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Journal articles on the topic 'GlycoGag'

Author: Grafiati

Published: 11 March 2023

Last updated: 31 July 2025

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1

Fujisawa, Ryuichi, Frank J. McAtee, Cynthia Favara, Stanley F. Hayes, and John L. Portis. "N-Terminal Cleavage Fragment of Glycosylated Gag Is Incorporated into Murine Oncornavirus Particles." Journal of Virology 75, no. 22 (2001): 11239–43. http://dx.doi.org/10.1128/jvi.75.22.11239-11243.2001.

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ABSTRACT Glycosylated Gag (Glycogag) is a transmembrane protein encoded by murine and feline oncornaviruses. While the protein is dispensible for virus replication, Glycogag-null mutants of a neurovirulent murine oncornavirus are slow to spread in vivo and exhibit a loss of pathogenicity. The function of this protein in the virus life cycle, however, is not understood. Glycogag is expressed at the plasma membrane of infected cells but has not been detected in virions. In the present study we have reexamined this issue and have found an N-terminal cleavage fragment of Glycogag which was pellete

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2

Usami, Yoshiko, Yuanfei Wu, and Heinrich G. Göttlinger. "SERINC3 and SERINC5 restrict HIV-1 infectivity and are counteracted by Nef." Nature 526, no. 7572 (2015): 218–23. https://doi.org/10.5281/zenodo.13533229.

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(Uploaded by Plazi for the Bat Literature Project) HIV-1 Nef and the unrelated mouse leukaemia virus glycosylated Gag (glycoGag) strongly enhance the infectivity of HIV-1 virions produced in certain cell types in a clathrin-dependent manner. Here we show that Nef and glycoGag prevent the incorporation of the multipass transmembrane proteins serine incorporator 3 (SERINC3) and SERINC5 into HIV-1 virions to an extent that correlates with infectivity enhancement. Silencing of both SERINC3 and SERINC5 precisely phenocopied the effects of Nef and glycoGag on HIV-1 infectivity. The infectivity of ne

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Usami, Yoshiko, Yuanfei Wu, and Heinrich G. Göttlinger. "SERINC3 and SERINC5 restrict HIV-1 infectivity and are counteracted by Nef." Nature 526, no. 7572 (2015): 218–23. https://doi.org/10.5281/zenodo.13533229.

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(Uploaded by Plazi for the Bat Literature Project) HIV-1 Nef and the unrelated mouse leukaemia virus glycosylated Gag (glycoGag) strongly enhance the infectivity of HIV-1 virions produced in certain cell types in a clathrin-dependent manner. Here we show that Nef and glycoGag prevent the incorporation of the multipass transmembrane proteins serine incorporator 3 (SERINC3) and SERINC5 into HIV-1 virions to an extent that correlates with infectivity enhancement. Silencing of both SERINC3 and SERINC5 precisely phenocopied the effects of Nef and glycoGag on HIV-1 infectivity. The infectivity of ne

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Gonzalez-Enriquez, Gracia Viviana, Martha Escoto-Delgadillo, Eduardo Vazquez-Valls, and Blanca Miriam Torres-Mendoza. "SERINC as a Restriction Factor to Inhibit Viral Infectivity and the Interaction with HIV." Journal of Immunology Research 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/1548905.

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The serine incorporator 5 (SERINC5) is a recently discovered restriction factor that inhibits viral infectivity by preventing fusion. Retroviruses have developed strategies to counteract the action of SERINC5, such as the expression of proteins like negative regulatory factor (Nef), S2, and glycosylated Gag (glycoGag). These accessory proteins downregulate SERINC5 from the plasma membrane for subsequent degradation in the lysosomes. The observed variability in the action of SERINC5 suggests the participation of other elements like the envelope glycoprotein (Env) that modulates susceptibility o

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5

Firrito, Claudia, Cinzia Bertelli, Teresa Vanzo, Ajit Chande, and Massimo Pizzato. "SERINC5 as a New Restriction Factor for Human Immunodeficiency Virus and Murine Leukemia Virus." Annual Review of Virology 5, no. 1 (2018): 323–40. http://dx.doi.org/10.1146/annurev-virology-092917-043308.

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SERINC genes encode for homologous multipass transmembrane proteins with unknown cellular function, despite being highly conserved across eukaryotes. Among the five SERINC genes found in humans, SERINC5 was shown to act as a powerful inhibitor of retroviruses. It is efficiently incorporated into virions and blocks the penetration of the viral core into target cells, by impairing the fusion process with a yet unclear mechanism. SERINC5 was also found to promote human immunodeficiency virus 1 (HIV-1) virion neutralization by antibodies, indicating a pleiotropic activity, which remains mostly une

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Cano-Ortiz, Lucía, Qinyong Gu, Patricia de Sousa-Pereira, et al. "Feline Leukemia Virus-B Envelope Together With its GlycoGag and Human Immunodeficiency Virus-1 Nef Mediate Resistance to Feline SERINC5." Journal of Molecular Biology 434, no. 6 (2022): 167421. http://dx.doi.org/10.1016/j.jmb.2021.167421.

