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1
Bertelli, Cinzia. « Antiviral activity and retroviral counteraction of SERINC genes ». Doctoral thesis, Università degli studi di Trento, 2021. http://hdl.handle.net/11572/321392.
Texte intégralRésumé :
SERINC5 is a restriction factor for retroviruses, antagonized by Nef of primate lentiviruses, by glycoGag of Moloney Murine Leukaemia Virus (MoMLV) and by S2 of Equine Infectious Anaemia virus (EIAV). In addition, SERINC5 sensitizes HIV-1 to neutralizing antibodies (nAbs) targeting the MPER in gp41. However, since the identification of SERINC5 as an inhibitor of retrovirus infectivity, many features of the host factor await clarification, notably the molecular mechanisms of restriction and viral counteraction. Furthermore, SERINC5 cellular role beyond restriction is still obscure. This thesis explores multiple aspects of the mutual antagonism governing the SERINC5 interplay with retroviruses. We first describe a contribution towards the determination of the structure of SERINC5 and the identification of the determinants crucial for antiviral activity, virus sensitization to neutralization and counteraction by retroviruses. By performing a structure-based mutagenesis screening, we identified SERINC5 ECL3, ECL5 and the interface between subdomains as regions essential for inhibition of HIV-1 infectivity and virus sensitization to 4E10 and 2F5 nAbs. The simultaneous impairment of both SERINC5 antiviral effects indicates that they are mechanistically related and support the hypothesis of a SERINC5-mediated impairment of the envelope glycoproteins. We included a comparative analysis of the antiviral activity of human SERINC paralogs and their sensitivity to retroviral counteraction. It has been previously established that SERINC3 inhibits HIV-1 infectivity less potently than SERINC5, while SERINC2 has no antiviral effects. We report here that similarly to SERINC3, SERINC1 is endowed with a modest antiviral activity; in contrast, SERINC4 severely inhibits HIV-1 infectivity, despite being poorly expressed. Irrespectively of their antiretroviral potency, all SERINC proteins are incorporated into virus particles. Interestingly, we observed that virion-associated SERINC2 is specifically cleaved by the viral protease, but proteolysis does not explain the lack of antiretroviral effects. Furthermore, SERINC5 and SERINC2 have different glycomic profiles, but diverse post-translational modification is irrelevant for their opposite activity against HIV-1. In addition, we reported that human SERINCs are differently targeted by retroviral counteracting factors, with SERINC5 being the paralog most efficiently downregulated, while SERINC1 being completely resistant. A cysteines cluster within ICL4 emerged as the major determinant of SERINC5 responsiveness to different nef alleles, while it proved irrelevant for internalization by MoMLV glycoGag and EIAV S2, indicating that diverse retroviral counteractors likely target the host factor differently. Though SERINC5 ICL4 harbours multiple motifs governing SERINC5 sensitivity to antagonization, insertion of this loop within SERINC2 was not enough to transfer susceptibility to Nef activity, suggesting that the overall conformation of the protein is essential for downregulation by Nef. Importantly, the cysteine stretch within ICL4 is palmitoylated, suggesting that this modification may be important for counteraction by the lentiviral factor. SERINC5 and CD4 downregulation by Nef are functionally related, as they both require AP-2 mediated endocytosis. However, regions in Nef selectively governing SERINC5 internalization are unknown. We reported here that Phe90 within Nef αA-helix genetically uncouples the activities on SERINC5 and CD4, being selectively involved in SERINC5 downregulation. In parallel, we explored SERINC5 antagonization by different glycoGag alleles and observed that the ability to target the host factor is not conserved across divergent γ-retroviruses. Finally, we observed that HIV-1 may evade SERINC5 restriction by direct cell-to-cell infection, suggesting that the host factor may have a broader role in retroviral spreading, requiring the evolution and the conservation of active viral counteraction. To this end, we preliminary investigated a positive contribution of SERINC5 to intracellular signalling.
2
Syed, Noor Afshan. « Regulation of glycogen synthase and glycogen phosphorylase by insulin in HepG2 cells ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ63926.pdf.
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3
Martin, Jennifer Louise. « Molecular interactions involving glycogen phosphorylase ». Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.253306.
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4
Ghosh, Paritosh. « De Novo Glycogen Biosynthesis by a Glycogen Primer Complex in the Obliquely Striated Skeletal Muscle of Ascaris suum ». Thesis, North Texas State University, 1987. https://digital.library.unt.edu/ark:/67531/metadc935639/.
Texte intégralRésumé :
During the purification of the enzyme glycogen synthase from the muscle of the nematode Ascaris suum, approximately 70% of the glycogen synthase activity can be separated from the bulk of cellular glycogen by centrifugation for 60 min at 105,000 x . The glycogen synthase in the supernatant fraction has an Mr of 1.2 x 106 as determined by Sepharose 4B gel filtration chromatography. The glycogen synthase in this high molecular weight complex (glycogen primer complex) can be further purified by ConA-Sepharose affinity chromatography; the enzyme activity was eluted with 100 .mM a-methylmannoside. The glycogen synthase in glycogen'primer complex is predominately in the glucose 6-phosphatedependent form. The glycogen primer complex can catalyze the transfer of glucosyl units from UDP-glucose to an endogenous acceptor in the absence of exogenous glycogen. Analysis by SDS-PAGE showed three proteins (Mr 140,000, 78,000 and 34,000) and a carbohydrate polymer. The carbohydrate polymer can be partially digested with a-amylase. The glycogen primer complex was further digested by acid hydrolysis, and upon descending paper chromatography analysis, eight different carbohydrates were isolated, two of which were tentatively identified as glucose and sialic acid. The [14 C]-autoradiograph showed that in vitro synthesis of a glycogen-like polysaccharide occurred on this carbohydrate polymer. Polyclonal antibodies have been made to the glycogen primer complex, and Western Blot analysis indicated that all three proteins of the glycogen primer complex were antigenic. Collectively, the data indicate that a glycogen-like polysaccharide is synthesized from a carbohydrate-associated protein primer in the muscle of this worm.
5
Karis, Nils David. « Design and Synthesis of 1,3-Disubstitiuted-2-Pyridones as a New Class of Glycogen Phosphorylase Inhibitors ». Thesis, Griffith University, 2009. http://hdl.handle.net/10072/365791.
Texte intégralRésumé :
Glycogen Phosphorylase (GP) is the regulatory enzyme that catalyses the first step in glycogen degradation and is a potential enzyme target for therapeutic intervention in the treatment of diabetes. The 16 amino acid C-terminal sequence of human Gl is the only known targeting subunit that binds to GPa. Blocking the interactions between Gl and GPa should reduce high blood glucose levels in a diabetic person. A segment of the 16 amino acid segment was chosen for a small molecule peptidomimetric approach, and de nova design from this segment identified the pyridone ring as apotential scaffold. This thesis reports the design and synthesis of 1.3-disubstituted pyridones as new class of GPa inhibitors.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Eskitis Institute for Cell and Molecular Therapies
Science, Environment, Engineering and Technology
Full Text
6
Street, Ian Philip. « Protein - carbohydrate interactions in glycogen phosphorylase ». Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/25049.
Texte intégralRésumé :
It has long been observed that some organo-fluorine compounds exhibit enhanced biological activity over their non-fluorinated precursors, however reasons for these unusual properties still remain poorly understood. An explanation which has been widely used relates to the ability of the C-F fragment of the analog to participate in hydrogen-bonding interactions with its protein receptor. For this reason, fluorinated carbohydrates have been used as hydrogen-bonding probes with a number of proteins.
Thus there exists a need for a systematic investigation into the hydrogen-bonding ability of the C-F fragment, and the enzyme glycogen phosphorylase provides an excellent subject for such a study. The glucopyranose binding site in the inactive (T-state) conformation of the enzyme has been well characterised and high resolution crystallographic data is available. Thus by comparison of kinetic and crystallographic data for the natural effectors and the fluorinated substrate analogs considerable insight into the hydrogen bonding ability of the C-F fragment and the nature of carbohydrate-protein interactions should be gained.
Little is known about the active (R-state) conformation of the enzyme and about the T-state to R-state transition. Use of fluorinated analogs of the enzymes natural substrate, glucose-l-phosphate, could also shed light on these questions.
With these aims in mind, all of the isomeric mono-fluorinated derivatives of glucose and glucose-l-phosphate have been synthesised. Some deoxy and difluorinated analogs of glucose and mannose have also been prepared. Kinetic results obtained using the analogs of glucose indicate that the 3 and 6 positions of the sugar participate in strong hydrogen-bonding interactions with the protein while the other positions are only involved in relatively weak interactions. These results agree well with recent X-ray crystallographic data.
None of the analogs of glucose-l-phosphate exhibited any substrate activity. The 2-deoxyfluoro analog had a similar affinity to glucose-1-phosphate and therefore probably binds in the same mode. The lack of substrate activity in this case can be explained by the destabi1isation of the putative oxo-carbonium ion intermediate at C(l), by the adjacent fluorine substituent.
