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Glycogen Metabolism

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Glc inhibits pancreatic -cells from secreting glucagon. ... Glucagon receptors on liver cells respond to glucagon binding by activating AC causing [cAMP] ... – PowerPoint PPT presentation

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Title: Glycogen Metabolism


1
Glycogen Metabolism
Chapter 18
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glycogen phosphorylase activation glycogen
converted to G-1-P
4
Figure 18-22 The enzymatic activities of
phosphorylase a and glycogen synthase in mouse
liver in response to an infusion of glucose.
Page 648
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Figure 18-2c X-Ray structure of rabbit muscle
glycogen phosphorylase. (c) An interpretive
low-resolution drawing of Part b showing the
enzymes various ligand-binding sites.
Page 628
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Figure 19-21 Schematic diagram of a typical
mammalian AC.
Page 682
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Figure 19-57 Activation of PKC.
Page 713
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Figure 18-9 The control of glycogen phosphorylase
activity.
Page 635
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Figure 18-12 A bicyclic enzyme cascade.
Page 638
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Figure 18-13 Schematic diagram of the major
enzymatic modification/demodification systems
involved in the control of glycogen metabolism in
muscle.
Page 639
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Figure 18-19 Schematic diagram of the
Ca2CaM-dependent activation of protein kinases.
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Figure 18-24 Formation and degradation of
?-D-fructose-2,6-bisphosphate as catalyzed by
PFK-2 and FBPase-2.
Page 649
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Figure 18-26b The livers response to stress. (b)
The participation of two second messenger systems.
Page 652
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In response to stress (i.e., release of
epinephrine) the liver EXPORTS glucose (to
muscle tissue fight or flight)
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Figure 18-21 The antagonistic effects of insulin
and epinephrine on glycogen metabolism in muscle.
Page 645
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Maintaining Blood Glucose Levels
  • During exercise or long after meals, the liver
    releases glc into the bloodstream
  • Glc inhibits pancreatic ?-cells from secreting
    glucagon. Inhibition is released when glc levels
    fall.
  • Glucagon receptors on liver cells respond to
    glucagon binding by activating AC causing ?
    cAMP.
  • ? cAMP increases the rate of glycogen breakdown
    and increased G6P.
  • G6P cannot pass through cell membranes.
    However, the liver, which doesnt rely on glc for
    a major energy source, has a G6P hydrolase to
    release glc.

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Table 18-1 Hereditary Glycogen Storage Diseases.
Page 651
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Figure 18-27 The ADP concentration in human
forearm muscles during rest and following
exertion in normal individuals and those with
McArdles disease.
Page 653
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Figure 18-26a The livers response to stress.
(a) Stimulation of ?-adrenoreceptors by
epinephrine activates phospholipase C to
hydrolyze PIP2 to IP3 and DAG.
Page 652
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Figure 19-64 Insulin signal transduction.
Page 719
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Figure 18-26a The livers response to stress.
(a) Stimulation of ?-adrenoreceptors by
epinephrine activates phospholipase C to
hydrolyze PIP2 to IP3 and DAG.
Page 652
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Signal Transduction--Ch 19
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Figure 19-1a Classification of hormones. (a)
Endocrine signals are directed at distant cells
through the intermediacy of the bloodstream.
Page 658
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Figure 19-1b Classification of hormones. (b)
Paracrine signals are directed at nearby cells.
Page 658
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Figure 19-1c Classification of hormones. (c)
Autocrine signals are directed at the cell that
produced them.
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Figure 19-2 Major glands of the human endocrine
system.
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Table 19-1 Some Human Hormones Polypeptides.
Page 659
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Table 19-1 (continued) Some Human Hormones
Polypeptides.
Page 659
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Table 19-1 (continued) Some Human Hormones
Steroids.
Page 659
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Table 19-1 (continued) Some Human Hormones
Amino Acid Derivatives.
Page 659
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Fig. 19-16 Receptor-mediated activation/inhibitio
n of Adenylate Cyclase
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Figure 19-13 Activation/deactivation cycle for
hormonally stimulated AC.
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Figure 19-14 General structure of a G
protein-coupled receptor (GPCR).
Page 674
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Figure 19-51 Role of PIP2 in intracellular
signaling.
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Figure 19-21 Schematic diagram of a typical
mammalian AC.
Page 682
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Figure 19-50 Molecular formula of the
phosphatidylinositides.
Page 707
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Figure 19-52 A phospholipase is named according
to the bond that it cleaves on a
glycerophospholipid.
Page 709
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Figure 19-57 Activation of PKC.
Page 713
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Figure 19-64 Insulin signal transduction.
Page 719
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