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7

Shi, Yuhang, Sydney Simpson, Shahad K. Ahmed, et al. "The Antiviral Factor SERINC5 Impairs the Expression of Non-Self-DNA." Viruses 15, no. 9 (2023): 1961. http://dx.doi.org/10.3390/v15091961.

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SERINC5 is a restriction factor that becomes incorporated into nascent retroviral particles, impairing their ability to infect target cells. In turn, retroviruses have evolved countermeasures against SERINC5. For instance, the primate lentiviruses (HIV and SIV) use Nef, Moloney Murine Leukemia Virus (MLV) uses GlycoGag, and Equine Infectious Anemia Virus (EIAV) uses S2 to remove SERINC5 from the plasma membrane, preventing its incorporation into progeny virions. Recent studies have shown that SERINC5 also restricts other viruses, such as Hepatitis B Virus (HBV) and Classical Swine Fever Virus

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8

Diehl, William E., Mehmet H. Guney, Teresa Vanzo, et al. "Influence of Different Glycoproteins and of the Virion Core on SERINC5 Antiviral Activity." Viruses 13, no. 7 (2021): 1279. http://dx.doi.org/10.3390/v13071279.

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Host plasma membrane protein SERINC5 is incorporated into budding retrovirus particles where it blocks subsequent entry into susceptible target cells. Three structurally unrelated proteins encoded by diverse retroviruses, human immunodeficiency virus type 1 (HIV-1) Nef, equine infectious anemia virus (EIAV) S2, and ecotropic murine leukemia virus (MLV) GlycoGag, disrupt SERINC5 antiviral activity by redirecting SERINC5 from the site of virion assembly on the plasma membrane to an internal RAB7+ endosomal compartment. Pseudotyping retroviruses with particular glycoproteins, e.g., vesicular stom

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9

Li, Minghua, Abdul A. Waheed, Jingyou Yu, et al. "TIM-mediated inhibition of HIV-1 release is antagonized by Nef but potentiated by SERINC proteins." Proceedings of the National Academy of Sciences 116, no. 12 (2019): 5705–14. http://dx.doi.org/10.1073/pnas.1819475116.

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The T cell Ig and mucin domain (TIM) proteins inhibit release of HIV-1 and other enveloped viruses by interacting with cell- and virion-associated phosphatidylserine (PS). Here, we show that the Nef proteins of HIV-1 and other lentiviruses antagonize TIM-mediated restriction. TIM-1 more potently inhibits the release of Nef-deficient relative to Nef-expressing HIV-1, and ectopic expression of Nef relieves restriction. HIV-1 Nef does not down-regulate the overall level of TIM-1 expression, but promotes its internalization from the plasma membrane and sequesters its expression in intracellular co

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10

Chande, Ajit, Emilia Cristiana Cuccurullo, Annachiara Rosa, Serena Ziglio, Susan Carpenter, and Massimo Pizzato. "S2 from equine infectious anemia virus is an infectivity factor which counteracts the retroviral inhibitors SERINC5 and SERINC3." Proceedings of the National Academy of Sciences 113, no. 46 (2016): 13197–202. http://dx.doi.org/10.1073/pnas.1612044113.

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The lentivirus equine infectious anemia virus (EIAV) encodes the small protein S2, a pathogenic determinant that is important for virus replication and disease progression in horses. No molecular function had been linked to this accessory protein. We report that S2 can replace the activity of Negative factor (Nef) in HIV-1 infectivity, being required to antagonize the inhibitory activity of Serine incorporator (SERINC) proteins on Nef-defective HIV-1. Like Nef, S2 excludes SERINC5 from virus particles and requires an ExxxLL motif predicted to recruit the clathrin adaptor, Adaptor protein 2 (AP

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Donaldo, Emiliano Silva López, Irlanda Méndez Ynostroza Sussan, Alejandra Solano Mendoza Alma, Paola Contreras Sáenz Claudia, Isabel Díaz de León Guzmán Ana, and Villaseñor Alcalá Noemí. "Pediatric Considerations in Pompe Disease: A Comprehensive Review." INTERNATIONAL JOURNAL OF MEDICAL SCIENCE AND CLINICAL RESEARCH STUDIES ISSN 04, no. 04 (2024): 651–54. https://doi.org/10.5281/zenodo.10964704.

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Pompe disease, also known as glycogen storage disease type II, is a rare inherited disorder caused by a deficiency of the enzyme acid alpha-glucosidase (GAA), leading to the accumulation of glycogen in various tissues, particularly muscles. While Pompe disease can affect individuals of all ages, its presentation and management in pediatric patients present unique challenges. This review aims to provide a comprehensive overview of the clinical manifestations, diagnosis, and management of Pompe disease in pediatric populations. Special considerations in the areas of respiratory support, nutritio

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Ma, Yulong, Yanhui Cai, Doutong Yu, et al. "Astrocytic Glycogen Mobilization in Cerebral Ischemia/Reperfusion Injury." Neuroscience and Neurological Surgery 11, no. 3 (2022): 01–05. http://dx.doi.org/10.31579/2578-8868/228.