The other analogs of glucose-l-phosphate showed lower affinity for the enzyme. The similar inhibition constants obtained for these compounds suggested a binding mode in which the glucopyranose ring contributes little to the overall binding energy. This has led to the proposal of a molecular mechanism for the T-state to R-state transition.Science, Faculty of
Chemistry, Department of
Graduate
7
Stambolic, Vuk. « Regulation of glycogen synthase kinase-3 ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0003/NQ27730.pdf.
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8
Fraser, Bernadine Heather. « Glycogen and glucose metabolism in cardioprotection ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0028/NQ34764.pdf.
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9
Henning, Sarah Louise. « Myocardial glycogen metabolism and its regulation ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ61107.pdf.
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10
Barford, D. « Crystallographic studies on glycogen phosphorylase b ». Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233473.
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11
McLaughlin, P. J. « Crystallographic studies on glycogen phosphorylase b ». Thesis, University of Oxford, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.370290.
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12
Bichard, Claire J. F. « Synthesis of potential glycogen phosphorylase inhibitors ». Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260115.
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13
Hu, Shu-Hong. « Crystallographic studies on activated glycogen phosphorylase ». Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.291283.
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14
Stambolic, Vuk. « Regulation of glycogen synthase kinase-3 ». Ottawa : National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.nlc-bnc.ca/obj/s4/f2/dsk2/tape16/PQDD%5F0003/NQ27730.pdf.
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15
Higuita, Juan Carlos. « Molecular consequences of cellular UDP-glucose deficiency / ». Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-901-3/.
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16
Hannigan, Linda L. (Linda Lucile). « Purification and characterization of glycogen synthase from Ascaris suum ». Thesis, North Texas State University, 1985. https://digital.library.unt.edu/ark:/67531/metadc798067/.
Texte intégralRésumé :
Glycogen synthase, the enzyme that catalyzes the rate-limiting reaction of glycogen syntheses has been purified and characterized from Ascaris suum muscle. Glycogen in the crude extract was digested to release the enzyme, eluted from a DE52 cellulose column and then applied to a Sepharose affinity column. The purified Ascaris enzyme was found to be homologous to the mammalian enzyme with regard to subunit and holoenzyme Mr^3 allosteric activation, substrate affinity and covalent modification. However, the association between Ascaris glycogen synthase and endogenous glycogen differed from that in mammalian systems.
17
Mitchell, Edward Peter. « Cryocrystallographic and mechanistic studies on glycogen phosphorylase ». Thesis, University of Oxford, 1994. https://ora.ox.ac.uk/objects/uuid:d562f4f6-0a93-43a6-ad74-d480697d1b8c.
Texte intégralRésumé :
Glycogen phosphorylase (GPb) regulates the degradation of glycogen to glucose-1-phosphate and catalyses the first step of the reaction. Many studies have provided insights into the essentials of the catalytic mechanism. Previous time resolved crystallographic work using heptenitol has revealed a putative phosphate binding site at the active site of phosphorylase. Using nojirimycin tetrazole, a transition state analogue, complexed with phosphate and both T and R state GPb crystals, this work has conclusively located the phosphate binding site and the concomitant active site conformational changes. This has confirmed the previous heptenitol results. Using R state crystals complexed with tetrazole and phosphate, data were collected to 2.5Ã
resolution, higher than for the original 2.8Ã
resolution native structure, and used to position water molecules in the R state model. Further to this, direct observation of the phosphate ion orientation was made possible using flash-frozen T state crystals to collect 1.7Ã
resolution data at 100K. As part of this cryocrystallographic work the relationship of cryoprotectant concentration with crystal mosaicity was established, aiding the systematic search for flash-freezing cryoprotectant conditions for all protein crystals. Collection of a new native T state data set to 1.5Ã
resolution was made possible using the flash-freezing technique. Refinement has produced a new higher precision native model (R factor currently 22.8%) containing additional N terminal residues (14-18) and 330 new water molecules. A molecule of glycerol, the cryoprotectant, was located at the active site. This study represents a considerable improvement over the 1.9Ã
resolution room temperature native data, and is also the first time such high resolution data have been collected from such a large enzyme. In a further analysis of the phosphate binding properties, a link between structure, atomic charges and the ability of a ligand to bind phosphate at the phosphorylase active site was established. In order of phosphate binding ability, the nojirimycin tetrazole, nitroglucal, glucal and glucose complexes with T state GPb and phosphate were structurally analysed. As the charge difference between the pyranose ring oxygen (or equivalent atom) and anomeric atom becomes more negative (charges estimated using MOPAC) the tendency to bind phosphate decreases. The ligand must possess a half-chair conformation as this is essential to bind phosphate; glucose, having the most negative charge difference and a full chair conformation, does not bind phosphate significantly in the crystal. A novel surface binding site for nitroglucal (covalently linked to His 73) was also located during this work. As part of an ongoing search for potential drugs for diabetes, two gluco-hydantoin inhibitors of GPb were investigated. One proved to be the best inhibitor to date, and the inhibition was rationalised using the structural results from this work. A new improved inhibitor has been proposed on the basis of these results.
18
Nitschke, Felix. « Phosphorylation of polyglycans, especially glycogen and starch ». Phd thesis, Universität Potsdam, 2013. http://opus.kobv.de/ubp/volltexte/2013/6739/.
Texte intégralRésumé :
Functional metabolism of storage carbohydrates is vital to plants and animals. The water-soluble glycogen in animal cells and the amylopectin which is the major component of water-insoluble starch granules residing in plant plastids are chemically similar as they consist of α-1,6 branched α-1,4 glucan chains. Synthesis and degradation of transitory starch and of glycogen are accomplished by a set of enzymatic activities that to some extend are also similar in plants and animals. Chain elongation, branching, and debranching are achieved by synthases, branching enzymes, and debranching enzymes, respectively. Similarly, both types of polyglucans contain low amounts of phosphate esters whose abundance varies depending on species and organs. Starch is selectively phosphorylated by at least two dikinases (GWD and PWD) at the glucosyl carbons C6 and C3 and dephosphorylated by the phosphatase SEX4 and SEX4-like enzymes. In Arabidopsis insufficiency in starch phosphorylation or dephosphorylation results in largely impaired starch turnover, starch accumulation, and often in retardation of growth. In humans the progressive neurodegenerative epilepsy, Lafora disease, is the result of a defective enzyme (laforin) that is functional equivalent to the starch phosphatase SEX4 and capable of glycogen dephosphorylation. Patients lacking laforin progressively accumulate unphysiologically structured insoluble glycogen-derived particles (Lafora bodies) in many tissues including brain. Previous results concerning the carbon position of glycogen phosphate are contradictory. Currently it is believed that glycogen is esterified exclusively at the carbon positions C2 and C3 and that the monophosphate esters, being incorporated via a side reaction of glycogen synthase (GS), lack any specific function but are rather an enzymatic error that needs to be corrected.
In this study a versatile and highly sensitive enzymatic cycling assay was established that enables quantification of very small G6P amounts in the presence of high concentrations of non-target compounds as present in hydrolysates of polysaccharides, such as starch, glycogen, or cytosolic heteroglycans in plants. Following validation of the G6P determination by analyzing previously characterized starches G6P was quantified in hydrolysates of various glycogen samples and in plant heteroglycans. Interestingly, glucosyl C6 phosphate is present in all glycogen preparations examined, the abundance varying between glycogens of different sources. Additionally, it was shown that carbon C6 is severely hyperphosphorylated in glycogen of Lafora disease mouse model and that laforin is capable of removing C6 phosphate from glycogen. After enrichment of phosphoglucans from amylolytically degraded glycogen, several techniques of two-dimensional NMR were applied that independently proved the existence of 6-phosphoglucosyl residues in glycogen and confirmed the recently described phosphorylation sites C2 and C3. C6 phosphate is neither Lafora disease- nor species-, or organ-specific as it was demonstrated in liver glycogen from laforin-deficient mice and in that of wild type rabbit skeletal muscle. The distribution of 6-phosphoglucosyl residues was analyzed in glycogen molecules and has been found to be uneven. Gradual degradation experiments revealed that C6 phosphate is more abundant in central parts of the glycogen molecules and in molecules possessing longer glucan chains. Glycogen of Lafora disease mice consistently contains a higher proportion of longer chains while most short chains were reduced as compared to wild type.
