in the synthesis of pulmonary surfactants. (
  • Glycogen starts to accumulate in the fetal cells about 26 weeks into gestation and helps in the synthesis of pulmonary surfactants.The growth of the bacteria, sporulation of yeast are all found to be interlinked with glycogen storage. (
  • Development of Glycogen synthase kinase-3 (GSK-3) inhibit. (
  • Proof of concept studies have accumulated supporting the targeting of glycogen synthase kinase-3 (GSK-3) for the treatment of diabetes and CNS conditions. (
  • Since the mid-1990s there has been a near exponential rise in the level of glycogen synthase kinase-3 (GSK-3) related research. (
  • To mark this surge in interest, LeadDiscovery have recently produced a full report "Glycogen synthase kinase 3 (GSK-3) inhibitors:Proof of concept and therapeutic opportunities for the treatment of diabetes, Alzheimer's disease, stroke & bipolar disorders" ( click here for access). (
  • Preparation of pyrroledione derivatives as inhibitors of glycogen synthase kinase-3. (
  • Glycogen synthase kinase-3 signaling in Alzheimer's. (
  • Mechanisms linking diabetes mellitus to the development of atherosclerosis: a role for endoplasmic reticulum stress and glycogen synthase kinase-3This paper is one of a selection of papers published in this Special Issue, entitled Young Investigator's Forum. (
  • Recently, inhibition of glycogen synthase kinase-3 has been shown to exert anti-tumor effects on pancreatic cancer cells by suppressing NF-kappaB. (
  • Glycogen synthase kinase 3 (GSK3) proteins (GSK3α and GSK3β) are key mediators of signaling pathways, with crucial roles in coordinating fundamental biological processes during neural development. (
  • Glycogen synthase kinase 3 (GSK3) proteins (GSK3α or GSK3β) are key mediators of signaling pathways, especially in the CNS but poorly described in the retina. (
  • It activated phosphatidylinositol 3-kinase and induced phosphorylation of Akt at Ser-473/Thr-308, and concurrently activated downstream p70 S6 kinase as well as glycogen synthase kinase-3. (
  • This enzyme is found only in liver cells, where it breaks down glycogen into a type of sugar called glucose-1-phosphate. (
  • In their study glycogen content, fat oxidation, and CS and HAD enzyme activity were higher in the twice every other day group, but performance was equally increased in both groups. (
  • One unit of isoamylase activity is the amount of enzyme required to release one µmole of D-glucose reducing sugar equivalent in the presence of oyster glycogen per min at pH 4.0 and 40 o C. (
  • Pure Isoamylase (Glycogen 6-glucanohydrolase) for use in biochemical enzyme assays and in vitro diagnostic analysis. (
  • Mutation of the gene coding this enzyme is the cause of McArdle disease (GLYCOGEN STORAGE DISEASE TYPE V). (
  • Muscle cells lack the enzyme needed for a complete breakdown of glycogen to glucose. (
  • glycogen de-branching enzyme (GDE) breaks it down. (
  • Neonatal type IV glycogen storage disease associated with "null" mutations in glycogen branching enzyme 1. (
  • Glycogen and Starch are two main sources of glucose that gives human body the energy needed in order to perform day to day tasks. (
  • Glycogen, also known as animal starch, is a source of energy that can be found in animals only. (
  • Starch, the same with glycogen, is another source of energy that can be found in plants only. (
  • Glycogen and starch are a good source of energy aside from the energy that the human body produces. (
  • Glycogen has a single molecule while the starch has double molecules. (
  • In terms of the structure, glycogens are branched out purely whereas the starch consists of branch and chain components. (
  • Well, the obvious difference between glycogen and starch, without delving into its structures and molecules, is where they are coming from. (
  • Glycogens come from animals only and starch from plants only. (
  • Glycogens are solely coming from animals, specifically made by the liver and the muscles, while the starch solely comes from the green plants and staple foods like potatoes and cassavas. (
  • Glycogen has a single molecule only whereas starch has two molecules. (
  • In terms of structure, glycogen structures are branched purely and starch structure is composed of branch and chain components. (
  • Both glycogen and starch are white powders in their dried form. (
  • In addition, glycogen and starch are both sparingly soluble in water at room temperature. (
  • macromolecule that makes up muscle, skin, organs, hair: protein: carbohydrates are made up of monomers called : monosaccharides: a disaccharide contains: two monosaccarides: polysaccharide that plants use to store energy: starch: polysaccharide animals use to store energy: glycogen: this organ stores glucose in the form of glycogen: liver: polysaccharide used … Which macromolecule stores energy, insulates us, and makes up the cell membrane? (
  • Exercise training resulted in an increase in the skeletal muscle glycogen content. (
  • Furthermore, the whey protein group significantly increased the skeletal muscle glycogen content compared with the casein group. (
  • Postmortem muscle color is associated with energy content of the diet, antemortem muscle glycogen content, postmortem muscle pH decline, and ultimate pH, all of which are affected by the degree and amount of physiological stress induced before slaughter. (
