Glycogen Structure and Synthesis and Glycogen Metabolism Flashcards
Where does glycogen synthesis and storage take place?
cytosol in liver and skeletal muscle
What determines the storage capacity for glycogen?
number of glycogenin molecules and physical restriction
What is the energy cost of turning each free glucose molecule into glycogen?
2ATP
How often does branching occur?
every 8 to 10 glucose units, closer together at core
glycogenin
protein at gore of each glycogen particle, first carbon linked to hydroxyl group of a specific tyrosine side chain of glycogenin via the autocatalytic activity of glycogenin
What is the effect of insulin on muscle and liver?
in muscle, insulin recruits GLUT4 transporters to the surface of the plasma membrane, making more intracellular glucose available.
In liver, insulin induces synthesis of glucokinase thereby ensuring continued uptake of glucose
What are the consequences of branching?
increased solubility
increased number of nonreducing ends
increased potential for rapid mobilization and deposition of glucose
What are the conditions that promote glycogen synthesis?
high carb meal
hyperglycemia
priorities for disposal of intracellular glucose: meet immediate energy needs of the cell, store as glycogen, conversion to fat
hormonal changes: increase in insulin/glucagon ratio
insulin promotes fuel storage and dephosphorylation of key enzymes involved in fuel storage. The effects are antagonized by glucagon and epinephrin.
Describe the effects of insulin on glycogen synthesis.
insulin activates protein phosphatase
insulin results in decreased cAMP (cAMP inhibits protein phosphatase and activates protein kinase A)
What stimulates glycogen degradation?
increase in glucagon or elevation in blood epinephrin levels
AMP accumulation in muscle
Describe the allosteric regulation differences of liver and muscle glycogen phosphorylase.
AMP important allosteric activator in skeletal muscle
Glucose - important allosteric inhibitor in liver
Describe the activation of muscle phosphorylase.
hormonal activation by epinephrin B: binding of epinephrine to beta-adrenergic receptors increase cAMP levels in muscle cell, while binding to alpha adrenergic receptors - increases Ca2+ concentration. Both cAMP and Ca2+ act as second messengers to activate protein kinase: phosphorylation of a specific serine residue and activation of glyogen phosphorylase.
neural activation by Ca2+ dependent mechanism - synchronizes muscle contraction with glycogenolysis. Ca2+ activates phosphorylse kinase
allosteric activation by AMP0 inactive dephospho form of glycogen phosphorylase allosterically activated by accumulation of AMP. Occurs under conditions of anoxia and ATP depletion.
Allosteric inhibition by indicators of high energy state- accumulation of glucose 6 phosphate or ATP - inhibit glycogen phosphorylase
Describe activation of liver phosphorylase
Hormonal activation by glucagon or by epinephrine. Binding of glucagon to its receptor or of epinephrine to beta-adrenergic receptors involves a cAMP dependent cascade which activates protein kinases
hormonal activation by epinephrine binding to alpha1 receptors - mediated by second messengers (IP3 and Ca2+)
glycogen phosphorylase is inhibited by glucose, glucose 6 phosphate and ATP
Inactivation of phosphorylase by protein phosphatse 1.
protein phosphatase1 is stimulated by insulin adn inhibited by increase in cAMP. Protein inhibitor 1 will act as an inhibitor only after cAMP dependent phosphorylation. Same signal results in activation of glycogen phosphorylase - keepin in active state preventing dephophorylation
Protein inhibitor 1 mediates inhibitory effect of cAMP on protein phosphatase 1keeping glycogen phosphorylase in active form
Describe the role of cAMP in glycogen metabolism
synthesis of cAMP is stimulated by epinephrin (liver and muscle and glucagon (liver). Degredation by cAMP phosphodiesterase is activated by insulin and inhibited by caffeine.
Phosphorylase is activated and synthase is inhibited by cAMP