Together with results recently published (Nitschke et al., 2013) the findings of this work completely unhinge the hypothesis of GS-mediated phosphate incorporation as the respective reaction mechanism excludes phosphorylation of this glucosyl carbon, and as it is difficult to explain an uneven distribution of C6 phosphate by a stochastic event. Indeed the results rather point to a specific function of 6-phosphoglucosyl residues in the metabolism of polysaccharides as they are present in starch, glycogen, and, as described in this study, in heteroglycans of Arabidopsis. In the latter the function of phosphate remains unclear but this study provides evidence that in starch and glycogen it is related to branching. Moreover a role of C6 phosphate in the early stages of glycogen synthesis is suggested. By rejecting the current view on glycogen phosphate to be a stochastic biochemical error the results permit a wider view on putative roles of glycogen phosphate and on alternative biochemical ways of glycogen phosphorylation which for many reasons are likely to be mediated by distinct phosphorylating enzymes as it is realized in starch metabolism of plants. Better understanding of the enzymology underlying glycogen phosphorylation implies new possibilities of Lafora disease treatment.Pflanzen und Tiere speichern Glukose in hochmolekularen Kohlenhydraten, um diese bei Bedarf unter anderem zur Gewinnung von Energie zu nutzen. Amylopectin, der größte Bestandteil des pflanzlichen Speicherkohlenhydrats Stärke, und das tierische Äquivalent Glykogen sind chemisch betrachtet ähnlich, denn sie bestehen aus verzweigten Ketten, deren Bausteine (Glukosylreste) auf identische Weise miteinander verbunden sind. Zudem kommen in beiden Kohlenhydraten kleine aber ähnliche Mengen von Phosphatgruppen vor, die offenbar eine tragende Rolle in Pflanzen und Tieren spielen. Ist in Pflanzen der Einbau oder die Entfernung von Phosphatgruppen in bzw. aus Stärke gestört, so ist oft der gesamte Stärkestoffwechsel beeinträchtigt. Dies zeigt sich unter anderem in der übermäßigen Akkumulation von Stärke und in Wachstumsverzögerungen der gesamten Pflanze. Beim Menschen und anderen Säugern beruht eine schwere Form der Epilepsie (Lafora disease) auf einer Störung des Glykogenstoffwechsels. Sie wird durch das erblich bedingte Fehlen eines Enzyms ausgelöst, das Phosphatgruppen aus dem Glykogen entfernt. Während die Enzyme, die für die Entfernung des Phosphats aus Stärke und Glykogen verantwortlich sind, hohe Ähnlichkeit aufweisen, ist momentan die Ansicht weit verbreitet, dass der Einbau von Phosphat in beide Speicherkohlenhydrate auf höchst unterschiedliche Weise erfolgt. In Pflanzen sind zwei Enzyme bekannt, die Phosphatgruppen an unterschiedlichen Stellen in Glukosylreste einbauen (Kohlenstoffatome 6 und 3). In Tieren soll eine seltene, unvermeidbare und zufällig auftretende Nebenreaktion eines Enzyms, das eigentlich die Ketten des Glykogens verlängert (Glykogen-Synthase), den Einbau von Phosphat bewirken, der somit als unwillkürlich gilt und weithin als „biochemischer Fehler“ (mit fatalen Konsequenzen bei ausbleibender Korrektur) betrachtet wird. In den Glukosylresten des Glykogens sollen ausschließlich die C-Atome 2 und 3 phosphoryliert sein. Die Ergebnisse dieser Arbeit zeigen mittels zweier unabhängiger Methoden, dass Glykogen auch am Glukosyl-Kohlenstoff 6 phosphoryliert ist, der Phosphatposition, die in der Stärke am häufigsten vorkommt. Die Tatsache, dass in dieser Arbeit Phosphat neben Stärke auch erstmals an Glukosylresten von anderen pflanzlichen Kohlenhydraten (wasserlösliche Heteroglykane) nachgewiesen werden konnte, lässt vermuten, dass Phosphorylierung ein generelles Phänomen bei Polysacchariden ist. Des Weiteren wiesen die Ergebnisse darauf hin, dass Phosphat im Glykogen, wie auch in der Stärke, einem bestimmten Zweck dient, der im Zusammenhang mit der Regulation von Kettenverzweigung steht, und dass kein zufälliges biochemisches Ereignis für den Einbau verantwortlich sein kann. Aufgrund der grundlegenden Ähnlichkeiten im Stärke- und Glykogenstoffwechsel, liegt es nahe, dass die Phosphorylierung von Glykogen, ähnlich der von Stärke, ebenfalls durch spezifische Enzyme bewirkt wird. Ein besseres Verständnis der Mechanismen, die der Glykogen-Phosphorylierung zugrunde liegen, kann neue Möglichkeiten der Behandlung von Lafora disease aufzeigen.
19
Duke, Elizabeth Mary Helen. « X-ray diffraction studies on glycogen phosphorylase ». Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336092.
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20
Kensley, Joy A. « Glycogen metabolism in Corynebacterium glutamicum ATCC 13032 ». Doctoral thesis, University of Cape Town, 2004. http://hdl.handle.net/11427/4279.
Texte intégralRésumé :
Includes bibliographical references (leaves 108-123).Corynebacterium glutamicum is a Gram-positive facultative aerobe particularly known for its industrial application in the synthesis of amino acids, such as L-glutamate and Llysine. The central metabolic pathways of this organism has been an area of much research by many groups. Linked to glycolysis is the synthesis of glycogen, previously considered a storage molecule of excess glucose. No information concerning the role of glycogen or its metabolism in C. glutamicum was known, and the aim of this work was to elucidate glycogen metabolism in this industrially important organism.
21
Allen, Tara J. « Characterization of vascular smooth muscle oxidative metabolism using ¹³C-isotopomer analysis of glutamate ». free to MU campus, to others for purchase, 2000. http://wwwlib.umi.com/cr/mo/fullcit?p9988641.
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22
Puthanveetil, Prasanth Nair. « Glucocorticoid and its effect on cardiac glucose utilization ». Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/5038.
Texte intégralRésumé :
Glycogen is an immediate source of glucose for cardiac tissue to maintain its metabolic
homeostasis. However, its excess brings about cardiac structural and physiological
impairments. Previously, we have demonstrated that in hearts from dexamethasone
(DEX) treated animals, glycogen accumulation was enhanced. We examined the
influence of DEX on glucose entry and glycogen synthase as a means of regulating the
accumulation of this stored polysaccharide. Following DEX, cardiac tissue had limited
contribution towards the development of whole body insulin resistance. Measurement of
GLUT4 at the plasma membrane revealed an excess presence of this transporter protein
at this location. Interestingly, this was accompanied by an increase in GLUT4 in the
intracellular membrane fraction, an effect that was well correlated to an increased
GLUT4 mR.NA. Both total and phosphorylated AMPK increased following DEX.
Immunoprecipitation of AS 160 followed by Western blotting demonstrated no change in
Akt phosphorylation at Ser473 and Thr308 in DEX treated hearts. However, there was a
significant increase in AMPK phosphorylation at Thr172, which correlated well with
AS 160 phosphorylation. In DEX hearts, there was a considerable reduction in the
phosphorylation of glycogen synthase, whereas GSK-3-β phosphorylation was
augmented. Our data suggest that AMPK mediated glucose entry, combined with
activation of glycogen synthase and reduction in glucose oxidation (Qi, D., et al. Diabetes
53:1790, 2004), act together to promote glycogen storage. Our data suggest that in the
presence of intact insulin signaling, AMPK mediated glucose entry, combined with
activation of glycogen synthase and the previously reported reduction in glucose
oxidation, act together to promote glycogen storage. Should these effects persist chronically, they may explain the increased morbidity and mortality observed with long
term excesses in endogenous or exogenous glucocorticoids.
23
Watson, Kimberly Ann. « Crystallographic studies on phosphorylase : sugar recognition properties ». Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.259849.
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24
Bruce, Mark. « Amino acid metabolism during exercise and recovery in human subjects ». Thesis, Loughborough University, 2001. https://dspace.lboro.ac.uk/2134/33569.
Texte intégralRésumé :
The depletion of muscle and liver glycogen observed during prolonged submaximal exercise is associated with fatigue. Re-synthesis of glycogen stores during the recovery period after exercise is therefore essential for the recovery of endurance exercise capacity. In recent years, attention has focussed on the supplementation of protein in addition to glucose-polymer during recovery from exercise in an attempt to further increase glycogen synthesis. The aims of the first and second studies in this thesis were to investigate the effect of glucose-polymer and amino acid ingestion, and solely amino acid ingestion upon amino acid and carbohydrate metabolism during recovery from glycogen-depleting exercise.
25
Green, Andrew R. « Interaction of phosphorylase and glycogen synthase in the defective control of glycogen metabolism in hepatocytes from the Zucker fatty rat ». Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413954.
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26
Lees, Simon J. « The effects of fatigue on glycogen, glycogen phosphorylase, and calcium uptake associated with the sarcoplasmic reticulum of rat skeletal muscle ». Thesis, Virginia Tech, 2000. http://hdl.handle.net/10919/35506.
Texte intégralRésumé :
Skeletal muscle fatigue can be defined as the inability to produce a desired amount of force. Fatigue can not only limit athletic performance and rehabilitation, but it can affect one's ability to perform every day activity as well. Despite extensive investigation of muscle fatigue, little is known about the exact mechanisms that result in decreased muscle performance. It likely involves several factors that are themselves dependent upon activation patterns and intensity. The process of excitation-contraction (EC) coupling is of particular importance with respect to regulation of force production. The release of calcium (Ca2+) from the sarcoplasmic reticulum (SR), which is stimulated by the depolarization of the sarcolemma, causes muscle contraction. The SR Ca2+-adenosine triphosphatase (ATPase) drives the translocation of two Ca2+ ions into the SR, utilizing the energy derived from the hydrolysis of one adenosine triphosphate (ATP) molecule. The process of SR Ca2+ uptake causes muscle relaxation. It has been proposed that both glycogen and glycolytic enzymes are associated with the SR membrane (SR-glycogenolytic complex). Interestingly, glycogen phosphorylase, an enzyme involved in glycogen breakdown, seems to be associated with the SR-glycogenolytic complex through its binding to glycogen. The presence of the SR-glycogenolytic system may serve to locally regenerate ATP utilized by the SR Ca2+-ATPase.
