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Journal articles on the topic 'Glycogène'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 January 2025

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1

Jimenez, Liliana. "Régime hyperlipidique et glycogène musculaire." Science & Sports 14, no. 3 (May 1999): 157. http://dx.doi.org/10.1016/s0765-1597(99)80061-6.

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2

Péronnet, François, Bruce Jacks, Guy Thibault, Hélène Perrault, and Daniel Cousineau. "Contrôle de l'activité du système sympathique à l'exercice prolongé : rôle de la glycémie." STAPS 6, no. 11 (1985): 47–56. http://dx.doi.org/10.3406/staps.1985.1429.

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Chez le Chien à l’exercice prolongé sous sotatol, la réponse de la catécholaminémie qui est plus importante chez le Chien normal apparaît reliée à la chute marquée de la glycémie. Il en est de même chez l’homme effectuant un exercice prolongé avec des réserves de glycogène basses. Au contraire, lorsque les réserves de glycogène sont normales ou élevées, la glycémie ne subit pas de chute significative et la catécholaminémie est moins haute que lorsque les réserves de glycogène sont basses. De la même façon l’administration régulière de glucose par voie orale au cours d’un exercice prolongé limite la chute de la glycémie et réduit considérablement la réponse sympathique. Cette réduction affecte la concentration plasmatique d’adrénaline et de noradrénaline. Ces observations, qui sont concordantes avec d’autres données rapportées dans la littérature confirment que la glycémie participe au contrôle de l’activité sympathique au cours de l’exercice prolongé.
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3

Mayeuf-Louchart, Alicia, and Hélène Duez. "Du glycogène à la gouttelette lipidique." médecine/sciences 36, no. 6-7 (June 2020): 577–79. http://dx.doi.org/10.1051/medsci/2020102.

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4

Hickner, RC, JS Fischer, and PA Hansen. "Resynthèse du glycogène musculaire chez le sportif." Science & Sports 13, no. 2 (January 1998): 98. http://dx.doi.org/10.1016/s0765-1597(97)86911-0.

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5

Chiasson, JL, P. Dupuis, and AK Srivastava. "Métabolisme anormal du glycogène musculaire dans le diabète." médecine/sciences 7, no. 4 (1991): 368. http://dx.doi.org/10.4267/10608/4362.

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6

C., M. "Neurones : la synthèse du glycogène est strictement inhibée." Revue Médicale Suisse 3, no. 131 (2007): 2510. http://dx.doi.org/10.53738/revmed.2007.3.131.2510_2.

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7

HOCQUETTE, J. F., I. ORTIGUES-MARTY, M. DAMON, P. HERPIN, and Y. GEAY. "Métabolisme énergétique des muscles squelettiques chez les animaux producteurs de viande." INRAE Productions Animales 13, no. 3 (June 18, 2000): 185–200. http://dx.doi.org/10.20870/productions-animales.2000.13.3.3780.

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Le muscle est d’importance économique majeure chez les animaux producteurs de viande. Ses principales fonctions physiologiques sont la thermogenèse, la posture et l’activité physique de l’animal. Ces fonctions et la croissance du muscle ont des besoins spécifiques en énergie, entraînant parfois des compétitions pour l’utilisation des différents nutriments. Ces régulations métaboliques modifient les efficacités de production et d’utilisation de l’ATP, et certaines caractéristiques musculaires déterminantes pour les qualités de la viande. Par exemple, un métabolisme musculaire plus glycolytique est associé à une meilleure utilisation du glucose, à une plus grande sensibilité du muscle à l’insuline, à un développement accru du muscle, à une réduction de ses dépenses énergétiques, et à une augmentation de sa teneur en glycogène. L’amélioration de la croissance musculaire par la sélection génétique induit un métabolisme musculaire moins oxydatif avec, comme conséquence, moins de lipides intramusculaires. Une augmentation des apports énergétiques favorise les dépôts de protéines, de glycogène et de lipides intramusculaires. Toutefois, des apports excessifs induisent une résistance du muscle à l’insuline favorisant le développement des tissus adipeux de la carcasse. Le turnover des nutriments et leur répartition entre les voies anaboliques (lipogenèse, glycogenèse) ou cataboliques (glycolyse, lipolyse, oxydation) intramusculaires restent à préciser. L’activité physique des animaux et la lutte contre le froid modifient les caractéristiques musculaires en favorisant le métabolisme oxydatif. La question qui se pose aujourd’hui est donc : l’optimisation des efficacités de production et d’utilisation de l’ATP est-elle compatible avec l’amélioration des qualités de la viande, déterminées notamment par les taux de glycogène et de lipides intramusculaire.
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8

Burlet-Godinot, Sophie, Pierre Magistretti, and Jean-Marie Petit. "Glycogène cérébral et sommeil : une régulation à sens unique ?" Médecine du Sommeil 13, no. 1 (January 2016): 48–49. http://dx.doi.org/10.1016/j.msom.2016.01.045.

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9

LARZUL, C., P. E ROY, G. MONIN, and P. SELLIER. "Variabilité génétique du potentiel glycolytique du muscle chez le porc." INRAE Productions Animales 11, no. 3 (June 3, 1998): 183–97. http://dx.doi.org/10.20870/productions-animales.1998.11.3.3937.