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Glycogen is an important energy reserve in the brain and can be rapidly degraded to maintain metabolic homeostasis during cerebral blood vessel occlusion. Recent studies have pointed out the alterations in glycogen and its underlying mechanism during reperfusion after ischemic stroke. In addition, glycogen metabolism may work as a promising therapeutic target to relieve reperfusion injury. Here, we summarize the progress of glycogen metabolism during reperfusion injury and its corresponding application in patients suffering from ischemic stroke.

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13

Kanungo, Shibani, Kimberly Wells, Taylor Tribett, and Areeg El-Gharbawy. "Glycogen metabolism and glycogen storage disorders." Annals of Translational Medicine 6, no. 24 (2018): 474. http://dx.doi.org/10.21037/atm.2018.10.59.

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14

Frolow, Jason, and C. Louise Milligan. "Hormonal regulation of glycogen metabolism in white muscle slices from rainbow trout (Oncorhynchus mykiss Walbaum)." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, no. 6 (2004): R1344—R1353. http://dx.doi.org/10.1152/ajpregu.00532.2003.

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To test the hypothesis that cortisol and epinephrine have direct regulatory roles in muscle glycogen metabolism and to determine what those roles might be, we developed an in vitro white muscle slice preparation from rainbow trout ( Oncorhynchus mykiss Walbaum). In the absence of hormones, glycogen-depleted muscle slices obtained from exercised trout were capable of significant glycogen synthesis, and the amount of glycogen synthesized was inversely correlated with the initial postexercise glycogen content. When postexercise glycogen levels were <5 μmol/g, about 4.3 μmol/g of glycogen were

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15

Nanware, Sanjay Shamrao, Habib Mohammed Hasmi, and Dhanraj Balbhim Bhure. "Glycogen Content in Moniezia Expansa and its Host Intestine." Indian Journal of Applied Research 4, no. 5 (2011): 651–52. http://dx.doi.org/10.15373/2249555x/may2014/206.

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16

Coderre, L., A. K. Srivastava, and J. L. Chiasson. "Effect of hypercorticism on regulation of skeletal muscle glycogen metabolism by insulin." American Journal of Physiology-Endocrinology and Metabolism 262, no. 4 (1992): E427—E433. http://dx.doi.org/10.1152/ajpendo.1992.262.4.e427.

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The effects of hypercorticism on the regulation of glycogen metabolism by insulin in skeletal muscles was examined by using the hindlimb perfusion technique. Rats were injected daily with either saline or dexamethasone (0.4 mg.kg-1.day-1) for 14 days and were studied in the fed or fasted (24 h) state under saline or insulin (1 mU/ml) treatment. In fed controls, insulin resulted in glycogen synthase activation and in enhanced glycogen synthesis. In dexamethasone-treated animals, basal muscle glycogen concentration remained normal, but glycogen synthase activity ratio was decreased in white and

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17

Kuipers, H., D. L. Costill, D. A. Porter, W. J. Fink, and W. M. Morse. "Glucose feeding and exercise in trained rats: mechanisms for glycogen sparing." Journal of Applied Physiology 61, no. 3 (1986): 859–63. http://dx.doi.org/10.1152/jappl.1986.61.3.859.

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This investigation studied the effect of an oral glucose feeding on glycogen sparing during exercise in non-glycogen-depleted and glycogen-depleted endurance-trained rats. The non-glycogen-depleted rats received via a stomach tube 2 ml of a 20% glucose solution labeled with [U-14C]glucose just prior to exercise (1 h at 25 m/min). Another group of rats ran for 40 min at higher intensity to deplete glycogen stores, after which they received the same glucose feeding and continued running for 1 h at 25 m/min. The initial 40-min run depleted glycogen in heart, skeletal muscle, and liver. In the non

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18

Shockey Breslin, Joanette, and Robert R. Cardell. "Morphometric analysis and autoradiography of the smooth endoplasmic reticulum during glycogen deposition in the fetal mouse hepatocyte." Proceedings, annual meeting, Electron Microscopy Society of America 48, no. 3 (1990): 544–45. http://dx.doi.org/10.1017/s0424820100160273.

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Analyses of adult hepatic glycogen deposition by numerous investigators have determined that the smooth endoplasmic reticulum (SER) proliferates immediately prior to glycogen deposition and during the early stages of glycogen accumulation, then decreases as glycogen levels reach their maximum, suggesting that SER participates in adult hepatic glycogen metabolism. Less is known regarding fetal hepatic glycogen synthesis and the participation of the fetal SER. The studies described here test the hypothesis that the SER functions in the synthesis of fetal hepatic glycogen. Quantitative analysis o

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19

McNulty, P. H., C. Ng, W. X. Liu, et al. "Autoregulation of myocardial glycogen concentration during intermittent hypoxia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 2 (1996): R311—R319. http://dx.doi.org/10.1152/ajpregu.1996.271.2.r311.