The purpose of the present study was to investigate the effects of prolonged muscle contraction on glycogen concentration, glycogen phosphorylase content and activity, and maximum Ca2+ uptake rate associated with the SR. Tetanic contractions, elicited once per second for 15 minutes, significantly reduced glycogen associated with SR to 5.1% of control from 401.17 ± 79.81 to 20.46 ± 2.16 mg/mg SR protein (p⠤0.05). The optical density of glycogen phosphorylase from SDS-PAGE was significantly reduced to 21.2% of control (p⠤0.05). Activity of glycogen phosphorylase, in the direction of glycogen breakdown, was significantly reduced to 4.1% of control (p⠤0.05). Pyridoxal 5'-phosphate (PLP) concentration, a quantitative indicator of glycogen phosphorylase content, was significantly reduced to 3.3% of control (£ 0.05). Maximum SR Ca2+ uptake rates were significantly reduced to 80.8% of control (£ 0.05). These data suggest reduced glycogen and glycogen phosphorylase may be involved, either directly or indirectly, in a mechanism that causes decreased SR Ca2+ uptake normally found in fatigue.
Master of Science
27
au, R. Jacob@central murdoch edu, et Robin Henry Jacob. « Optimising the concentration of glycogen in lamb meat ». Murdoch University, 2003. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20040513.153312.
Texte intégralRésumé :
The lamb industry is actively seeking to improve the quality of lamb meat produced in Australia. Ultimate pH (pHu) is a key determinant of red meat eating quality although this measurement has not been adopted formally by the Australian lamb meat industry. Muscle glycogen concentration is a major determinant of pHu in red meat. This thesis investigates glycogen concentration in lamb muscle and the ultimate pH (pHu) of lamb meat under commercial industry conditions as well as exploring by experimentation, some of the factors that control muscle glycogen concentration in lamb muscle. The results of this work has contributed to an understanding of the significance of high pHu meat to the lamb industry and will assist with developing new management strategies for lambs that avoid low muscle glycogen concentration at the point of slaughter, thus high pHu in meat derived from lambs.
The first part of the study (Experiments 1 and 2) undertook to determine the ranges of muscle glycogen concentration and lamb meat pHu found under commercial conditions and to measure any changes in these parameters associated with consignment of lambs from farm to abattoir and lairage at abattoirs. This study utilised a new biopsy technique that allowed muscle collection from lambs on farm. Some 16 different consignments of lambs and 3 consignments of lactating ewes were intensively monitored on farm and at abattoirs over a range of lairage times. Sensory evaluation tests were done using meat from 6 of these consignments.
The results showed there to be considerable variation between lamb consignments with some consignments having a very high and other consignments having a very low incidence of meat with a high pHu. On balance on farm factors were concluded to have a greater impact on muscle glycogen concentration at slaughter than post farm gate factors. However, there was evidence that muscle glycogen concentrations decreased during the farm curfew and transport period for some consignments so both on farm and post farm gate factors can be important. Characteristically glycogen loss occurred during the farm curfew and transport period in consignments of Merino lambs that had high muscle glycogen concentrations prior to consignment. Holding lambs in lairage caused no negative effects on muscle glycogen concentration although there was some evidence that very short lairage periods may increase meat pHu without causing a change in muscle glycogen concentration. It was concluded from these experiments that the mean muscle glycogen concentration of a group of lambs needs to be greater than 1.5 g/100g on farm in order for the pHu of lamb meat to be less than 5.7.
Subsequent to this industry study, an experiment (Experiment 3) was done to gain an understanding of muscle glycogen concentration as being an integral part of whole body glucose metabolism. This experiment investigated the effects of exercise on a range of different muscles and tissues of lambs including liver, kidney, skin and gastrointestinal tract. Interactions between glycogen concentrations in the liver and muscle with time after exercise showed that glycogen repletion occurred in the liver before muscle tissue. This effect was a unique finding and could explain in part the slow rate of glycogen repletion in muscle tissue that is characteristic for ruminants. Another major finding was an accumulation of glycogen concentration in skin during the recovery period after exercise. It was postulated that this effect may be due to the supply of glucose to glycolytic tissues being continued even when demand for glucose in the skin was low and the capacity to store glycogen in muscle was very high.
Experiment 3 confirmed the existence of a relationship between metabolisable energy (ME) intake and glycogen repletion in muscle tissues and found a slightly different relationship between ME intake and glycogen repletion in the liver tissue of lambs. Muscle glycogen concentration did not change in fasted lambs and the rate of glycogen repletion in muscle after exercise was dependent on ME intake. Differences were observed between different muscles, particularly between M. longissimus thoracis et lumborum (LTL) and all other muscles, in relation to the change in glycogen concentration with time after exercise. Glycogen concentrations changed less rapidly in the LTL than other muscles. Glycogen concentration in the liver was associated negatively with time after exercise in fasted lambs and positively with time after exercise in fed lambs.
Several experiments (Experiments 4, 5 and 6) were conducted to determine the affects of different nutritional factors on muscle glycogen concentration in lambs, both on farm and after commercial slaughter. These studies showed that short term increases in ME intake will increase muscle glycogen concentration to a maximum level over a period of about 7 days (Experiment 4). Diet composition did not affect the change in muscle glycogen concentration associated with an increase in ME intake although results from this experiment (Experiment 5) were not entirely conclusive. There was evidence that the type of feeding and finishing system may influence the susceptibility of muscle glycogen concentration to change during consignment of lambs to slaughter. Results from these experiments demonstrated that a goal for muscle glycogen concentration in lambs on farm of 1.5g/100g is quite achievable with contemporaneous management systems.
Finally this study highlighted the need for further research in a number of key areas in order that muscle glycogen concentration in lambs to be fully understood. In particular, the role of muscle glycogen turnover in relation to muscle glycogen concentration was noted as an area for which further research is warranted.
28
Varvill, Katherine Mary. « X-ray crystallographic studies on glycogen phosphorylase b ». Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.352921.
Texte intégral
29
Mung, Kwan-long, et 蒙君朗. « Regulation of glycogen phosphorylase in hypoxic cancer cells ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2015. http://hdl.handle.net/10722/211148.
Texte intégralRésumé :
Compared to normal cells, many tumor cells have to subsist in a hypoxic intratumoral environment that has an unstable supply of oxygen and nutrients including glucose. How tumor cells may survive the metabolic stress arising from tumor hypoxia is not yet fully understood. Recent studies revealed that tumor cells are able to accumulate large quantities of intracellular glycogen. Whether glycogen would serve as fuel reserve in hypoxic tumor cells is presently not clear. This question is being addressed in this study.
When HeLa, HT29, HEK293 and HepG2 cells were incubated under hypoxic condition in the absence of glucose, the steady state intracellular glycogen level dropped by more than 50% in 3 hours. The specific pharmacological inhibition of the liver isoform glycogen phosphorylase (PYGL) (CAS 648926-15-2) partially inhibited hypoxia-induced glycogen degradation. More complete inhibition was achieved by combined incubation using the pharmacological inhibitor and 2-deoxyglucose. Inhibition of glycogen degradation resulted in decrease in hypoxia-induced lactate formation, supporting the idea that glycogen serves as a fuel reserve in hypoxic cancer cells.
Inhibition of autophagy or alpha-glucosidase failed to prevent glycogen degradation in hypoxic condition, suggesting that cytosolic glycogen phosphorylase is the major enzyme involved in glycogen degradation. The mRNA, protein and phosphorylation levels of glycogen phosphorylase were unaltered by hypoxia. The siRNA-mediated knockdown of the brain form of glycogen phosphorylase (PYGB) resulted in markedly greater inhibition of glycogen degradation than did the knockdown of PYGL. Whereas the enzyme activity of PYGB can be markedly stimulated by AMP, the activity of PYGL is only slightly stimulated in the presence of AMP. The relative proportion of AMP-sensitive and AMP-insensitive GP activity is little affected by acute hypoxia.
In conclusion, direct evidence is provided in this study that glycogen may serve as an intracellular fuel reserve in tumor cells. The involvement of the brain form of glycogen phosphorylase is for the first time demonstrated to be involved in the mobilization of this fuel reserve in tumor cells.published_or_final_version
Biochemistry
Master
Master of Philosophy
30
Pascoe, David D. « Glycogen synthesis in skeletal muscle following resistive exercise ». Virtual Press, 1990. http://liblink.bsu.edu/uhtbin/catkey/720309.