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Le potentiel glycolytique du muscle (PG) se réfère à la teneur en glycogène musculaire chez l’animal vivant et est défini comme le potentiel de production d’acide lactique lors de la glycolyse post mortem. Le PG varie selon le muscle considéré : il est plus fort dans les muscles de type blanc que dans les muscles de type rouge. La valeur du PG dépend aussi du moment de la mesure : elle est plus élevée lorsque le muscle est prélevé par biopsie sur l’animal au repos que lorsqu’il est prélevé sur la carcasse dans l’heure qui suit l’abattage. Une relation de type linéaire puis en plateau lie le pH ultime au PG, et la valeur-seuil de PG au-delà de laquelle le pH ultime reste constant dépend du muscle considéré. La valeur du PG est très fortement influencée par le gène majeur RN (viande acide), qui est à l’origine de la position très particulière occupée de ce point de vue par la race Hampshire ("effet Hampshire"). L’allèle RN-, responsable de l’augmentation substantielle (+ 70 %) de la teneur en glycogène des muscles de type blanc rapide (Long dorsal par exemple), est presque complètement dominant. En dehors du gène RN, le PG présente une variabilité polygénique appréciable (héritabilité de 20-25 %). Ce caractère est lié positivement au rapport muscle/gras de la carcasse et à la teneur en glycogène résiduel de la viande. Il est lié négativement au pH ultime et au rendement à la cuisson de la viande. Les animaux porteurs de l’allèle RN-se caractérisent par une forte élévation du rapport eau/protéines du muscle. Plusieurs faits indiquent que le métabolisme énergétique du muscle est à tendance plus oxydative chez les animaux à PG génétiquement plus fort. Le potentiel glycolytique du muscle, caractère mesurable chez l’animal vivant (sur une biopsie du Long dorsal), est un critère de sélection à prendre en considération pour l’amélioration génétique de la qualité de la viande de porc.
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10

Pérés, Gilbert. "Approche biologique : la récupération des réserves de glycogène après l'exercice d'endurance." Les Cahiers de l'INSEP 14, no. 1 (1996): 67–73. http://dx.doi.org/10.3406/insep.1996.1166.

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11

Paulin, A., M. Lord, M. Nadeau, and J. M. Lavoie. "Influence du niveau de glycogène hépatique sur le métabolisme à l'exercice: effets d'une vagotomie hépatique." Science & Sports 2, no. 3 (November 1987): 231–32. http://dx.doi.org/10.1016/s0765-1597(87)80063-1.

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12

Grably, S., M. Verdys, and A. Rossi. "Activités des enzymes du métabolisme du glycogène cardiaque: Etude dans un protocole d'hypoxiein situchez le rat." Archives Internationales de Physiologie et de Biochimie 97, no. 2 (January 1989): 185–96. http://dx.doi.org/10.3109/13813458909104538.

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13

MILAN, D., A. ROBIC, P. CHARDON, N. IANNUCCELLI, J. C. CARITEZ, M. YERLE, J. GELLIN, et al. "Exemple de cartographie fine : le cas du gène RN chez le porc." INRAE Productions Animales 13, HS (December 22, 2000): 137–39. http://dx.doi.org/10.20870/productions-animales.2000.13.hs.3825.

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En 1986, un gène majeur ayant un effet défavorable sur le rendement à la cuisson de la viande de porc a été mis en évidence. La constitution de familles informatives nous a permis de cartographier ce gène appelé RN sur le chromosome 15. Pour identifier le gène RN, nous avons successivement réalisé : la cartographie génétique fine de RN, la cartographie cytogénétique de marqueurs proches, des études de carte comparée, le développement de cartes d’irradiation de la région de RN chez le porc et chez l’Homme, le développement d’un contig de BAC couvrant près de 2 Mb, le développement d’une carte du déséquilibre de liaison de la région de RN chez le porc, le séquençage d’un BAC contenant le gène RN, l’identification d’un gène encore inconnu membre d’une famille de gènes impliqués dans le métabolisme du glucose/glycogène, l’identification d’une mutation causale dans la séquence codante de ce gène.
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14

Ferry, A., I. Amiridis, and M. Rieu. "Aptitudes différentes des muscles squelettiques du rat à resynthétiser leur glycogène: effet de l'entraînement et de l'insuline." Science & Sports 6, no. 1 (March 1991): 37–42. http://dx.doi.org/10.1016/s0765-1597(05)80233-3.

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15

Martinez-Morales, Patricia, Irene Morán Cruz, Lorena Roa-de la Cruz, Paola Maycotte, Juan Salvador Reyes Salinas, Victor Javier Vazquez Zamora, Claudia Teresita Gutierrez Quiroz, Alvaro Jose Montiel-Jarquin, and Verónica Vallejo-Ruiz. "Hallmarks of glycogene expression and glycosylation pathways in squamous and adenocarcinoma cervical cancer." PeerJ 9 (August 31, 2021): e12081. http://dx.doi.org/10.7717/peerj.12081.

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Background Dysregulation of glycogene expression in cancer can lead to aberrant glycan expression, which can promote tumorigenesis. Cervical cancer (CC) displays an increased expression of glycogenes involved in sialylation and sialylated glycans. Here, we show a comprehensive analysis of glycogene expression in CC to identify glycogene expression signatures and the possible glycosylation pathways altered. Methods First, we performed a microarray expression assay to compare glycogene expression changes between normal and cervical cancer tissues. Second, we used 401 glycogenes to analyze glycogene expression in adenocarcinoma and squamous carcinoma from RNA-seq data at the cBioPortal for Cancer Genomics. Results The analysis of the microarray expression assay indicated that CC displayed an increase in glycogenes related to GPI-anchored biosynthesis and a decrease in genes associated with chondroitin and dermatan sulfate with respect to normal tissue. Also, the glycogene analysis of CC samples by the RNA-seq showed that the glycogenes involved in the chondroitin and dermatan sulfate pathway were downregulated. Interestingly the adenocarcinoma tumors displayed a unique glycogene expression signature compared to squamous cancer that shows heterogeneous glycogene expression divided into six types. Squamous carcinoma type 5 (SCC-5) showed increased expression of genes implicated in keratan and heparan sulfate synthesis, glycosaminoglycan degradation, ganglio, and globo glycosphingolipid synthesis was related to poorly differentiated tumors and poor survival. Squamous carcinoma type 6 (SCC-6) displayed an increased expression of genes involved in chondroitin/dermatan sulfate synthesis and lacto and neolacto glycosphingolipid synthesis and was associated with nonkeratinizing squamous cancer and good survival. In summary, our study showed that CC tumors are not a uniform entity, and their glycome signatures could be related to different clinicopathological characteristics.
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16