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During hypoxia, the heart consumes glycogen to generate ATP. Tolerance of repetitive hypoxia logically requires prompt replenishment of glycogen, a process whose regulation is not fully understood. To examine this, we imposed a defined hypoxic stimulus on the rat heart while varying its workload. In intact rats, hypoxia reduced myocardial glycogen approximately 30% and increased both the fraction of glycogen synthase in its physiologically active (GS I) form (from 0.24 +/- 0.06 to 0.82 +/- 0.07; P < 0.005) and glycogen synthesis (from 0.087 +/- 0.011 to 0.375 +/- 0.046 mumol.g-1.min-1; P &l

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20

FRANCH, Jesper, Rune ASLESEN, and Jørgen JENSEN. "Regulation of glycogen synthesis in rat skeletal muscle after glycogen-depleting contractile activity: effects of adrenaline on glycogen synthesis and activation of glycogen synthase and glycogen phosphorylase." Biochemical Journal 344, no. 1 (1999): 231–35. http://dx.doi.org/10.1042/bj3440231.

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We investigated the effects of insulin and adrenaline on the rate of glycogen synthesis in skeletal muscles after electrical stimulation in vitro. The contractile activity decreased the glycogen concentration by 62%. After contractile activity, the glycogen stores were fully replenished at a constant and high rate for 3 h when 10 m-i.u./ml insulin was present. In the absence of insulin, only 65% of the initial glycogen stores was replenished. Adrenaline decreased insulin-stimulated glycogen synthesis. Surprisingly, adrenaline did not inhibit glycogen synthesis stimulated by glycogen-depleting

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21

Talmadge, R. J., and H. Silverman. "Glyconeogenic and glycogenic enzymes in chronically active and normal skeletal muscle." Journal of Applied Physiology 71, no. 1 (1991): 182–91. http://dx.doi.org/10.1152/jappl.1991.71.1.182.

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The chronically active (pseudomyotonic) gastrocnemius muscle in the C57B16J dy2J/dy2J mouse contains both elevated lactate and glycogen as well as fibers that have high amounts of glycogen and enhanced glyconeogenic activity. In the present study we analyze the activities of some key glyconeogenic enzymes to assess the causes of elevated muscle glycogen and to determine the pathway for glycogen synthesis from lactate. Glycogen synthase, malate dehydrogenase, phosphoenolpyruvate carboxykinase, and malic enzyme were all elevated in homogenates of the chronically active muscle. Activities of glyc

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Wilson, Wayne A., Michael P. Boyer, Keri D. Davis, Michael Burke, and Peter J. Roach. "The subcellular localization of yeast glycogen synthase is dependent upon glycogen content." Canadian Journal of Microbiology 56, no. 5 (2010): 408–20. http://dx.doi.org/10.1139/w10-027.

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The budding yeast, Saccharomyces cerevisiae , accumulates the storage polysaccharide glycogen in response to nutrient limitation. Glycogen synthase, the major form of which is encoded by the GSY2 gene, catalyzes the key regulated step in glycogen storage. Here, we utilized Gsy2p fusions to green fluorescent protein (GFP) to determine where glycogen synthase was located within cells. We demonstrated that the localization pattern of Gsy2-GFP depended upon the glycogen content of the cell. When glycogen was abundant, Gsy2-GFP was found uniformly throughout the cytoplasm, but under low glycogen co

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Shiose, Keisuke, Yosuke Yamada, Keiko Motonaga, and Hideyuki Takahashi. "Muscle glycogen depletion does not alter segmental extracellular and intracellular water distribution measured using bioimpedance spectroscopy." Journal of Applied Physiology 124, no. 6 (2018): 1420–25. http://dx.doi.org/10.1152/japplphysiol.00666.2017.

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Although each gram of glycogen is well known to bind 2.7–4.0 g of water, no studies have been conducted on the effect of muscle glycogen depletion on body water distribution. We investigated changes in extracellular and intracellular water (ECW and ICW) distribution in each body segment in muscle glycogen-depletion and glycogen-recovery condition using segmental bioimpedance spectroscopy technique (BIS). Twelve male subjects consumed 7.0 g/kg body mass of indigestible (glycogen-depleted group) or digestible (glycogen-recovered group) carbohydrate for 24 h after a glycogen-depletion cycling exe

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Ragano-Caracciolo, Maria, William K. Berlin, Mill W. Miller, and John A. Hanover. "Nuclear Glycogen and Glycogen Synthase Kinase 3." Biochemical and Biophysical Research Communications 249, no. 2 (1998): 422–27. http://dx.doi.org/10.1006/bbrc.1998.9159.

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Vardanis, Alexander. "Particulate glycogen of mammalian liver: specificity in binding phosphorylase and glycogen synthase." Biochemistry and Cell Biology 70, no. 7 (1992): 523–27. http://dx.doi.org/10.1139/o92-081.

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The glycogen particle – glycogen metabolizing enzyme complex was investigated to gain some understanding of its physiological significance. Fractionations of populations of particles from mouse liver were carried out utilising open column and high performance liquid chromatography, and based either on the molecular weight of the particles or the hydrophobic interactions of the glycogen-associated proteins. The activities of glycogen phosphorylase and glycogen synthase were measured in these fractions. Fractionations were of tissue in different stages of glycogen deposition or mobilization. In

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Shearer, Jane, and Terry E. Graham. "New Perspectives on the Storage and Organization of Muscle Glycogen." Canadian Journal of Applied Physiology 27, no. 2 (2002): 179–203. http://dx.doi.org/10.1139/h02-012.