  • Glycogen also plays an important part in regulating metabolic signalling , interacting with particular proteins in cells to alter their activity. (
  • 2005). Low muscle glycogen amplifies the activation of signalling proteins (in particular AMPK and MAPK for those who are interested). (
  • Don't waste your money on expensive proteins just for your body to inefficiently waste them by converting them into glycogen slowly over time. (
  • Because liver cells cannot break down glycogen into glucose, individuals with GSDVI can have hypoglycemia and may use fats for energy, resulting in ketosis. (
  • Evaluation of glycogen storage disease as a cause of ketotic hypoglycemia in children. (
  • the deficiencies may occur in the liver or muscles and cause hypoglycemia or deposition of abnormal amounts or types of glycogen (or its intermediate metabolites) in tissues. (
  • AAV vector-mediated reversal of hypoglycemia in canine and murine glycogen storage disease type Ia. (
  • Glycogen storage disease type 1a (GSD1a) is an inborn genetic disease caused by glucose-6-phosphatase-α (G6Pase-α) deficiency and is often observed to lead to endogenous glucose production disorders manifesting as hypoglycemia, hyperuricemia, hyperlipidemia, lactic acidemia, hepatomegaly, and nephromegaly. (
  • With an unavailability of fatty acids, the body resorts to using glucose and glycogen for its energy, which then leads to hypoglycemia. (
  • That "flat" feeling is from a lack of glycogen in the muscle - you used it all up at the gym and your body is scrambling to take every-thing you throw at it to fill them back up again. (
  • Neuropathological study of skeletal muscle, heart, liver, and brain in a neonatal form of glycogen storage disease type IV associated with a new mutation in GBE1 gene. (
  • The classic infantile form of glycogen storage disease type II is characterized by severe muscle weakness (myopathy) and abnormally diminished muscle tone (hypotonia) without muscle wasting. (
  • The nonclassic infantile form of glycogen storage disease type II usually presents within the first year of life. (
  • In the late-onset form of glycogen storage disease type II, symptoms may not be evident until childhood, adolescence, or adulthood. (
  • Dr Baar's fellow scholars at the University of Birmingham even created a training session specifically designed to increase the signalling function of glycogen. (
  • Hence it is an important function of glycogen, the storage of glucose within cells. (
  • During intense exercise, your muscles use glucose and glycogen for energy. (
  • Therefore, accumulation of glycogen in liver, muscle and nerve cells results in gradual dysfunction of these organs. (
  • The accumulation of glycogen in hepatocytes and proximal renal tubules leads to hepatomegaly and nephromegaly. (
  • We know from studies that training at high intensity activates AMPK at a greater rate, plus we know this effect is improved when training at lower glycogen levels, so this session gives twice the activation," Baar explains. (
  • Because the group was training in a lower glycogen state. (
  • However, hepatic total glycogen synthase activity and mRNA expression were similar with the two diets. (
  • Total glycogen synthase activity in the skeletal muscle in the whey protein group was significantly higher than that in the casein group. (
  • There was significant decrease in total glycogen content of the experimental tissues as compare to the control tissue. (
  • Glycogen synthase activity was significantly increased immediately after exercise in both groups. (
  • This is the reason glycogen behaves differently to Amylopectin. (
  • Hydrolysis of (1,6)-α-D-glucosidic branch linkages in glycogen, amylopectin and their β-limit dextrins. (
  • Glycogen is your body's carbohydrate stores that serve essentially as your on-board battery. (
  • Skeletal muscles collectively store about ___% of the body's glycogen stores. (
  • The animal liver and muscles are responsible in the creation of glycogens. (
  • Glycogen can be found solely from animals and is created by the liver and the muscles and can sometimes be made in small amount by the brains and stomachs. (
  • Glycogen storage disease type V, also known as McArdle disease , is a glycogen storage disease caused by a deficiency of myophosphorylase, which is responsible for glycogen storage in skeletal muscles . (
  • In the case of starvation, glycogen stored in the liver and the skeletal muscles undergo glycogenolysis to form glucose for utilization. (
  • Glycogen in skeletal muscles provides energy only for the functioning of the muscles and not the entire body. (
  • There is not a form of carbohydrates anywhere known to man that is more pure or refined or that can deliver glycogen directly to the muscles any faster. (
  • Glycogen accumulation within the muscles, peripheral nerves, and the anterior horn cells causes this weakness. (
  • During exercise, muscles use up stored glucose (called glycogen) and you'll feel shaky and tired. (
  • At the same time, after you drink, your liver and muscles don't do a great job of storing sugar as glycogen for later. (