Texte intégralRésumé :
The purpose of this investigation was to determine the influence of post exercise carbohydrate (CHO) intake on the rate of muscle glycogen restorage after high intensity weight resistance exercise in untrained subjects. In a cross over design, eight male subjects performed sets (mean= 8.8) of 6 single leg knee extensions at 70% of one repletion max until 50% of full knee extension was no longer possible. Total force application was equated between trials using a strain gauge interfaced to a computer. Post exercise supplementation was administered at 0 and 1 hrs consisting of either a 23% CHO solution (1.5g•kg-1•hr-1) or an equal volume of water (H20). Total force production, pre-exercise muscle glycogen content, and degree of depletion (-40.6 and -44.3 mmol•kg-1) were not significantly different between H2O and CHO trials, respectively. During the initial 2 hrs recovery, the CHO trial had a significantly greater rate of muscle glycogen resynthesis as compared to the H2O trial. In the final 4 hrs of recovery no difference in repletion rates were observed. The glycogen content (mmol•kg-1 w.w.) and rates of restorage (mmol•kg-1 w.w.) during the recovery period were (mean + SE):TrialPost2 Hr6 HrRate (0-2 hrs)H2O101.3+ 13.1105.1+ 13.1105.5+ 13.01.3+ 2.2CHO91.7+ 11.8117.6+ 16.5123.4+ 15.1 *12.9+ 4.0*significance between trials, p <0.01Only the CHO supplementation trial restored pre-exercise muscle glycogen content after 6 hrs. The spectrophotometric analysis of glycogen stained muscle sections (PAS) indicated no difference between trials in the pre and post glycogen content for Type I and II fibers. The change in absorbance, when these samples were combined demonstrate greater glycogenolysis in the Type II (0.284 + 0.58) as compared to Type I (0.014 ± 0.076). During the recovery period, the change in absorbance supports greater glycogenesis in the Type II ( 0.096 + 0.060) when compared to no observed change in absorbance in the Type I fibers.Supported by a grant from Ross Laboratories.Human Performance Laboratory
31
Halse, Reza. « Control of glycogen synthesis in cultured human muscle ». Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310172.
Texte intégral
32
Rusbridge, Nicholas Mercer. « Tryptic proteolysis of glycogen phosphorylase b in vitro ». Thesis, University of Liverpool, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317367.
Texte intégral
33
McConchie, Stephen Mark. « Molecular heterogeneity of human muscle glycogen phosphorylase deficiency ». Thesis, University of Liverpool, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317266.
Texte intégral
34
Jiang, Xianguo. « Investigating adrenoceptor regulation of the astroglial glycogen reserve ». Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/40130.
Texte intégralRésumé :
There is increasing evidence that astrocytes can play crucial roles in signalling within the central nervous system. In particular, astrocytes can communicate with each other and also with neurons, the latter interaction giving rise to the concept of the “tripartite synapse”. Thus, as well as astrocytes playing a homeostatic role to maintain an optimal extracellular environment within the brain, this cell-type may play roles in an array of CNS processes, including neurotransmission and synaptic activity. Astrocytes appear to be unique within the CNS in that they can store glucose in the form of glycogen. This constitutes the only energy reserve of the brain, and has been shown to play an important role not only at times of metabolic crisis, but also in supporting normal physiological brain function, including higher functions, such as learning and memory. Primary rat cerebral cortex (and cerebellar) astrocytes have been studied to advance our understanding of how cell-surface receptors control glycogen turnover, focusing on the roles played by the key neurotransmitter, noradrenaline. Evidence is presented for the presence of multiple adrenoceptor subtypes in astrocytes, including β1-, α1- and α2-adrenoceptors. β1-adrenoceptor activation resulted in robust accumulation of adenosine 3’,5’-cyclic-monophosphate (cAMP), with ≤5% of the maximal cAMP response elicited by noradrenaline being sufficient to activate near-maximally glycogenolysis. The observed cAMP response to noradrenaline in astrocytes is the sum of stimulatory β1-adrenoceptor-, and inhibitory α2-adrenoceptor-mediated effects. Because of the amplification of signal observed between cAMP and glycogenolysis, the inhibitory α2-adrenoceptor-mediated effect is only observed at the level of the glycogenolytic response over a small concentration range that may nevertheless coincide with the physiological range for noradrenaline effects on astrocytic function. Interestingly, α2-adrenoceptor activation also appears to increase the rate of glycogen re-synthesis and to have a “glycogen-loading” effect on astrocytes, increasing resting glycogen concentrations in cells. In contrast, while noradrenaline also stimulated a robust increase in intracellular Ca2+ concentration ([Ca2+]i), no evidence was found of this α1-adrenoceptor-mediated effect being able to contribute to the glycogenolytic response. Thus, while the sarco/endoplasmic reticular Ca2+-ATPase inhibitor, thapsigargin, and membrane depolarization (by increasing [K+]o) could each evoke increases in [Ca2+]i and stimulate glycogenolyis, addition of α1-adrenoceptor-selective agonists did not. These data increase our understanding of how the neurotransmitter, noradrenaline exerts its actions in astrocytes to regulate glycogenolysis, as well as a variety of other signal transduction pathways.
35
Харченко, Каріна Олександрівна, et Олександра Юріївна Кушнір. « Glycogen in the liver of streptozotocin diabetic rats ». Thesis, 39th International Medical Scientific Congress, 2016. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/11214.
Texte intégral
36
Pimentel, Helena Isabel da Costa Antunes. « Glycogen synthase kinase 3ß modulation in axonal regeneration ». Master's thesis, Universidade de Aveiro, 2011. http://hdl.handle.net/10773/5284.
Texte intégralRésumé :
Mestrado em Biomedicina MolecularA espinal medula de mamíferos adultos não possui capacidade de regeneração ao contrário do nervo periférico lesionado. De forma a compreender os mecanismos que potenciem a regeneração do sistema nervoso central, o modelo de lesão condicionante foi usado. Neste, uma lesão no ramo periférico dos neurónios da raiz dorsal cerca de uma semana antes de uma lesão no ramo central dos mesmos neurónios, promove a regeneração do último. Através de abordagens proteómicas concluiu-se que a Glycogen Synthase Kinase 3β (GSK3β) e proteínas que interagem com esta, estavam diferencialmente regulados após lesão condicionante, explicando possivelmente o maior potencial regenerativo nesta condição. Com este projecto, pretendemos compreender o mecanismo de regulação da GSK3β que leva à regeneração axonal. Primeiro observámos nos neurónios da raiz dorsal, um aumento da fosforilação da Akt (a cinase que inactiva a GSK3β através de fosforilação da S9), um aumento da pGSK3β(S9) (forma inactiva) e diminuição dos níveis de pGSK3β(Y216) (forma activa) após lesão condicionante validando os resultados da proteómica. Relativamente à espinal medula (local de lesão), verificou-se a diminuição de pGSK3β(Y216) após lesão condicionante em comparação com a lesão na espinal medula sugerindo que a GSK3β se encontra inibida após lesão condicionante por modulação deste resíduo. Relativamente aos substratos da GSK3β, na espinal medula a fosforilação do CRMP2 encontra-se diminuída e os níveis de pMAP1b encontram-se aumentados após lesão condicionante. De forma a perceber o papel da fosforilação da GSK3β(Y216) na regeneração axonal tratámos culturas de neurónios da raiz dorsal condicionados com ácido lisofosfatídico, um indutor da fosforilação da GSK3β(Y216), o qual reduziu o efeito de condicionamento. Para além disso, o inibidor VII (inibidor da GSK3) provocou um aumento da extensão axonal em neurónios adultos da raiz dorsal possivelmente por diminuição da fosforilação da GSK3β(Y216). Analisámos também o mecanismo responsável pela modulação da fosforilação da GSK3β(Y216). Os nossos resultados sugerem que a Fyn seja um bom candidato, uma vez que observámos na espinal medula níveis aumentados da forma inactiva da Fyn após lesão condicionante. De forma a determinar o papel da GSK3β in vivo, a regeneração axonal foi avaliada utilizando ratinhos GSK3βS9A knockin (KI). Tanto as culturas de neurónios da raiz dorsal de ratinhos GSK3βS9A KI não lesionados como após condicionamento, tiveram crescimento axonal semelhante à dos ratinhos wild type mostrando que a modulação da GSK3β através de fosforilação da GSK3β(S9) não é necessária para o efeito de condicionamento. Os nossos resultados sugerem que a fosforilação da GSK3β(Y216) tem um papel importante na regeneração axonal apesar de a literatura se focar no mecanismo inibitório da fosforilação da GSK3β(S9). A identificação da importância que a GSK3β possa ter no potenciamento da regeneração axonal após lesão condicionante, pode ser positiva no desenvolvimento de novas terapias para lesões na espinal medula.