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Due to its large mass, skeletal muscle contains the largest depot of stored carbohydrate in the body in the form of muscle glycogen. Readily visualized by the electron microscope, glycogen granules appear as bead-like structures localized to specific subcellular locales. Each glycogen granule is a functional unit, not only containing carbohydrate, but also enzymes and other proteins needed for its metabolism. These proteins are not static, but rather associate and dissociate depending on the carbohydrate balance in the muscle. This review examines glycogen-associated proteins, their interactio

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Pfeiffer-Guglielmi, Brigitte, and Ralf-Peter Jansen. "The Motor Neuron-Like Cell Line NSC-34 and Its Parent Cell Line N18TG2 Have Glycogen that is Degraded Under Cellular Stress." Neurochemical Research 46, no. 6 (2021): 1567–76. http://dx.doi.org/10.1007/s11064-021-03297-y.

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AbstractBrain glycogen has a long and versatile history: Primarily regarded as an evolutionary remnant, it was then thought of as an unspecific emergency fuel store. A dynamic role for glycogen in normal brain function has been proposed later but exclusively attributed to astrocytes, its main storage site. Neuronal glycogen had long been neglected, but came into focus when sensitive technical methods allowed quantification of glycogen at low concentration range and the detection of glycogen metabolizing enzymes in cells and cell lysates. Recently, an active role of neuronal glycogen and even i

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Jensen, Jørgen, Einar Jebens, Erlend O. Brennesvik, et al. "Muscle glycogen inharmoniously regulates glycogen synthase activity, glucose uptake, and proximal insulin signaling." American Journal of Physiology-Endocrinology and Metabolism 290, no. 1 (2006): E154—E162. http://dx.doi.org/10.1152/ajpendo.00330.2005.

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Insulin-stimulated glucose uptake and incorporation of glucose into skeletal muscle glycogen contribute to physiological regulation of blood glucose concentration. In the present study, glucose handling and insulin signaling in isolated rat muscles with low glycogen (LG, 24-h fasting) and high glycogen (HG, refed for 24 h) content were compared with muscles with normal glycogen (NG, rats kept on their normal diet). In LG, basal and insulin-stimulated glycogen synthesis and glycogen synthase activation were higher and glycogen synthase phosphorylation (Ser645, Ser649, Ser653, Ser657) lower than

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Napit, Prabhat R., Abdulrahman Alhamyani, Khaggeswar Bheemanapally, Paul W. Sylvester, and Karen P. Briski. "Sex-Dimorphic Glucocorticoid Receptor Regulation of Hypothalamic Primary Astrocyte Glycogen Metabolism: Interaction with Norepinephrine." Neuroglia 3, no. 4 (2022): 144–57. http://dx.doi.org/10.3390/neuroglia3040010.

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Astrocyte glycogen is a critical metabolic variable that affects hypothalamic control of glucostasis. Glucocorticoid hormones regulate peripheral glycogen, but their impact on hypothalamic glycogen is not known. A hypothalamic astrocyte primary culture model was used to investigate the premise that glucocorticoids impose sex-dimorphic independent and interactive control of glycogen metabolic enzyme protein expression and glycogen accumulation. The glucocorticoid receptor (GR) agonist dexamethasone (DEX) down-regulated glycogen synthase (GS), glycogen phosphorylase (GP)–brain type (GPbb), and G

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Montell, Eulàlia, Alexandra Arias, and Anna M. Gómez-Foix. "Glycogen depletion rather than glucose 6-P increments controls early glycogen recovery in human cultured muscle." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 5 (1999): R1489—R1495. http://dx.doi.org/10.1152/ajpregu.1999.276.5.r1489.

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In glycogen-containing muscle, glycogenesis appears to be controlled by glucose 6-phosphate (6- P) provision, but after glycogen depletion, an autoinhibitory control of glycogen could be a determinant. We analyzed in cultured human muscle the contribution of glycogen depletion versus glucose 6- P in the control of glycogen recovery. Acute deglycogenation was achieved by engineering cells to overexpress glycogen phosphorylase (GP). Cells treated with AdCMV-MGP adenovirus to express 10 times higher active GP showed unaltered glycogen relative to controls at 25 mM glucose, but responded to 6-h gl

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Allen, Tara J., and Christopher D. Hardin. "Influence of glycogen storage on vascular smooth muscle metabolism." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 6 (2000): H1993—H2002. http://dx.doi.org/10.1152/ajpheart.2000.278.6.h1993.

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The role of glycogen as an oxidative substrate for vascular smooth muscle (VSM) remains controversial. To elucidate the importance of glycogen as an oxidative substrate and the influence of glycogen flux on VSM substrate selection, we systematically altered glycogen levels and measured metabolism of glucose, acetate, and glycogen. Hog carotid arteries with glycogen contents ranging from 1 to 11 μmol/g were isometrically contracted in physiological salt solution containing 5 mM [1-13C]glucose and 1 mM [1,2-13C]acetate at 37°C for 6 h. [1-13C]glucose, [1,2-13C]acetate, and glycogen oxidation wer

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Henriksen, E. J., C. R. Kirby, and M. E. Tischler. "Glycogen supercompensation in rat soleus muscle during recovery from nonweight bearing." Journal of Applied Physiology 66, no. 6 (1989): 2782–87. http://dx.doi.org/10.1152/jappl.1989.66.6.2782.