  • The liver and muscles store glycogen. (
  • In a glycogen molecule, the branching happens more frequently, almost after every six glucose units. (
  • This is the reason a glycogen molecule has a very high molecular weight. (
  • A hydrolysis experiment will suggest that in a glycogen molecule, one end group occurs after every ten to twelve units of glucose. (
  • But glycogen is a big and complex molecule, so it will not diffuse out of the cell membrane. (
  • But if glucose combines into one big molecule of glycogen, the problem does not occur. (
  • Glycogen consists of a single molecule and its structure is branched purely. (
  • Glycogen is composed of a single molecule. (
  • Correction of glycogen storage disease type 1a in a mouse model by gene therapy. (
  • It has been found that training in a glycogen depleted state enhances gene transcription of several markers of training adaptation (Yeo et al. (
  • Shen J, Liu HM, McConkie-Rosell A. Prenatal diagnosis of glycogen storage disease type IV using PCR-based DNA mutation analysis. (
  • An association has been curated linking Mir15b and negative regulation of glycogen biosynthetic process in Rattus norvegicus. (
  • Regulation of glycogen synthase. (
  • Dive into the research topics of 'Regulation of glycogen synthase. (
  • 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. (
  • High frequency of missense mutations in glycogen storage disease type VI. (
  • Glycogen storage disease type Ia and VI associated with hepatocellular carcinoma: two case reports. (
  • Glycogen storage disease type III diagnosis and management guidelines. (
  • Bijvoet AG, Van Hirtum H, Vermey M. Pathological features of glycogen storage disease type II highlighted in the knockout mouse model. (
  • Asami T, Kikuchi T, Asami K. Effect of clonidine on the height of a child with glycogen storage disease type VI: a 13 year follow-up study. (
  • Diagnosis and management of glycogen storage diseases type VI and IX: a clinical practice resource of the American College of Medical Genetics and Genomics (ACMG). (
  • Prognosis for and treatment of glycogen storage diseases vary by type, but treatment typically includes dietary supplementation with cornstarch to provide a sustained source of glucose for the hepatic forms of GSD and exercise avoidance for the muscle forms. (
  • Further studies using larger sample sizes are now required to quantify the interindividual variability of glycogen cost of match play (including muscle and fiber-type-specific responses), as well examining potential metabolic and ergogenic effects of CHO feeding. (
  • Glycogen storage disease type 1 (GSD1) is a rare inherited defect of endogenous glucose production. (
  • Glycogen storage disease type Ia (GSD-Ia) profoundly impairs glucose release by the liver due to glucose-6-phosphatase (G6Pase) deficiency. (
  • Glycogen storage disease type I (GSD I) is caused by a dysfunction of the glycoregulation, which. (
  • Glycogen storage disease type 1 (GSD 1) is caused by a dysfunction of the glycoregulation, which leads to mass storage of glycogen in organs. (
  • blood test for diabetes type 2 meds for blood sugar how to lower high blood sugar instantly Dr. Oz lower blood sugar if blood sugar is high, what do you do diabetes control medicine does glycogen lower blood sugar long-acting diabetes medications. (
  • Because the media's does glycogen lower blood sugar flawed side of Becki Pingree's character, which highlights his arrogance, ignorance, domineering, and second-hand side in the hearts of fans, just like they treated Cassano at the beginning Accepted the media to Maribel Fleishman shell of the fixed image that type 2 blood sugar. (
  • For the people of the border towns, the court wanted to solve type 2 diabetes check blood sugar problem of the Xiongnu once and for all, of does glycogen lower blood sugar what makes your blood sugar go down. (
  • Glycogen Storage Disease Type IV: A Rare Cause for Neuromuscular Disorders or Often Missed? (
  • Sandhu T, Polan M, Yu Z, Lu R, Makkar A. Case of Neonatal Fatality from Neuromuscular Variant of Glycogen Storage Disease Type IV. (
  • Variable clinical presentation of glycogen storage disease type IV: from severe hepatosplenomegaly to cardiac insufficiency. (
  • Liver histology in children with glycogen storage disorders type VI and IX. (
  • The potential of dietary treatment in patients with glycogen storage disease type IV. (
  • IMSEAR at SEARO: Glycogen storage disease type III. (
  • Most infants with glycogen storage disease type II cannot hold up their heads or move normally. (
  • Learn more about the symptoms of glycogen storage disease type II. (
  • Glycogen storage disease type 1a (GSD1a) is a rare autosomal recessive metabolic disorder characterized by hypoglycaemia, growth retardation, lactic acidosis , hepatomegaly , hyperlipidemia , and nephromegaly. (
  • In addition, four disorders (severe combined immunodeficiency, glycogen storage disease type II [Pompe disease], mucopolysaccharidosis type 1, and X-linked adrenoleukodystrophy) were added to the RUSP since 2006, for which screening was implemented in some states during the 3-year data collection time frame. (
  • Which hormone signals for the conversion of glucose to glycogen? (