Groth, Theodore, Rudiyanto Gunawan, and Sriram Neelamegham. "A systems-based framework to computationally describe putative transcription factors and signaling pathways regulating glycan biosynthesis." Beilstein Journal of Organic Chemistry 17 (July 22, 2021): 1712–24. http://dx.doi.org/10.3762/bjoc.17.119.

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Glycosylation is a common posttranslational modification, and glycan biosynthesis is regulated by a set of glycogenes. The role of transcription factors (TFs) in regulating the glycogenes and related glycosylation pathways is largely unknown. In this work, we performed data mining of TF–glycogene relationships from the Cistrome Cancer database (DB), which integrates chromatin immunoprecipitation sequencing (ChIP-Seq) and RNA-Seq data to constitute regulatory relationships. In total, we observed 22,654 potentially significant TF–glycogene relationships, which include interactions involving 526 unique TFs and 341 glycogenes that span 29 the Cancer Genome Atlas (TCGA) cancer types. Here, TF–glycogene interactions appeared in clusters or so-called communities, suggesting that changes in single TF expression during both health and disease may affect multiple carbohydrate structures. Upon applying the Fisher’s exact test along with glycogene pathway classification, we identified TFs that may specifically regulate the biosynthesis of individual glycan types. Integration with Reactome DB knowledge provided an avenue to relate cell-signaling pathways to TFs and cellular glycosylation state. Whereas analysis results are presented for all 29 cancer types, specific focus is placed on human luminal and basal breast cancer disease progression. Overall, the article presents a computational approach to describe TF–glycogene relationships, the starting point for experimental system-wide validation.
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17

Moreau, F., E. Auroux, E. Seyfritz, S. Ros, W. Bietiger, M. Pinget, N. Jeandidier, S. Sigrist, and L. Kessler. "P1052 Contenus du foie en triglycérides et glycogène et régénération hépatique dans un modèle de diabète insulinopénique induit par la streptozotocine." Diabetes & Metabolism 39 (March 2013): A44. http://dx.doi.org/10.1016/s1262-3636(13)71798-1.

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18

TESSERAUD, S., I. BOUVAREL, P. FRAYSSE, S. MÉTAYERCOUSTARD, A. COLLIN, M. LESSIRE, and C. BERRI. "Optimiser la composition corporelle et la qualité des viandes de volailles en modulant le métabolisme par les acides aminés alimentaires." INRAE Productions Animales 27, no. 5 (December 12, 2014): 337–46. http://dx.doi.org/10.20870/productions-animales.2014.27.5.3081.

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Pour optimiser la composition corporelle et la qualité des viandes tout en garantissant l’efficacité des systèmes de production, il faut comprendre et maîtriser les mécanismes régulant l'utilisation métabolique des nutriments. Dans cette synthèse, nous présentons les généralités concernant la régulation nutritionnelle du métabolisme. Quelques exemples choisis et représentatifs (i.e. apports en protéines et acides aminés, rythme d’apport) sont utilisés pour illustrer ce type de recherche en privilégiant les résultats obtenus lors d’études récentes et en précisant leur intérêt pratique. Nous détaillons leur incidence sur la qualité des produits, et plus généralement l’efficacité des systèmes de production de viande de volaille, au travers d’études impliquant des recherches fondamentales et appliquées. Sont abordés les aspects concernant la composition corporelle et la qualité de la viande en lien avec sa sensibilité à l’oxydation ou avec son pH. Par exemple, chez le poulet, le pH ultime constitue un élément clé dont dépendent plusieurs caractéristiques technologiques et sensorielles de la viande. Il est en grande partie déterminé par la teneur en glycogène du muscle au moment de la mort des animaux, qui dépend entre autres du statut nutritionnel des animaux. Le défi de l’ensemble de ces travaux est de générer des connaissances scientifiques originales, mais aussi de permettre d’optimiser les apports alimentaires (quantitatifs, qualitatifs et rythmes) au cours du développement et en fonction des objectifs de production.
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Pellerin-Massicotte, Jocelyne, Bruno Vincent, and Émilien Pelletier. "Évaluation écotoxicologique de la baie des Anglais à Baie-Comeau (Québec)." Water Quality Research Journal 28, no. 4 (November 1, 1993): 665–86. http://dx.doi.org/10.2166/wqrj.1993.035.