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The time course of glycogen changes in soleus muscle recovering from 3 days of nonweight bearing by hindlimb suspension was investigated. Within 15 min and up to 2 h, muscle glycogen decreased. Coincidentally, muscle glucose 6-phosphate and the fractional activity of glycogen phosphorylase, measured at the fresh muscle concentrations of AMP, increased. Increased fractional activity of glycogen synthase during this time was likely the result of greater glucose 6-phosphate and decreased glycogen. From 2 to 4 h, when the synthase activity remained elevated and the phosphorylase activity declined,

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Kolnes, Anders J., Jesper B. Birk, Einar Eilertsen, Jorid T. Stuenæs, Jørgen F. P. Wojtaszewski, and Jørgen Jensen. "Epinephrine-stimulated glycogen breakdown activates glycogen synthase and increases insulin-stimulated glucose uptake in epitrochlearis muscles." American Journal of Physiology-Endocrinology and Metabolism 308, no. 3 (2015): E231—E240. http://dx.doi.org/10.1152/ajpendo.00282.2014.

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Epinephrine increases glycogen synthase (GS) phosphorylation and decreases GS activity but also stimulates glycogen breakdown, and low glycogen content normally activates GS. To test the hypothesis that glycogen content directly regulates GS phosphorylation, glycogen breakdown was stimulated in condition with decreased GS activation. Saline or epinephrine (0.02 mg/100 g rat) was injected subcutaneously in Wistar rats (∼130 g) with low (24-h-fasted), normal (normal diet), and high glycogen content (fasted-refed), and epitrochlearis muscles were removed after 3 h and incubated ex vivo, eliminati

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Ortmeyer, Heidi K., and Noni L. Bodkin. "Lack of defect in insulin action on hepatic glycogen synthase and phosphorylase in insulin-resistant monkeys." American Journal of Physiology-Gastrointestinal and Liver Physiology 274, no. 6 (1998): G1005—G1010. http://dx.doi.org/10.1152/ajpgi.1998.274.6.g1005.

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It is well known that an alteration in insulin activation of skeletal muscle glycogen synthase is associated with insulin resistance. To determine whether this defect in insulin action is specific to skeletal muscle, or also present in liver, simultaneous biopsies of these tissues were obtained before and during a euglycemic hyperinsulinemic clamp in spontaneously obese insulin-resistant male rhesus monkeys. The activities of glycogen synthase and glycogen phosphorylase and the concentrations of glucose 6-phosphate and glycogen were measured. There were no differences between basal and insulin

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Lynch, R. M., C. P. Kuettner, and R. J. Paul. "Glycogen metabolism during tension generation and maintenance in vascular smooth muscle." American Journal of Physiology-Cell Physiology 257, no. 4 (1989): C736—C742. http://dx.doi.org/10.1152/ajpcell.1989.257.4.c736.

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To study the regulation of glycogen utilization in vascular smooth muscle, we measured the content of glycogen and glucose 6-phosphate and the activity of the glycogen phosphorylase and glycogen debrancher enzymes in porcine carotid artery. During active contraction, the rates of glycogen phosphorylase and glycogenolysis were as high as expected. Despite this, glycogen content did not decrease to less than approximately 50% of control levels even after sustained contractions. The activity of glycogen debrancher enzyme was found to be limiting glycogen utilization at this point. Although glycog

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Wu, Chien-Yu, Tsung-Han Lee, and Deng-Yu Tseng. "Glucocorticoid Receptor Mediates Cortisol Regulation of Glycogen Metabolism in Gills of the Euryhaline Tilapia (Oreochromis mossambicus)." Fishes 8, no. 5 (2023): 267. http://dx.doi.org/10.3390/fishes8050267.

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In this study, we investigated the effects of cortisol on the regulation of the glycogen metabolism biomarkers glycogen synthase (GS) and glycogen phosphorylase (GP) in the glycogen-rich cells of the gills of tilapia (Oreochromis mossambicus). In the gills of tilapia, GP, GS, and glycogen were immunocytochemically colocalized in a specific group of glycogen-rich cells adjacent to the gills’ main ionocytes and mitochondria-rich cells. Cortisol plays a vital role in the regulation of physiological functions in animals, including energy metabolism, respiration, immune response, and ion regulation

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Pérez-Torrado, R., J. V. Gimeno-Alcañiz, and E. Matallana. "Wine Yeast Strains Engineered for Glycogen Overproduction Display Enhanced Viability under Glucose Deprivation Conditions." Applied and Environmental Microbiology 68, no. 7 (2002): 3339–44. http://dx.doi.org/10.1128/aem.68.7.3339-3344.2002.