  • The natural history of glycogen storage disease types VI and IX: Long-term outcome from the largest metabolic center in Canada. (
  • This glucose obtained from glycogen, is released into the bloodstream, and the blood glucose level is revived. (
  • Glucagon causes the liver to convert stored glycogen into glucose, which is released into the bloodstream. (
  • If you think glycogen is the stored form of carbohydrate we use to produce the energy required for cycling, you would be correct. (
  • Generally, athletes of all levels are told to have a carbohydrate-rich meal two to three hours before any training occurs, ensuring their glycogen levels are fully topped up. (
  • Racing shorter distances for an hour or less requires a faster speed, meaning that your body has to burn carbohydrate no matter what, so glycogen signalling is largely irrelevant. (
  • To better understand the carbohydrate (CHO) requirement of Australian Football (AF) match play by quantifying muscle glycogen utilization during an in-season AF match. (
  • After 4 wk of supplementation, subjects performed a supramaximal bout of cycling exercise to deplete muscle glycogen, which was followed by high-glycemic carbohydrate feedings for the next 24 h. (
  • Approximately 1/3 of your total carbohydrate energy is from lactate, the rest is from blood glucose and muscle glycogen. (
  • Purified Glycogen (PG) is a extremely hyper branched carbohydrate, characterised by excessive water solubility and really average enhance in viscosity. (
  • Glycogen accumulates within liver cells, causing these cells to become enlarged and dysfunctional. (
  • Whereas, in muscle, where glycogen is the primary energy source, glycogen accumulates and muscle weakness and cramping occurs, exercise intolerance is present, and myoglobinuria is detectable. (
  • Glycogen is the storage form of carbohydrates found in animals, bacteria and fungi. (
  • Consuming carbohydrates as part of a post workout snack helps replenish depleted glycogen stores and boosts the immune system. (
  • A. carbohydrates and lipids, carbohydrates are stored in the liver as glycogen and lipids are stored underneath the skin. (
  • Apart from glucagon, hormones like cortisol, epinephrine and norepinephrine also stimulate the breakdown of glycogen. (
  • Cortisone stimulates the breakdown of glycogen into glucose. (
  • We investigated the effect of different types of dietary protein on glycogen content in liver and skeletal muscle of exercise-trained rats. (
  • The increase in glycogen content in liver was significantly greater in rats fed the whey protein diet compared with those fed the casein diet. (
  • The present study is the first to demonstrate that a diet based on whey protein may increase glycogen content in liver and skeletal muscle of exercise-trained rats. (
  • Which hormone signals the liver to convert glycogen to glucose? (
  • This would be interesting but not practically useful were it not for one crucial point, the scientists showed our signalling function can be improved by training when glycogen stores are low, which is a radical break from conventional wisdom. (
  • It is possible, and perhaps likely, that training with low glycogen stores could result in negative consequences for shorter events. (
  • Glycogen and triglycerides are the two energy stores found in animals. (
  • Training with weights severely depletes your glycogen stores and drains the battery. (
  • The more lactate you use during exercise, the less muscle glycogen you have to use, which means your glycogen stores will last longer and this equates to more energy. (
  • When your body fasts - for example, during sleep - glycogen stores are depleted. (
  • And because glycogen stores are depleted, your body will burn fat, rather than readily available energy. (
  • Glycogen storage diseases. (
  • Diagnosis of glycogen storage diseases is suspected by history, examination, and detection of glycogen and intermediate metabolites in tissues by MRI or biopsy. (
  • Total metal accumulation and the levels of total protein and glycogen were measured in Palaemonetes pugio after exposing the animals to 0.05, 0.1 and 0.2 ppm concentrations of chromium over 1, 7 and 15 days. (
  • Metal accumulation in tisuues was measured using atomic absorbtion spectrophotometric techniques and the levels of total protein and glycogen were determined Lowry and Anthron methods, respectively. (
  • Total metal accumulation increased with increasing concentrations of chromium at given exposure period while total protein and glycogen levels showed a decrease on day 15th compared with day 1. (
  • Flying solo with protein only after a workout means that your body will very slowly digest this protein, convert most of it into glucose and push it into the cell as glycogen. (
  • That translates into a lot of wasted time, effort, and money on your part and leaves no protein in the end to build and repair with since it has all been converted into glycogen. (
  • Toxicity tests were conducted on freshwater fish, Channa gachua and glycogen content of the tissues like liver and gonad were calculated after acute exposure of toxicants like Confidor and Bavistin upto acute exposure at specific time interval of 24, 48, 72 and 96hrs. (