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Résumé La baie des Anglais à Baie-Comeau (Québec) est un site industriel reconnu comme étant contaminé aux hydrocarbures et aux biphényls polychlorés (BPC). Une expérience de transfert à moyen terme de deux bivalves marins, Mya arenaria et Mytilus edulis L., a été réalisée entre un site de référence en aval de la baie des Anglais (Franquelin) et des sites contaminés près de Baie-Comeau suivant un gradient de contamination déterminé selon des données physico-chimiques antérieures. Les analyses chimiques de contaminants ont montré qu’il n’y a pas eu d’enrichissement en hydrocarbures, au mercure et en BPC pour toute la durée du protocole mais, parmi les sondes bioanalytiques choisies pour évaluer l’état de santé de cet écosystème, celles qui se sont avérées les plus sensibles chez Mya arenaria furent le glycogène et les lipides dans les gonades, et pour les deux bivalves, la fragilité de la membrane lysosomale de la glande digestive qui est un excellent indicateur de stress toxique. Les présents résultats sont compatibles avec un modèle qui consisterait à établir une évaluation ecotoxicologique d’un écosystème que l’on soupçonne perturbé par la pollution par (i) l’analyse de la bioaccumulation des substances toxiques que l’on croit présentes dans l’écosystème (hydrocarbures, BPC et métaux lourds) et (ii) l’évaluation des effets physiologiques et biochimiques des polluants à l’aide de sondes bioanalytiques appropriées.
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Cimino, Rita, Sukhvir Kaur Bhangu, Anshul Baral, Muthupandian Ashokkumar, and Francesca Cavalieri. "Ultrasound-Assisted Microencapsulation of Soybean Oil and Vitamin D Using Bare Glycogen Nanoparticles." Molecules 26, no. 17 (August 25, 2021): 5157. http://dx.doi.org/10.3390/molecules26175157.

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Ultrasonically synthesized core-shell microcapsules can be made of synthetic polymers or natural biopolymers, such as proteins and polysaccharides, and have found applications in food, drug delivery and cosmetics. This study reports on the ultrasonic synthesis of microcapsules using unmodified (natural) and biodegradable glycogen nanoparticles derived from various sources, such as rabbit and bovine liver, oyster and sweet corn, for the encapsulation of soybean oil and vitamin D. Depending on their source, glycogen nanoparticles exhibited differences in size and ‘bound’ proteins. We optimized various synthetic parameters, such as ultrasonic power, time and concentration of glycogens and the oil phase to obtain stable core-shell microcapsules. Particularly, under ultrasound-induced emulsification conditions (sonication time 45 s and sonication power 160 W), native glycogens formed microcapsules with diameter between 0.3 μm and 8 μm. It was found that the size of glycogen as well as the protein component play an important role in stabilizing the Pickering emulsion and the microcapsules shell. This study highlights that native glycogen nanoparticles without any further tedious chemical modification steps can be successfully used for the encapsulation of nutrients.
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21

Figeac, F., B. Uzan, B. Portha, and J. Movassat. "P57 L’inhibition de la Glycogène Synthase Kinase 3β stimule la prolifération des cellules β dans le pancréas néonatal du rat. Implication de la voie Wnt/β-caténine." Diabetes & Metabolism 34 (March 2008): H58. http://dx.doi.org/10.1016/s1262-3636(08)72969-0.

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22

Beauvieux, M. C., P. Couzigou, H. Gin, V. Rigalleau, and J. L. Gallis. "P175 Les flux unidirectionnels du métabolisme du glycogène du foie isolé sont inhibés par la perfusion d’éthanol 10 mM en présence d’insuline. Étude RMN chez le rat." Diabetes & Metabolism 34 (March 2008): H89. http://dx.doi.org/10.1016/s1262-3636(08)73087-8.

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23

LEBRET, B., S. PRACHE, C. BERRI, F. LEFÈVRE, D. BAUCHART, B. PICARD, G. CORRAZE, F. MÉDALE, J. FAURE, and H. ALAMI-DURANTE. "Qualités des viandes : influences des caractéristiques des animaux et de leurs conditions d'élevage." INRA Productions Animales 28, no. 2 (January 13, 2020): 151–68. http://dx.doi.org/10.20870/productions-animales.2015.28.2.3022.

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Cette synthèse présente l’influence des caractéristiques des animaux et de leurs conditions d’élevage sur les qualités des viandes et des chairs des principales espèces animales d’élevage (porc, bovins, ovins, poulets, poissons). Les dimensions intrinsèques (composition des carcasses, qualités sensorielle, nutritionnelle et technologique) et extrinsèques (interactions entre productions animales et environnement, bien-être des animaux, origine des produits, authenticité des pratiques de production…) de la qualité des produits sont considérées. Dans toutes les espèces, le type génétique et la conduite alimentaire sont les principaux déterminants de la composition des carcasses. La nature de l’alimentation des animaux constitue le principal levier pour moduler la qualité nutritionnelle, toutefois le niveau d’enrichissement des viandes et chairs en acides gras, minéraux ou vitamines favorables à la santé humaine varie selon les espèces. Pour une espèce donnée, les caractéristiques des animaux, leurs conditions d’élevage et d’abattage interagissent pour déterminer les propriétés (teneurs en lipides, glycogène, myoglobine…) et le métabolisme péri et post-mortem des muscles, et consécutivement la qualité sensorielle des viandes ou chairs et de leurs produits. A l’inverse, la qualité technologique, composante importante dans les filières porc, poulet et poisson résulte essentiellement du type génétique et des conditions d’abattage des animaux et de transformation des viandes. Dans les différentes filières animales, les qualités extrinsèques des produits font partie intégrante de certaines démarches collectives ou privées et sont garanties aux consommateurs au travers des signes officiels de qualité. Elles visent à améliorer les interactions favorables entre les productions animales et l’environnement et/ou le bien-être des animaux, garantir l’origine des produits et/ou valoriser l’authenticité des méthodes de production et de transformation. Différents exemples sont développés pour illustrer la prise en compte par les acteurs des filières de cette demande croissante des consommateurs et plus largement des citoyens envers leur alimentation.
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Zeng, Ruichao, Ahmed Mohamed, Kum Kum Khanna, and Michelle M. Hill. "Differential Regulation of Lacto-/Neolacto- Glycosphingolipid Biosynthesis Pathway Reveals Transcription Factors as Potential Candidates in Triple-Negative Breast Cancer." Cancers 13, no. 13 (July 2, 2021): 3330. http://dx.doi.org/10.3390/cancers13133330.