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ABSTRACT We used metabolic engineering to produce wine yeasts with enhanced resistance to glucose deprivation conditions. Glycogen metabolism was genetically modified to overproduce glycogen by increasing the glycogen synthase activity and eliminating glycogen phosphorylase activity. All of the modified strains had a higher glycogen content at the stationary phase, but accumulation was still regulated during growth. Strains lacking GPH1, which encodes glycogen phosphorylase, are unable to mobilize glycogen. Enhanced viability under glucose deprivation conditions occurs when glycogen accumulate

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Udoh, Uduak S., Telisha M. Swain, Ashley N. Filiano, Karen L. Gamble, Martin E. Young, and Shannon M. Bailey. "Chronic ethanol consumption disrupts diurnal rhythms of hepatic glycogen metabolism in mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 308, no. 11 (2015): G964—G974. http://dx.doi.org/10.1152/ajpgi.00081.2015.

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Chronic ethanol consumption has been shown to significantly decrease hepatic glycogen content; however, the mechanisms responsible for this adverse metabolic effect are unknown. In this study, we examined the impact chronic ethanol consumption has on time-of-day-dependent oscillations (rhythms) in glycogen metabolism processes in the liver. For this, male C57BL/6J mice were fed either a control or ethanol-containing liquid diet for 5 wk, and livers were collected every 4 h for 24 h and analyzed for changes in various genes and proteins involved in hepatic glycogen metabolism. Glycogen displaye

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Swanson, Raymond A. "Physiologic coupling of glial glycogen metabolism to neuronal activity in brain." Canadian Journal of Physiology and Pharmacology 70, S1 (1992): S138—S144. http://dx.doi.org/10.1139/y92-255.

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Brain glycogen is localized almost exclusively to glia, where it undergoes continuous utilization and resynthesis. We have shown that glycogen utilization increases during tactile stimulation of the rat face and vibrissae. Conversely, decreased neuronal activity during hibernation and anesthesia is accompanied by a marked increase in brain glycogen content. These observations support a link between neuronal activity and glial glycogen metabolism. The energetics of glycogen metabolism suggest that glial glycogen is mobilized to meet increased metabolic demands of glia rather than to serve as a

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Roach, Peter J., Anna A. Depaoli-Roach, Thomas D. Hurley, and Vincent S. Tagliabracci. "Glycogen and its metabolism: some new developments and old themes." Biochemical Journal 441, no. 3 (2012): 763–87. http://dx.doi.org/10.1042/bj20111416.

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Glycogen is a branched polymer of glucose that acts as a store of energy in times of nutritional sufficiency for utilization in times of need. Its metabolism has been the subject of extensive investigation and much is known about its regulation by hormones such as insulin, glucagon and adrenaline (epinephrine). There has been debate over the relative importance of allosteric compared with covalent control of the key biosynthetic enzyme, glycogen synthase, as well as the relative importance of glucose entry into cells compared with glycogen synthase regulation in determining glycogen accumulati

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Saez, Isabel, Jordi Duran, Christopher Sinadinos, et al. "Neurons Have an Active Glycogen Metabolism that Contributes to Tolerance to Hypoxia." Journal of Cerebral Blood Flow & Metabolism 34, no. 6 (2014): 945–55. http://dx.doi.org/10.1038/jcbfm.2014.33.

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Glycogen is present in the brain, where it has been found mainly in glial cells but not in neurons. Therefore, all physiologic roles of brain glycogen have been attributed exclusively to astrocytic glycogen. Working with primary cultured neurons, as well as with genetically modified mice and flies, here we report that—against general belief—neurons contain a low but measurable amount of glycogen. Moreover, we also show that these cells express the brain isoform of glycogen Phosphorylase, allowing glycogen to be fully metabolized. Most importantly, we show an active neuronal glycogen metabolism

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Huang, D., I. Farkas, and P. J. Roach. "Pho85p, a cyclin-dependent protein kinase, and the Snf1p protein kinase act antagonistically to control glycogen accumulation in Saccharomyces cerevisiae." Molecular and Cellular Biology 16, no. 8 (1996): 4357–65. http://dx.doi.org/10.1128/mcb.16.8.4357.

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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 PHO

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Shearer, Jane, Karen D. Ross, Curtis C. Hughey, Virginia L. Johnsen, Dustin S. Hittel, and David L. Severson. "Exercise training does not correct abnormal cardiac glycogen accumulation in the db/db mouse model of type 2 diabetes." American Journal of Physiology-Endocrinology and Metabolism 301, no. 1 (2011): E31—E39. http://dx.doi.org/10.1152/ajpendo.00525.2010.

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Substrate imbalance is a well-recognized feature of diabetic cardiomyopathy. Insulin resistance effectively limits carbohydrate oxidation, resulting in abnormal cardiac glycogen accumulation. Aims of the present study were to 1) characterize the role of glycogen-associated proteins involved in excessive glycogen accumulation in type 2 diabetic hearts and 2) determine if exercise training can attenuate abnormal cardiac glycogen accumulation. Control ( db+) and genetically diabetic ( db/db) C57BL/KsJ-lepr db/lepr db mice were subjected to sedentary or treadmill exercise regimens. Exercise traini

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Greenberg, Cynthia C., Arpad M. Danos, and Matthew J. Brady. "Central Role for Protein Targeting to Glycogen in the Maintenance of Cellular Glycogen Stores in 3T3-L1 Adipocytes." Molecular and Cellular Biology 26, no. 1 (2006): 334–42. http://dx.doi.org/10.1128/mcb.26.1.334-342.2006.