The adult mammalian spinal cord fails to regenerate, contrarily to the injured peripheral nerve. In order to shed light on the mechanisms enabling central nervous system axonal regeneration, the conditioning lesion model was used. In this model, an injury in the peripheral branch of the dorsal root ganglia (DRG), approximately one week prior to an injury in the central branch of the DRG, promotes regeneration of the latter. To identify putative candidates differentially regulated in the DRG following conditioning lesion in comparison to spinal cord injury (SCI) alone, two proteomic approaches were used. From these analysis, Glycogen Synthase Kinase 3β (GSK3β) and interacting proteins, were identified as being differentially regulated following conditioning lesion, possibly explaining the increased regeneration in this condition. In this study we aimed to understand how GSK3β is modulated in order to promote axonal regeneration. We observed in the DRG increased levels of pAkt (the kinase that inactivates GSK3β through S9 phosphorylation), an increase of pGSK3β(S9) (inactive form) and decreased pGSK3β(Y216) (active form) levels in the conditioning lesion model, validating the proteomic results. Concerning the spinal cord injury site, we observed a decrease in pGSK3β(Y216) after conditioning lesion when compared to SCI, suggesting that the GSK3β activity is downregulated through modulation of this residue. Regarding the GSK3β substrates, CRMP2 phoshorylation levels are decreased and MAP1b is increasingly phosphorylated following conditioning lesion when compared with SCI alone in the spinal cord injury site. In order to evaluate the role of GSK3β(Y216) phosphorylation in axonal regeneration we treated conditioned DRG neurons with lysophosphatidic acid, an inducer of Y216 phosphorylation, which reduced the conditioning effect. On the other hand, the GSK3 inhibitor VII increased axon growth of adult DRG neurons possibly through a decrease of GSK3β(Y216) phosphorylation. We also analysed the mechanism responsible for the modulation of GSK3β(Y216) phosphorylation. Our results suggest that Fyn is a good candidate as we observed increased levels of the inactive form of Fyn after conditioning lesion in the spinal cord injury site. To evaluate the role of GSK3β in vivo, we assessed axonal regeneration in GSK3βS9A knockin (KI) mice. Both uninjured and conditioned DRG neuronal cultures from GSK3βS9A KI mice had similar neurite outgrowth to cultures performed with wild type mice showing that modulation of GSK3β through GSK3β(S9) phosphorylation is not required for the conditioning effect. In summary, our results suggest that GSK3β(Y216) phosphorylation has an important role in axonal regeneration, though the literature focuses on the inhibitory mechanism of GSK3β(S9) phosphorylation. Determining the role of GSK3β in the promotion of axonal regeneration after conditioning lesion, might impact in the development of new therapies for SCI.
37
Sucic, Joseph F. « Regulation of glycogen phosphorylase genes in Dictyostelium discoideum ». Diss., This resource online, 1992. http://scholar.lib.vt.edu/theses/available/etd-06062008-170101/.
Texte intégral
38
Seibold, Gerd Michael. « Charakterisierung des Glycogen- und Maltosestoffwechsels von Corynebacterium glutamicum ». [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-63818.
Texte intégral
39
Jacob, Robin Henry. « Optimising the concentration of glycogen in lamb meat ». Thesis, Jacob, Robin Henry (2003) Optimising the concentration of glycogen in lamb meat. PhD thesis, Murdoch University, 2003. https://researchrepository.murdoch.edu.au/id/eprint/110/.
Texte intégralRésumé :
The lamb industry is actively seeking to improve the quality of lamb meat produced in Australia. Ultimate pH (pHu) is a key determinant of red meat eating quality although this measurement has not been adopted formally by the Australian lamb meat industry. Muscle glycogen concentration is a major determinant of pHu in red meat. This thesis investigates glycogen concentration in lamb muscle and the ultimate pH (pHu) of lamb meat under commercial industry conditions as well as exploring by experimentation, some of the factors that control muscle glycogen concentration in lamb muscle. The results of this work has contributed to an understanding of the significance of high pHu meat to the lamb industry and will assist with developing new management strategies for lambs that avoid low muscle glycogen concentration at the point of slaughter, thus high pHu in meat derived from lambs.
The first part of the study (Experiments 1 and 2) undertook to determine the ranges of muscle glycogen concentration and lamb meat pHu found under commercial conditions and to measure any changes in these parameters associated with consignment of lambs from farm to abattoir and lairage at abattoirs. This study utilised a new biopsy technique that allowed muscle collection from lambs on farm. Some 16 different consignments of lambs and 3 consignments of lactating ewes were intensively monitored on farm and at abattoirs over a range of lairage times. Sensory evaluation tests were done using meat from 6 of these consignments.
The results showed there to be considerable variation between lamb consignments with some consignments having a very high and other consignments having a very low incidence of meat with a high pHu. On balance 'on farm' factors were concluded to have a greater impact on muscle glycogen concentration at slaughter than 'post farm gate' factors. However, there was evidence that muscle glycogen concentrations decreased during the farm curfew and transport period for some consignments so both 'on farm' and 'post farm gate factors' can be important. Characteristically glycogen loss occurred during the farm curfew and transport period in consignments of Merino lambs that had high muscle glycogen concentrations prior to consignment. Holding lambs in lairage caused no negative effects on muscle glycogen concentration although there was some evidence that very short lairage periods may increase meat pHu without causing a change in muscle glycogen concentration. It was concluded from these experiments that the mean muscle glycogen concentration of a group of lambs needs to be greater than 1.5 g/100g on farm in order for the pHu of lamb meat to be less than 5.7.
Subsequent to this industry study, an experiment (Experiment 3) was done to gain an understanding of muscle glycogen concentration as being an integral part of whole body glucose metabolism. This experiment investigated the effects of exercise on a range of different muscles and tissues of lambs including liver, kidney, skin and gastrointestinal tract. Interactions between glycogen concentrations in the liver and muscle with time after exercise showed that glycogen repletion occurred in the liver before muscle tissue. This effect was a unique finding and could explain in part the slow rate of glycogen repletion in muscle tissue that is characteristic for ruminants. Another major finding was an accumulation of glycogen concentration in skin during the recovery period after exercise. It was postulated that this effect may be due to the supply of glucose to glycolytic tissues being continued even when demand for glucose in the skin was low and the capacity to store glycogen in muscle was very high.
Experiment 3 confirmed the existence of a relationship between metabolisable energy (ME) intake and glycogen repletion in muscle tissues and found a slightly different relationship between ME intake and glycogen repletion in the liver tissue of lambs. Muscle glycogen concentration did not change in fasted lambs and the rate of glycogen repletion in muscle after exercise was dependent on ME intake. Differences were observed between different muscles, particularly between M. longissimus thoracis et lumborum (LTL) and all other muscles, in relation to the change in glycogen concentration with time after exercise. Glycogen concentrations changed less rapidly in the LTL than other muscles. Glycogen concentration in the liver was associated negatively with time after exercise in fasted lambs and positively with time after exercise in fed lambs.
Several experiments (Experiments 4, 5 and 6) were conducted to determine the affects of different nutritional factors on muscle glycogen concentration in lambs, both on farm and after commercial slaughter. These studies showed that short term increases in ME intake will increase muscle glycogen concentration to a maximum level over a period of about 7 days (Experiment 4). Diet composition did not affect the change in muscle glycogen concentration associated with an increase in ME intake although results from this experiment (Experiment 5) were not entirely conclusive. There was evidence that the type of feeding and finishing system may influence the susceptibility of muscle glycogen concentration to change during consignment of lambs to slaughter. Results from these experiments demonstrated that a goal for muscle glycogen concentration in lambs on farm of 1.5g/100g is quite achievable with contemporaneous management systems.
Finally this study highlighted the need for further research in a number of key areas in order that muscle glycogen concentration in lambs to be fully understood. In particular, the role of muscle glycogen turnover in relation to muscle glycogen concentration was noted as an area for which further research is warranted.
40
Jacob, Robin Henry. « Optimising the concentration of glycogen in lamb meat ». Jacob, Robin Henry (2003) Optimising the concentration of glycogen in lamb meat. PhD thesis, Murdoch University, 2003. http://researchrepository.murdoch.edu.au/110/.
Texte intégralRésumé :
The lamb industry is actively seeking to improve the quality of lamb meat produced in Australia. Ultimate pH (pHu) is a key determinant of red meat eating quality although this measurement has not been adopted formally by the Australian lamb meat industry. Muscle glycogen concentration is a major determinant of pHu in red meat. This thesis investigates glycogen concentration in lamb muscle and the ultimate pH (pHu) of lamb meat under commercial industry conditions as well as exploring by experimentation, some of the factors that control muscle glycogen concentration in lamb muscle. The results of this work has contributed to an understanding of the significance of high pHu meat to the lamb industry and will assist with developing new management strategies for lambs that avoid low muscle glycogen concentration at the point of slaughter, thus high pHu in meat derived from lambs.
The first part of the study (Experiments 1 and 2) undertook to determine the ranges of muscle glycogen concentration and lamb meat pHu found under commercial conditions and to measure any changes in these parameters associated with consignment of lambs from farm to abattoir and lairage at abattoirs. This study utilised a new biopsy technique that allowed muscle collection from lambs on farm. Some 16 different consignments of lambs and 3 consignments of lactating ewes were intensively monitored on farm and at abattoirs over a range of lairage times. Sensory evaluation tests were done using meat from 6 of these consignments.