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Triple-negative breast cancer (TNBC) is an aggressive breast cancer with limited treatment options. Glycosylation has been implicated in cancer development, but TNBC-specific glycosylation pathways have not been examined. Here, we applied bioinformatic analyses on public datasets to discover TNBC-specific glycogenes and pathways, as well as their upstream regulatory mechanisms. Unsupervised clustering of 345 glycogene expressions in breast cancer datasets revealed a relative homogenous expression pattern in basal-like TNBC subtype. Differential expression analyses of the 345 glycogenes between basal-like TNBC (hereafter termed TNBC) and other BC subtypes, or normal controls, revealed 84 differential glycogenes in TNBC. Pathway enrichment showed two common TNBC-enriched pathways across all three datasets, cell cycle and lacto-/neolacto- glycosphingolipid (GSL) biosynthesis, while a total of four glycosylation-related pathways were significantly enriched in TNBC. We applied a selection criterion of the top 50% differential anabolic/catabolic glycogenes in the enriched pathways to define 34 TNBC-specific glycogenes. The lacto-/neolacto- GSL biosynthesis pathway was the most highly enriched, with seven glycogenes all up-regulated in TNBC. This data led us to investigate the hypothesis that a common upstream mechanism in TNBC up-regulates the lacto-/neolacto-GSL biosynthesis pathway. Using public multi-omic datasets, we excluded the involvement of copy-number alteration and DNA methylation, but identified three transcription factors (AR, GATA3 and ZNG622) that each target three candidate genes in the lacto-/neolacto- GSL biosynthesis pathway. Interestingly, a subset of TNBC has been reported to express AR and GATA3, and AR antagonists are being trialed for TNBC. Our findings suggest that AR and GATA3 may contribute to TNBC via GSL regulation, and provide a list of candidate glycogenes for further investigation.
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25

Kauffman, Matthew R., and Justin R. DiAngelo. "Glut1 Functions in Insulin-Producing Neurons to Regulate Lipid and Carbohydrate Storage in Drosophila." Biomolecules 14, no. 8 (August 20, 2024): 1037. http://dx.doi.org/10.3390/biom14081037.

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Obesity remains one of the largest health problems in the world, arising from the excess storage of triglycerides (TAGs). However, the full complement of genes that are important for regulating TAG storage is not known. The Glut1 gene encodes a Drosophila glucose transporter that has been identified as a potential obesity gene through genetic screening. Yet, the tissue-specific metabolic functions of Glut1 are not fully understood. Here, we characterized the role of Glut1 in the fly brain by decreasing neuronal Glut1 levels with RNAi and measuring glycogen and TAGs. Glut1RNAi flies had decreased TAG and glycogen levels, suggesting a nonautonomous role of Glut1 in the fly brain to regulate nutrient storage. A group of hormones that regulate metabolism and are expressed in the fly brain are Drosophila insulin-like peptides (Ilps) 2, 3, and 5. Interestingly, we observed blunted Ilp3 and Ilp5 expression in neuronal Glut1RNAi flies, suggesting Glut1 functions in insulin-producing neurons (IPCs) to regulate whole-organism TAG and glycogen storage. Consistent with this hypothesis, we also saw fewer TAGs and glycogens and decreased expression of Ilp3 and Ilp5 in flies with IPC-specific Glut1RNAi. Together, these data suggest Glut1 functions as a nutrient sensor in IPCs, controlling TAG and glycogen storage and regulating systemic energy homeostasis.
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Beauvieux, M. C., H. Gin, H. Roumes, V. Rigalleau, and J. L. Gallis. "P207 - Intérêt des fibres alimentaires : un lien métabolique entre le cyclage du glycogène et le taux de renouvellement de l’ATP mitochondrial étudié dans le foie de rats nourris en butyrate ou glucose+butyrate." Diabetes & Metabolism 37, no. 1 (March 2011): A82. http://dx.doi.org/10.1016/s1262-3636(11)70833-3.

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27

Chen, Yen-Hsieh, and Yuh-Shan Jou. "Abstract 6215: Systematic identification and clinical implications of glycogenes in cancer research: An integrative omics approach." Cancer Research 84, no. 6_Supplement (March 22, 2024): 6215. http://dx.doi.org/10.1158/1538-7445.am2024-6215.

