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The anaerobic glycogen consumption and the question of post-anaerobic glycogen resynthesis in some invertebratesCleary, Mary Baptist, January 1948 (has links)
Thesis--Catholic Univ. of America. / "Literature cited": p. 17-18.
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A chemical study of glycogen and its preparation ...McBride, James Joseph, January 1929 (has links)
Thesis (PH. D.)--Columbia University, 1930. / Vita. Bibliography: p. [29].
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Ein beitrag zur physiologie des glykogens ...Adamoff, Wera. January 1904 (has links)
Innaug.-Diss.--Bern.
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Crystallographic studies on phosphorylase : sugar recognition propertiesWatson, Kimberly Ann January 1994 (has links)
No description available.
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Glucocorticoid and its effect on cardiac glucose utilizationPuthanveetil, Prasanth Nair 11 1900 (has links)
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.
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Glucocorticoid and its effect on cardiac glucose utilizationPuthanveetil, Prasanth Nair 11 1900 (has links)
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.
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The role of glycogen synthase kinase 3-beta in interferon beta biology /Wang, Huizhi, January 2009 (has links) (PDF)
Thesis (Ph. D.)--University of Louisville, 2009. / Department of Microbiology and Immunology. Vita. "May 2009." Includes bibliographical references (leaves 64-76).
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Glycogen resynthesis following submaximal and supramasimal exhaustive exercise in manOkocha, Augustine Emefiene. January 1984 (has links)
Thesis (Ph. D.)--University of Wisconsin--Madison, 1984. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 109-119).
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Amino acid metabolism during exercise and recovery in human subjectsBruce, Mark January 2001 (has links)
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.
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Glucocorticoid and its effect on cardiac glucose utilizationPuthanveetil, Prasanth Nair 11 1900 (has links)
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. / Pharmaceutical Sciences, Faculty of / Graduate
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