The results showed there to be considerable variation between lamb consignments with some consignments having a very high and other consignments having a very low incidence of meat with a high pHu. On balance 'on farm' factors were concluded to have a greater impact on muscle glycogen concentration at slaughter than 'post farm gate' factors. However, there was evidence that muscle glycogen concentrations decreased during the farm curfew and transport period for some consignments so both 'on farm' and 'post farm gate factors' can be important. Characteristically glycogen loss occurred during the farm curfew and transport period in consignments of Merino lambs that had high muscle glycogen concentrations prior to consignment. Holding lambs in lairage caused no negative effects on muscle glycogen concentration although there was some evidence that very short lairage periods may increase meat pHu without causing a change in muscle glycogen concentration. It was concluded from these experiments that the mean muscle glycogen concentration of a group of lambs needs to be greater than 1.5 g/100g on farm in order for the pHu of lamb meat to be less than 5.7.
Subsequent to this industry study, an experiment (Experiment 3) was done to gain an understanding of muscle glycogen concentration as being an integral part of whole body glucose metabolism. This experiment investigated the effects of exercise on a range of different muscles and tissues of lambs including liver, kidney, skin and gastrointestinal tract. Interactions between glycogen concentrations in the liver and muscle with time after exercise showed that glycogen repletion occurred in the liver before muscle tissue. This effect was a unique finding and could explain in part the slow rate of glycogen repletion in muscle tissue that is characteristic for ruminants. Another major finding was an accumulation of glycogen concentration in skin during the recovery period after exercise. It was postulated that this effect may be due to the supply of glucose to glycolytic tissues being continued even when demand for glucose in the skin was low and the capacity to store glycogen in muscle was very high.
Experiment 3 confirmed the existence of a relationship between metabolisable energy (ME) intake and glycogen repletion in muscle tissues and found a slightly different relationship between ME intake and glycogen repletion in the liver tissue of lambs. Muscle glycogen concentration did not change in fasted lambs and the rate of glycogen repletion in muscle after exercise was dependent on ME intake. Differences were observed between different muscles, particularly between M. longissimus thoracis et lumborum (LTL) and all other muscles, in relation to the change in glycogen concentration with time after exercise. Glycogen concentrations changed less rapidly in the LTL than other muscles. Glycogen concentration in the liver was associated negatively with time after exercise in fasted lambs and positively with time after exercise in fed lambs.
Several experiments (Experiments 4, 5 and 6) were conducted to determine the affects of different nutritional factors on muscle glycogen concentration in lambs, both on farm and after commercial slaughter. These studies showed that short term increases in ME intake will increase muscle glycogen concentration to a maximum level over a period of about 7 days (Experiment 4). Diet composition did not affect the change in muscle glycogen concentration associated with an increase in ME intake although results from this experiment (Experiment 5) were not entirely conclusive. There was evidence that the type of feeding and finishing system may influence the susceptibility of muscle glycogen concentration to change during consignment of lambs to slaughter. Results from these experiments demonstrated that a goal for muscle glycogen concentration in lambs on farm of 1.5g/100g is quite achievable with contemporaneous management systems.
Finally this study highlighted the need for further research in a number of key areas in order that muscle glycogen concentration in lambs to be fully understood. In particular, the role of muscle glycogen turnover in relation to muscle glycogen concentration was noted as an area for which further research is warranted.
41
Ferguson, Donna Catherine. « Skeletal Muscle and Hepatic Glycogen Content in Birds ». Thesis, The University of Arizona, 2010. http://hdl.handle.net/10150/146240.
Texte intégral
42
Semiz, Sabina. « Effects of diabetes, insulin, and vanadium on regulation of glycogen synthesis : roles of glycogen synthase kinase-3 and protein phosphatase-1 ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ61172.pdf.
Texte intégral
43
Naperalsky, Michael E. « Effect of post-exercise environmental temperature on glycogen resynthesis ». The University of Montana, 2009. http://etd.lib.umt.edu/theses/available/etd-06052009-115319/.
Texte intégralRésumé :
Hotter environments can often alter the normal exercises responses of metabolism and work performance compared to exercise in a more neutral condition. The goal of this study was to determine the effects of a hot (H) and room temperature (RT) environment on glycogen resynthesis during recovery from exercise. Recreationally active males (n = 9) completed two trials, each with 60-min of cycling exercise at 60% of maximum watts in a temperature-controlled chamber (32.6°C), followed by 4 hours of recovery at the same temperature (H) or 22.2°C (RT). Subjects were fed a carbohydrate beverage (1.8 g/kg bodyweight) at 0 and 2 hours post-exercise. Muscle biopsies were taken from the vastus lateralis at 0, 2, and 4 hours post-exercise for analysis of muscle glycogen. Blood samples were collected at 0, 30, 60, 120, 150, 180, and 240 minutes of recovery for glucose and insulin analysis. Ambient and core temperatures were monitored for the duration of the trial. Expired gas was collected prior to 2- and 4-hour biopsies for calculation of whole-body carbohydrate (CHO) oxidation. Glycogen, core temperature, CHO oxidation, and blood marker values were analyzed using two-way ANOVA with repeated measures. Average core temperature was significantly higher in H compared to RT (38.1°C ± 0.01° vs. 37.9°C ± 0.08°, p<0.05) during recovery. Glycogen was not different at 0 and 2 hours post-exercise. However, at 4 hours post-exercise muscle glycogen was significantly higher in RT vs. H (105 ± 28 vs. 88 ± 24 mmolkg-1 wet weight, respectively). Blood glucose levels were similar between H and RT for the first two hours, but showed lower values (p<0.05) in RT compared to H at time points 150, 180, and 240 minutes post-exercise. CHO oxidation during recovery was higher in H compared to RT (0.36 ± 0.04 g/min vs. 0.22 ± 0.03 g/min, respectively, p<0.05), with greater CHO oxidation at 4-hours post-exercise in both trials. Glycogen resynthesis during recovery is impaired in a hot environment, likely due to increased oxidation of CHO instead of synthesis.
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Munoz, Nicole. « Glucosamine reduces glycogen storage in L6 skeletal muscle cells ». Online access for everyone, 2007. http://www.dissertations.wsu.edu/Thesis/Fall2007/n_munoz_112507.pdf.
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Forsyth, Robert J. « The contribution of astrocyte glycogen to brain energy homeostasis ». Thesis, University of Newcastle Upon Tyne, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361387.
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Chao, Feng Zhi. « The role of myocardial glycogen in the ischaemic heart ». Thesis, University of Edinburgh, 1998. http://hdl.handle.net/1842/21139.
Texte intégralRésumé :
More than half of the total mortality from coronary heart disease results from sudden cardiac death, primarily from ventricular fibrillation (VF). The metabolic changes due to ischaemia are believed to play an important role in the genesis of the arrhythmia. Two of the main mechanisms of myocyte cell death in severe ischaemia are inadequate supply of glycolytically produced adenosine triphosphate (ATP) and increased circulating catecholamines (Opie, 1993). Glucose-insulin-potassium (GIK) protects ischaemic myocardium. However, the role of glycolytic ATP is questioned by the results that preconditioned animals have a better recovery although myocardial glycogen was decreased. The precise effect of GIK is still poorly understood. There has been no evidence for the effects of myocardial glycogen on ischaemic noradrenaline (NA) release. Such a study could provide an alternative explanation for the protective effect of myocardial glycogen on VF. Attention was focused on the effects of myocardial glycogen raised by fasting or GIK infusion on the ischaemic myocardium. Isolated perfused rat hearts were used and retrogradely perfused. Myocardial metabolites and coronary lactate production were measured. The effects of insulin on total anoxia induced NA release were examined. Regional myocardial glycogen levels in the non-ischaemic and ischaemic myocardium of fibrillating and non-fibrillating hearts were also studied. Hearts were freeze clamped at the onset on VF for the measurement of myocardial metabolites. Anaesthetics were necessary to do these studies. However, the effects of anaesthetics on myocardial glycogen levels are unknown and were examined. Enhanced myocardial glycogen levels obtained by the use of a perfusate containing high glucose (15 mM) and/or insulin and fasting did not reduce the incidence of ischaemia-induced VF. Pre-perfusion of hearts under normoxic conditions with insulin decreased anoxic NA overflow under conditions of low K+ (3 mM) concentrations. The myocardial glycogen in situ did not increase after 24 hours fasting, but after 48 hours fasting it did increase. However, this did not affect the incidence of ischaemia-induced VF in vitro. The myocardial glycogen levels raised by fasting were normalised within 10 minutes of isolated perfusion with 5.5 mM glucose. Pentobarbitone, which gave the highest myocardial glycogen levels, can be used for glycogen studies in vitro, provided that hypoxia is prevented during the induction of the anaesthesia. In conclusion: The results in this thesis suggest that the method used to increase myocardial glycogen concentration is more important than the glycogen level itself in protecting the heart against ischaemia.
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Williamson, Brian. « Cloning and characterization of glycogen synthase from Dictyostelium discoideum ». Diss., Virginia Tech, 1995. http://hdl.handle.net/10919/40221.
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Batts, Timothy Wayne. « The Effect of Glycogen Depletion on Sarcoplasmic Reticulum Function ». Thesis, Virginia Tech, 1997. http://hdl.handle.net/10919/31095.