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Abstract Glycosylation and its products are crucial in clinical routines but are overshadowed by a framework embedding genomic participants in cancer development. The glycosylation scheme varies between research groups, presenting clinical concerns that demand understanding in cancer research beyond the glycome. Our work aims (a) to enhance the canonical framework by identifying potential glycosylation-associated genes (glycogenes) and (b) to advance translational cancer study, offering a unified perspective on integrative omics and explainable machine learning with glycogene integration. The expansion of the glycosylation framework involved initial text mining from curated databases like OMIM, InterPro, and Reactome. Dysregulation of identified genes was affirmed across 29 TCGA solid cancers, encompassing over 7,000 patients with primary tumors. And healthy tissue data from GTEx facilitated tumor-normal comparisons. Subsequently, integrative omic analysis, involving transcriptome and methylome, was applied to confirm the stratification feasibility of glycogenes and to revealed cancer clusters within the UMAP space. After cluster discovery, profiling from survival analysis and drug response prediction highlighted clinical differences between clusters. Employing a survival forest model and explainable artificial intelligence (XAI), personalized assessments, including a 5-year survival predictor and risk factors for individuals, were developed. Our study verified over 3,000 glycogenes, expanding the conventional configuration of glycosylation and constituting 10-30% of differentially expressed genes between tumors and healthy tissues. Whether transcriptome or methylome alone, glycogenes demonstrated stratification ability. Advanced omic integration further discovered 16 cancer clusters out of 29 TCGA cancers, associated with anatomical source, morphology, and genomic similarity. Utilizing drug resources from GDSC, this specialized geneset exhibited drug predicting ability, displaying a distinct drug response profile among the 16 clusters. To finalize the clinical potential, a survival forest for 5-year survival model construction concluded forecasters with a time-dependent AUC (0.77 to 0.92 on average) for each cancer cluster. With XAI implementation, survival risk factors were developed and assessed for each individual locally. Here we identified over 3,000 glycogenes, elaborating the classic glycosylation structure and emphasizing genomic importance in cancer research. Glycogenes demonstrated translational potential, supported by diverse survival distributions and drug responses across cancer clusters discovered by the integrative omic approach. The integration of XAI provided a tailored perspective for implementing glycogenes in clinical cancer research. Citation Format: Yen-Hsieh Chen, Yuh-Shan Jou. Systematic identification and clinical implications of glycogenes in cancer research: An integrative omics approach [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 6215.
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Martinez-Garcia, Marta, Marc C. A. Stuart, and Marc J. E. C. van der Maarel. "Characterization of the highly branched glycogen from the thermoacidophilic red microalga Galdieria sulphuraria and comparison with other glycogens." International Journal of Biological Macromolecules 89 (August 2016): 12–18. http://dx.doi.org/10.1016/j.ijbiomac.2016.04.051.

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Ma, Yulong, Yanhui Cai, Doutong Yu, Yuting Qiao, Haiyun Guo, Zejun Gao, and Li Guo. "Astrocytic Glycogen Mobilization in Cerebral Ischemia/Reperfusion Injury." Neuroscience and Neurological Surgery 11, no. 3 (February 21, 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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Nielsen, Niels A., H. Okkels, and C. Chr Stochholm-Borresen. "DETECTION HISTOCHIMIQUE DU GLYCOGENE." Acta Pathologica Microbiologica Scandinavica 9, no. 3 (February 4, 2010): 258–68. http://dx.doi.org/10.1111/j.1600-0463.1932.tb06542.x.

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31

Guindolet, Damien, Ashley M. Woodward, Eric E. Gabison, and Pablo Argüeso. "Glycogene Expression Profile of Human Limbal Epithelial Cells with Distinct Clonogenic Potential." Cells 11, no. 9 (May 7, 2022): 1575. http://dx.doi.org/10.3390/cells11091575.

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Glycans function as valuable markers of stem cells but also regulate the ability of these cells to self-renew and differentiate. Approximately 2% of the human genome encodes for proteins that are involved in the biosynthesis and recognition of glycans. In the present study, we evaluated the expression of a small subset of glycogenes in human limbal epithelial cells with distinct clonogenic potential. Individual clones were classified as abortive or clonogenic, based on the fraction of the terminal colonies produced; clones leading exclusively to terminal colonies were referred to as abortive while those with half or fewer terminal colonies were referred to as clonogenic. An analysis of glycogene expression in clonogenic cultures revealed a high content of transcripts regulating the galactose and mannose metabolic pathways. Abortive clones were characterized by increased levels of GCNT4 and FUCA2, genes that are responsible for the branching of mucin-type O-glycans and the hydrolysis of fucose residues on N-glycans, respectively. The expansion of primary cultures of human limbal epithelial cells for 10 days resulted in stratification and a concomitant increase in MUC16, GCNT4 and FUCA2 expression. These data indicate that the clonogenic potential of human limbal epithelial cells is associated with specific glycosylation pathways. Mucin-type O-glycan branching and increased fucose metabolism are linked to limbal epithelial cell differentiation.
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Kanungo, Shibani, Kimberly Wells, Taylor Tribett, and Areeg El-Gharbawy. "Glycogen metabolism and glycogen storage disorders." Annals of Translational Medicine 6, no. 24 (December 2018): 474. http://dx.doi.org/10.21037/atm.2018.10.59.

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33

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 (October 1, 2011): 651–52. http://dx.doi.org/10.15373/2249555x/may2014/206.

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34

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 (December 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 synthesized, but when postexercise glycogen levels were >5 μmol/g, only about 1.7 μmol/g of glycogen was synthesized. This difference in the amount of glycogen synthesized was reflected in the degree of activation of glycogen synthase. Postexercise glycogen content also influenced the response of the muscle to 10−8 M epinephrine and 10−8 M dexamethasone (a glucocorticoid analog). At high glycogen levels (>5 μmol/g), epinephrine and dexamethasone stimulated glycogen phosphorylase activity and net glycogenolysis, whereas at low (<5 μmol/g) glycogen levels, glycogenesis and activation of glycogen synthase activity prevailed. These data clearly indicate not only is trout muscle capable of in situ glycogenesis, but the amount of glycogen synthesized is a function of initial glycogen content. Furthermore, whereas dexamethasone and epinephrine directly stimulate muscle glycogen metabolism, the net effect is dependent on initial glycogen content.
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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 (August 1998): 422–27. http://dx.doi.org/10.1006/bbrc.1998.9159.

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36

Conway, V. D., and P. P. Zolin. "Glycogene metabolism in postresuscitation period." Pathophysiology 5 (June 1998): 229. http://dx.doi.org/10.1016/s0928-4680(98)81187-5.