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ABSTRACT Overexpression of the protein phosphatase 1 (PP1) subunit protein targeting to glycogen (PTG) markedly enhances cellular glycogen levels. In order to disrupt the endogenous PTG-PP1 complex, small interfering RNA (siRNA) constructs against PTG were identified. Infection of 3T3-L1 adipocytes with PTG siRNA adenovirus decreased PTG mRNA and protein levels by >90%. In parallel, PTG reduction resulted in a >85% decrease in glycogen levels 4 days after infection, supporting a critical role for PTG in glycogen metabolism. Total PP1, glycogen synthase, and GLUT4 levels, as well as insul

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HORI, Keiichi, Hiroshi NARITA, and Masanao SAIO. "A case of glycogen-rich clear cell carcinoma of the breast." Nihon Rinsho Geka Gakkai Zasshi (Journal of Japan Surgical Association) 69, no. 9 (2008): 2173–77. http://dx.doi.org/10.3919/jjsa.69.2173.

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McNulty, P. H., A. Darling, and J. M. Whiting. "Glycogen depletion contributes to ischemic preconditioning in the rat heart in vivo." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 6 (1996): H2283—H2289. http://dx.doi.org/10.1152/ajpheart.1996.271.6.h2283.

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Ischemic preconditioning depletes the myocardium of glycogen, thus blunting lactic acidosis during subsequent episodes of ischemia. Preconditioning also protects against reperfusion arrhythmias and infarction. To test whether glycogen depletion is necessary for this ischemic tolerance, we preconditioned two groups of intact rats with a series of 3-min coronary artery occlusions. In one group, preconditioning lowered the glycogen concentration of the ischemic region by approximately 50% (24.9 +/- 2.5 to 12.5 +/- 1.8 mumol/g; P < 0.01). In the other, the heart was first loaded with glycogen v

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Nitschke, Silvia, Sara Petković, Saija Ahonen, Berge A. Minassian та Felix Nitschke. "Sensitive quantification of α-glucans in mouse tissues, cell cultures, and human cerebrospinal fluid". Journal of Biological Chemistry 295, № 43 (2020): 14698–709. http://dx.doi.org/10.1074/jbc.ra120.015061.

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The soluble α-polyglucan glycogen is a central metabolite enabling transient glucose storage to suit cellular energy needs. Glycogen storage diseases (GSDs) comprise over 15 entities caused by generalized or tissue-specific defects in enzymes of glycogen metabolism. In several, e.g. in Lafora disease caused by the absence of the glycogen phosphatase laforin or its interacting partner malin, degradation-resistant abnormally structured insoluble glycogen accumulates. Sensitive quantification methods for soluble and insoluble glycogen are critical to research, including therapeutic studies, in su

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Shiose, Keisuke, Hideyuki Takahashi, and Yosuke Yamada. "Muscle Glycogen Assessment and Relationship with Body Hydration Status: A Narrative Review." Nutrients 15, no. 1 (2022): 155. http://dx.doi.org/10.3390/nu15010155.

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Muscle glycogen is a crucial energy source for exercise, and assessment of muscle glycogen storage contributes to the adequate manipulation of muscle glycogen levels in athletes before and after training and competition. Muscle biopsy is the traditional and gold standard method for measuring muscle glycogen; alternatively, 13C magnetic resonance spectroscopy (MRS) has been developed as a reliable and non-invasive method. Furthermore, outcomes of ultrasound and bioimpedance methods have been reported to change in association with muscle glycogen conditions. The physiological mechanisms underlyi

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Youn, J. H., and R. N. Bergman. "Patterns of glycogen turnover in liver characterized by computer modeling." American Journal of Physiology-Endocrinology and Metabolism 253, no. 4 (1987): E360—E369. http://dx.doi.org/10.1152/ajpendo.1987.253.4.e360.

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We used a computer model of liver glycogen turnover to reexamine the data of Devos and Hers, who reported the time course of accumulation in and loss from glycogen of label originating in [1-14C]galactose injected at different times after the start of refeeding of 40-h fasted mice or rats. In the present study computer representation of individual glycogen molecules was utilized to account for growth and degradation of glycogen according to specific hypothetical patterns. Using this model we could predict the accumulation and localization within glycogen of labeled glucose residues and compare

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Choi, Hyungseok, In-Seok Yeo, Godfrey Mwiti, et al. "Optimization of Microbial Glycogen Production by Saccharomyces cerevisiae CEY1." Fermentation 10, no. 8 (2024): 388. http://dx.doi.org/10.3390/fermentation10080388.

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Glycogen is a highly branched polyglucan utilized as a carbohydrate reserve in major living systems. Industrially, it is used as a prebiotic and in the nanoencapsulation of drugs and nutraceuticals. In this study, optimal fermentation conditions enabling the highest glycogen accumulation in Saccharomyces cerevisiae were experimentally evaluated for possible mass production. Production efficiency was assessed by comparing specific growth rates, specific glycogen production rates, and glycogen yields under each condition. The results demonstrated that fermentation at 30 °C with an aeration rate

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