Title: Regulation of Glycogen Metabolism
1Regulation of Glycogen Metabolism!!
2Figure 18-22 The enzymatic activities of
phosphorylase a and glycogen synthase in mouse
liver in response to an infusion of glucose.
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3Figure 18-9 The control of glycogen phosphorylase
activity.
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4Figure 18-13 Control of glycogen metabolism
in muscle.
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5Figure 18-16 X-Ray structure of rat testis
calmodulin.
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6Figure 18-19 Schematic diagram of the
Ca2CaM-dependent activation of protein
kinases.
7Figure 18-21 The antagonistic effects of insulin
and epinephrine on glycogen metabolism in muscle.
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8Maintaining 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.
9Figure 18-23 Comparison of the relative enzymatic
activities of hexokinase and glucokinase over the
physiological blood glucose range.
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10Figure 18-24 Formation and degradation of
?-D-fructose-2,6-bisphosphate as catalyzed by
PFK-2 and FBPase-2.
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11Figure 18-26a The livers response to stress.
(a) Stimulation of ?-adrenoreceptors by
epinephrine activates phospholipase C to
hydrolyze PIP2 to IP3 and DAG.
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12- Epinephrine and Norepinephrine
- Mention 2,5 BFP
13Figure 18-26b The livers response to stress. (b)
The participation of two second messenger systems.
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14Signal Transduction--Ch 19
15Figure 19-1a Classification of hormones. (a)
Endocrine signals are directed at distant cells
through the intermediacy of the bloodstream.
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16Figure 19-1b Classification of hormones. (b)
Paracrine signals are directed at nearby cells.
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17Figure 19-1c Classification of hormones. (c)
Autocrine signals are directed at the cell that
produced them.
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18Figure 19-2 Major glands of the human endocrine
system.
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19Table 19-1 Some Human Hormones Polypeptides.
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20Table 19-1 (continued) Some Human Hormones
Polypeptides.
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21Table 19-1 (continued) Some Human Hormones
Steroids.
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22Table 19-1 (continued) Some Human Hormones
Amino Acid Derivatives.
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23Fig. 19-16 Receptor-mediated activation/inhibitio
n of Adenylate Cyclase
24Figure 19-13 Activation/deactivation cycle for
hormonally stimulated AC.
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25Figure 19-14 General structure of a G
protein-coupled receptor (GPCR).
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26Figure 19-15 X-Ray structure of bovine rhodopsin.
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27Figure 19-51 Role of PIP2 in intracellular
signaling.
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28Figure 19-21 Schematic diagram of a typical
mammalian AC.
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29Figure 19-50 Molecular formula of the
phosphatidylinositides.
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30Figure 19-52 A phospholipase is named according
to the bond that it cleaves on a
glycerophospholipid.
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31Figure 19-57 Activation of PKC.
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32Figure 19-64 Insulin signal transduction.
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33Figure 19-18a X-Ray structure of the
hetero- trimeric G protein Gi.
G? subunit is violet with its Switch I, II,
and III segments green, blue, and red,
respectively
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34Figure 19-19 Mechanism of action of cholera toxin.
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35Figure 19-23 Domain organization in a variety of
receptor tyrosine kinase (RTK) subfamilies.
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36Figure 19-27a Growth pattern of vertebrate cells
in culture. (a) Normal cells stop growing
through contact inhibition once they have formed
a confluent monolayer.
(b) In contrast, transformed cells lack contact
inhibition they pile up to form a multilayer.
37Figure 19-28 Variation of the cancer death rate
in humanswith age.
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38Figure 19-29a Transformation of cultured chicken
fibroblasts by Rous sarcoma virus. (a) Normal
cells adhere to the surface of the culture
dish.(b) On infection with RVS, these cells
become rounded and cluster together in piles.
(a)
(b)
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39Figure 19-38 The Ras-activated MAP kinase cascade.
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40Figure 19-40 MAP kinase cascades in mammalian
cells.
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