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37

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 (April 1, 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 red gastrocnemius and plantaris muscles. Furthermore, insulin failed to activate glycogen synthase and glycogen synthesis. In the controls, fasting was associated with decreased glycogen concentrations and with increased glycogen synthase activity ratio in all four groups of muscles (P less than 0.01). Dexamethasone treatment, however, completely abolished the decrease in muscle glycogen content as well as the augmented glycogen synthase activity ratio associated with fasting. Insulin infusion stimulated glycogen synthesis in fasted controls but not in dexamethasone-treated rats. These data therefore indicate that dexamethasone treatment inhibits the stimulatory effect of insulin on glycogen synthase activity and on glycogen synthesis. Furthermore, hypercorticism suppresses the decrease in muscle glycogen content associated with fasting.
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38

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 (September 1, 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-glycogen-depleted rats the glucose feeding spared glycogen in the liver, primarily from the oxidation of blood-borne glucose in muscle. In the glycogen-depleted rats, muscle glycogen was repleted after the feeding, but sources other than the administered glucose also contributed to glycogen synthesis. The results suggest that glycogen depletion rather than the glucose feeding per se stimulates glycogen resynthesis in muscle during exercise in endurance-trained rats.
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39

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 (August 12, 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 of SER and glycogen levels during hepatic glycogen synthesis tests the existence of a correlation between glycogen and SER. Newly deposited labeled glycogen is localized via autoradiography and the extent of association between labeled glycogen and SER quantified, establishing whether glycogen is necessarily deposited near membranes of SER.Fetal mouse livers were harvested at daily intervals between days 14 and 19 of gestation, immersion fixed in 2% glutaraldehyde, 2% paraformaldehyde, post-fixed in 1 % OsO4 dehydrated in EtOH and embedded in Epon 812. Semi-thin (0.5μm) and ultra-thin sections (60 nm) were prepared for morphometric analysis.2
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40

McNulty, P. H., C. Ng, W. X. Liu, D. Jagasia, G. V. Letsou, J. C. Baldwin, and R. Soufer. "Autoregulation of myocardial glycogen concentration during intermittent hypoxia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 2 (August 1, 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 < 0.005). Reducing cardiac work (with propranolol or heterotopic transplantation) reduced glycogen breakdown, glycogen synthase activation, and glycogen synthesis in parallel, stepwise fashion in intact rats. Correspondingly, hypoxia increased GS I activity in the perfused heart in vitro, but only under conditions where glycogen was consumed. This suggests myocardial glycogen synthase is activated by systemic hypoxia and catalyzes rapid posthypoxic glycogen synthesis. Hypoxic glycogen synthase activation appears to be a proportionate, wholly intrinsic response to local glycogenolysis, operating to preserve myocardial glycogen stores independent of any extracardiac mediator of carbohydrate metabolism.
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41

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 (November 8, 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 contractile activity. In agreement with this, the fractional activity of glycogen synthase was high when adrenaline was present after exercise, whereas adrenaline decreased the fractional activity of glycogen synthase to a low level during stimulation with insulin. Furthermore, adrenaline activated glycogen phosphorylase almost completely during stimulation with insulin, whereas a much lower activation of glycogen phosphorylase was observed after contractile activity. Thus adrenaline does not inhibit contraction-stimulated glycogen synthesis.
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42

Talmadge, R. J., and H. Silverman. "Glyconeogenic and glycogenic enzymes in chronically active and normal skeletal muscle." Journal of Applied Physiology 71, no. 1 (July 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 glycogen phosphorylase and fructose 1,6-bisphosphatase were decreased in whole muscle homogenates. Histochemistry demonstrated that the high-glycogen fibers were typically fast-twitch glycolytic fibers that had high glycogen synthase, glycogen phosphorylase, and malic enzyme activities. Malate dehydrogenase activity followed succinate dehydrogenase activity and did not correlate to high-glycogen fibers. Thus the high-glycogen fibers have an elevated enzymatic capacity for glycogen synthesis from lactate, and the pathway may involve use of the pyruvate kinase bypass enzymes.
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43

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 (May 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 conditions, Gsy2-GFP localized to discrete spots within cells. Gsy2p is known to bind to glycogen, and we propose that the subcellular distribution of Gsy2-GFP reflects the distribution of glycogen particles. In the absence of glycogen, Gsy2p translocates into the nucleus. We hypothesize that Gsy2p is normally retained in the cytoplasm through its interaction with glycogen particles. When glycogen levels are reduced, Gsy2p loses this anchor and can traffic into the nucleus.
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44

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 (June 1, 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 exercise. Muscle glycogen content using 13C-magnetic resonance spectroscopy, blood hydration status, body composition, and ECW and ICW content of the arm, trunk, and leg using BIS were measured. Muscle glycogen content at the thigh muscles decreased immediately after exercise (glycogen-depleted group, 71.6 ± 12.1 to 25.5 ± 10.1 mmol/kg wet wt; glycogen-recovered group, 76.2 ± 16.4 to 28.1 ± 16.8 mmol/kg wet wt) and recovered in the glycogen-recovered group (72.7 ± 21.2 mmol/kg wet wt) but not in the glycogen-depleted group (33.2 ± 12.6 mmol/kg wet wt) 24 h postexercise. Fat-free mass decreased in the glycogen-depleted group ( P < 0.05) but not in the glycogen-recovered group 24 h postexercise. However, no changes were observed in ECW and ICW content at the leg in both groups. Our results suggested that glycogen depletion per se does not alter body water distribution as estimated via BIS. This information is valuable in assessing body composition using BIS in athletes who show variable glycogen status during training and recovery. NEW & NOTEWORTHY Segmental bioimpedance spectroscopy analysis reveals the effect of muscle glycogen depletion on body segmental water distribution in controlled conditions. Despite the significant difference in the muscle glycogen levels at the leg, no difference was observed in body resistance and the corresponding water content of the extracellular and intracellular compartments.
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45

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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46