Texte intégralRésumé :
The role of glycogen in endurance performance has been accepted in theory. It has been shown that higher resting muscle glycogen levels prolong endurance performance. On the other hand, low glycogen levels have been associated with fatigue. Ultimately, a personâ s muscle glycogen level dictates the duration in which an activity can be maintained at a maximal effort, after which time, performance will decrease. As of yet, there has been no evidence as to what happens to the fatigued muscle. Force production in skeletal muscle is dictated by the release and uptake of Ca2+ from the sarcoplasmic reticulum (SR). Force production is proportional to [Ca2+], as [Ca2+] increases so does force. At the point of fatigue, there is a decrease in force production. Since fatigue has been associated with glycogen depletion, it is likely that SR function has been altered causing this decrease in force.
The purpose of this study was to determine the effect of glycogen depletion on the SR. Twenty male Sprague-Dawley (Harlan Sprague-Dawley, Indianapolis, IN) rats weighing, 345 ± 70 gm were housed two per cage in the Virginia Tech Lab Animal Resources facility. They were fed ad libitum (Purina Rodent Laboratory Chow and water) until time of experiment. Ten of the rats were used as control animals and the other ten were assigned to the experimental group. Rats were allowed a minimum of 5 days to acclimate to their housing. On the morning of the day of testing, rats were selected in pairs according to the housing cage in an effort to decrease variations in food consumption. To reduce muscle glycogen levels, experimental rats were given an initial injection of either epinephrine (1mg/g: ip) while control rats were injected with saline (equal volume) at 0 hr. Thirty minutes later they received another injection of epinephrine or saline (0.5 mg/g: ip). At the end of the hour the rats were anesthetized with pentobarbital sodium (60 mg/kg:ip) for tissue harvesting. Upon reaching a surgical plane of anesthesia one gastrocnemious muscle was extracted for the muscle glycogen assay and the other removed for SR vesicle preparation. Rats were then euthanized with an overdose of pentobarbital sodium. The tissue was assayed for glycogen and glucose levels as well as for Ca2+ uptake and release and ATPase activity.
It was found that epinephrine animals had 23% less glycogen than did the control animals and almost twice the amount of glucose (control â 2.9 nmol/g and epinephrine â 5.9 nmol/g). Ca2+ uptake rates in epinephrine animals were significantly decreased by 19.7% (p < .05). Control animals had a release rate of 77.15 ± 1.26 nmol/mg/min and epinephrine animals had a release rate of 75.01 ± 1.86 nmol/mg/min. Ca2+ release rates were decreased but not significantly. Ca2+ stimulated ATPase activity was significanlty decreased by 17.7% in epinephrine animals (p < .05).
This is one of the first studies that demonstrate that glycogen reduction in a rested muscle causes altered SR function similar to those caused by exercise. This study shows that low glycogen levels are associated with decreased SR function, which is the primary reason for causing the loss of force in muscle. Ultimately, this study suggests that glycogen loading will enhance endurance performance.Master of Science
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Gardner, Graham Edwin. « Nutritional regulation of glycogen metabolism in cattle and sheep ». Thesis, Gardner, Graham Edwin ORCID : 0000-0001-7499-9986 (2001) Nutritional regulation of glycogen metabolism in cattle and sheep. PhD thesis, Murdoch University, 2001. https://researchrepository.murdoch.edu.au/id/eprint/41881/.
Texte intégralRésumé :
Dark cutting meat is a major economic problem within the cattle and sheep meat industries, and is linked to a shortage of muscle glycogen at slaughter. This study investigated various nutritional aspects involved in the regulation of muscle glycogen metabolism in sheep and cattle.
Initially, a repetitive muscle biopsy protocol was developed such that changes in muscle glycogen concentration over time could be measured. An exercise model for cattle (similar to an existing model for sheep) was then developed facilitating the controlled depletion of muscle glycogen such that rates of glycogen repletion could be measured. This model involved trotting cattle at 9 km/h for five 15-min intervals, with 15-min rest between each interval, depleting muscle glycogen by approximately 50%. The model was then used to assess the impact of various aspects of nutrition on muscle glycogen metabolism, and in a number of experiments the results were supported by data collected during commercial slaughter.
The first experiments carried out in sheep and cattle, compared the rate of glycogen repletion in animals maintained on roughage and cereal grain diets. In cattle there was a positive linear relationship between metabolisable energy (ME) intake and rate of muscle glycogen repletion following exercise. Muscle glycogen repletion following exercise in sheep was independent of ME intake, with animals on all diets repleting at the same rate, suggesting that physiologically sheep place a greater emphasis on recovery of the glycogen depot following stress.
An experiment was then run to determine the influence of dietary nitrogen on muscle glycogen metabolism. Cattle were maintained on grain based diets, formulated with 1, 2 or 3% urea, or 17, 35, 50 or 70% lupin grain. Following exercise there was no difference between any of the dietary treatments, however at slaughter muscle glycogen concentration demonstrated a negative linear relationship with increasing levels of urea inclusion in the diet. There were no differences between lupin treatments, thus the contrasting dietary urea effect may be associated with an increased rate of ammonia absorption from the rumen. Therefore, diets containing high levels of readily hydrolysed rumen degradable nitrogen may lead to reduced muscle glycogen concentration at slaughter.
The next trial investigated the impact of supplemental grain on basal muscle glycogen concentration in cattle previously maintained on roughage diets. After 6 days of supplementation, cattle receiving 6 kg/head/day of barley grain demonstrated the most marked increase in muscle glycogen concentration, however after 16 days all supplemented groups had equilibrated to a similar level of muscle glycogen concentration, all at a higher level than the control. This suggests that over a longer period, 2 kg/hd/day of barley grain can be as efficient as 6kg/hd/day for promoting higher muscle glycogen concentrations.
The use of carbohydrate supplements added to the water were trialed in sheep and cattle in an attempt to provide water-borne substrate for muscle glycogen repletion. Initially, sheep were drenched with various carbohydrate supplements showing that a combination drench of 70% glycerol and 30% propylene glycol produced the greatest hyperglycaemic response. Cattle and sheep were then offered the supplement at the rate of 3.5% glycerol and 1.5% propylene glycol, increasing the rate of muscle glycogen repletion following exercise, although not affecting muscle glycogen concentration at slaughter. The supplement increased water intakes during lairage, and reduced pHu in both species.
Magnesium oxide was supplemented in the feed of sheep and cattle, with an aim to reduce glycogen loss at slaughter, and to increase the rate of repletion following exercise. In sheep, the rate of muscle glycogen repletion was increased following exercise, and muscle glycogen concentration was increased at slaughter, however in cattle there was minimal response. Thus MgO appears to be a viable option for reducing glycogen loss in sheep at slaughter.
Lastly, the metabolism of muscle glycogen in Merino lambs was compared to first and second cross Merinos at slaughter. Increasing proportions of Merino genetics were associated with increased muscle glycogen loss during commercial slaughter. This suggests that Merino’s are more sensitive to stress than cross bred lambs, highlighting that extra care must be taken with the management and handling of this breed prior to slaughter.
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Benedict, Michael A. « Reliability in the measurement of muscle fiber composition and the histrochemical staining for glycogen ». Virtual Press, 1990. http://liblink.bsu.edu/uhtbin/catkey/722240.
Texte intégralRésumé :
This study was conducted to determine the variation in stain Intensity between serial sections of muscle biopsies following a periodic acid Schiff (PAS) staining procedure, to assess the reliability of the PAS staining technique for the quantitation of the glycogen content in muscle fibers, and to evaluate the variability in fiber composition between repeated biopsies of the vastus lateralis (VL) muscle. Eight randomly located biopsies (4 right leg and 4 left leg) were obtained from the VL of each of 16 healthy males (26.1 ± 1.1 years). Serial cross sections, 10 um thick, were cut from each biopsy and stained for myosin ATPase following an acid preincubation at pH=4.30 and for glycogen using a PAS staining procedure. No significant difference existed in the fiber composition between the eight repeated biopsies taken from an individual. The variation In type I fiber percentage, expressed as the coefficient of variation, between repeated biopsies of the same leg and between the right and left VL averaged 18.6% and 17.7%, respectively. In many cases, differences of greater than 20% In the percentage of type I fibers were observed between repeated samples. These data suggest an inhomogeneity with regard to the fiber type distribution in the VL of young males and an Inability to predict the fiber composition of a muscle with a single biopsy sample.The optical densities (OD) of the same 50 type I and 50 type II fibers were determined In each of three PAS stained serial sections per biopsy using a computer integrated photometric system. Mean total, fiber type specific, and Individual fiber OD did not differ significantly between the serial sections although a variability was observed. This variability appears to be primarily due to differences In sectional thickness. The comparison of biochemically determined glycogen content (41.0 - 191.0 mmol.kg-lwet weight) to mean total OD in sections from the same samples resulted in a poor relationship (r=0.47) between the two methods for the quantification of muscle glycogen. These results Indicate a variability in PAS stain intensity between serial sections of muscle biopsies and an inability to quantify muscle glycogen concentrations with the photometric determination of OD of the PAS stain in cross sections of muscle.School of Physical Education