Vardanis, Alexander. "Particulate glycogen of mammalian liver: specificity in binding phosphorylase and glycogen synthase." Biochemistry and Cell Biology 70, no. 7 (July 1, 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 animals fed ad libitum, glycogen synthase was associated with the whole spectrum of molecular weights, while the glycogen phosphorylase distribution was skewed in favour of the lower molecular weight species. Under conditions of glycogen mobilization, the phosphorylase distribution changed to include all molecular weights. The hydrophobic interaction separations demonstrated that glycogen synthase binds to a specific subpopulation of particles that is a minor proportion of the total. In general, there was a direct relationship of the total amount of phosphorylase and synthase bound during periods of mobilization and deposition, respectively. Two notable exceptions were the large amounts of glucose-6-P dependent synthase present during the early period of glycogen mobilization and the high amounts of active phosphorylase appearing shortly after food withdrawal, in spite of interim glycogen deposition from presumably already ingested food.Key words: glycogen particle, glycogenolysis, glycogenesis, glycogen phosphorylase, glycogen synthase.
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47

Shearer, Jane, and Terry E. Graham. "New Perspectives on the Storage and Organization of Muscle Glycogen." Canadian Journal of Applied Physiology 27, no. 2 (April 1, 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 interactions, and roles in regulating glycogen metabolism. While certain enzymes such as glycogen synthase and glycogen phosphorylase have been extensively studied, other proteins such as the glycogen initiating and targeting proteins are just beginning to be understood. Two metabolically distinct forms of glycogen, pro- and marcoglycogen have been identified that vary in their carbohydrate complement per molecule and have different sensitivities to glycogen synthesis and degradation. Glycogen regulation takes place not only by allosteric regulation of enzymes, but also due to other factors such as subcellular location, granule size, and association with various glycogen-related proteins. Keywords: glycogen-associated proteins, skeletal muscle, carbohydrate metabolism, proglycogen, macroglycogen.
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48

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 (March 30, 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 its contribution to neuronal survival could be demonstrated. We used the neuronal cell lines NSC-34 and N18TG2 and could demonstrate that they express the key-enzymes of glycogen metabolism, glycogen phosphorylase and glycogen synthase and contain glycogen which is mobilized on glucose deprivation and elevated potassium concentrations, but not by hormones stimulating cAMP formation. Conditions of metabolic stress, namely hypoxia, oxidative stress and pH lowering, induce glycogen degradation. Our studies revealed that glycogen can contribute to the energy supply of neuronal cell lines in situations of metabolic stress. These findings shed new light on the so far neglected role of neuronal glycogen. The key-enzyme in glycogen degradation is glycogen phosphorylase. Neurons express only the brain isoform of the enzyme that is supposed to be activated primarily by the allosteric activator AMP and less by covalent phosphorylation via the cAMP cascade. Our results indicate that neuronal glycogen is not degraded upon hormone action but by factors lowering the energy charge of the cells directly.
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Jensen, Jørgen, Einar Jebens, Erlend O. Brennesvik, Jérôme Ruzzin, Maria A. Soos, Ellen M. L. Engebretsen, Stephen O'Rahilly, and Jonathan P. Whitehead. "Muscle glycogen inharmoniously regulates glycogen synthase activity, glucose uptake, and proximal insulin signaling." American Journal of Physiology-Endocrinology and Metabolism 290, no. 1 (January 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 in NG. GLUT4 expression, insulin-stimulated glucose uptake, and PKB phosphorylation were higher in LG than in NG, whereas insulin receptor tyrosyl phosphorylation, insulin receptor substrate-1-associated phosphatidylinositol 3-kinase activity, and GSK-3 phosphorylation were unchanged. Muscles with HG showed lower insulin-stimulated glycogen synthesis and glycogen synthase activation than NG despite similar dephosphorylation. Insulin signaling, glucose uptake, and GLUT4 expression were similar in HG and NG. This discordant regulation of glucose uptake and glycogen synthesis in HG resulted in higher insulin-stimulated glucose 6-phosphate concentration, higher glycolytic flux, and intracellular accumulation of nonphosphorylated 2-deoxyglucose. In conclusion, elevated glycogen synthase activation, glucose uptake, and GLUT4 expression enhance glycogen resynthesis in muscles with low glycogen. High glycogen concentration per se does not impair proximal insulin signaling or glucose uptake. “Insulin resistance” is observed at the level of glycogen synthase, and the reduced glycogen synthesis leads to increased levels of glucose 6-phosphate, glycolytic flux, and accumulation of nonphosphorylated 2-deoxyglucose.
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50

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 (November 17, 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 GP–muscle type (GPmm) proteins in glucose-supplied male astrocytes, but enhanced these profiles in female. The catecholamine neurotransmitter norepinephrine (NE) did not alter these proteins, but amplified DEX inhibition of GS and GPbb in male or abolished GR stimulation of GPmm in female. In both sexes, DEX and NE individually increased glycogen content, but DEX attenuated the magnitude of noradrenergic stimulation. Glucoprivation suppressed GS, GPbb, and GPmm in male, but not female astrocytes, and elevated or diminished glycogen in these sexes, respectively. Glucose-deprived astrocytes exhibit GR-dependent induced glycogen accumulation in both sexes, and corresponding loss (male) or attenuation (female) of noradrenergic-dependent glycogen build-up. Current evidence for GR augmentation of hypothalamic astrocyte glycogen content in each sex, yet divergent effects on glycogen enzyme proteins infers that glucocorticoids may elicit opposite adjustments in glycogen turnover in each sex. Results document GR modulation of NE stimulation of glycogen accumulation in the presence (male and female) or absence (female) of glucose. Outcomes provide novel proof that astrocyte energy status influences the magnitude of GR and NE signal effects on glycogen mass.
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