Figure 5-38b, step 1

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Transcript Figure 5-38b, step 1

POWERPOINT® LECTURE SLIDE PRESENTATION
by LYNN CIALDELLA, MA, MBA, The University of Texas at Austin
UNIT 1
5
PART C
Membrane Dynamics
HUMAN PHYSIOLOGY
AN INTEGRATED APPROACH
DEE UNGLAUB SILVERTHORN
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FOURTH EDITION
The Body Is Mostly Water
Distribution of water volume in the three body fluid
compartments
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Figure 5-28
Osmosis and Osmotic Pressure
Osmolarity describes the number of particles in solution
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Figure 5-29
Osmosis and Osmotic Pressure
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Figure 5-29 (1 of 3)
Osmosis and Osmotic Pressure
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Figure 5-29 (2 of 3)
Osmosis and Osmotic Pressure
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Figure 5-29 (3 of 3)
Osmolarity: Comparing Solutions
 Solution A = 1 OsM Glucose
 Solution B = 2 OsM Glucose
 B is hyperosmotic to A
 A is hyposmotic to B
 What would be the osmolarity of a solution which is
isosmotic to A? to B?
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Tonicity
Tonicity describes the volume change of a cell placed
in a solution
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Tonicity
Tonicity depends on the relative concentrations
of nonpenetrating solutes
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Figure 5-30a
Tonicity
Tonicity depends on nonpenetrating solutes only
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Figure 5-30b
Electricity Review
 Law of conservation of electrical charges
 Opposite charges attract; like charges repel each other
 Separating positive charges from negative charges
requires energy
 Conductor versus insulator
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Separation of Electrical Charges
Resting membrane potential is the electrical gradient
between ECF and ICF
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Figure 5-32b
Separation of Electrical Charges
Resting membrane potential is the electrical gradient
between ECF and ICF
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Figure 5-32c
Potassium Equilibrium Potential
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Figure 5-34a
Potassium Equilibrium Potential
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Figure 5-34b
Potassium Equilibrium Potential
Resting membrane potential is due mostly
to potassium
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Figure 5-34c
Sodium Equilibrium Potential
Can be calculated using the Nernst Equation
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Figure 5-35
Changes in Membrane Potential
Terminology associated with changes in membrane
potential
PLAY Animation: Nervous I: The Membrane Potential
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Figure 5-37
Insulin Secretion and
Membrane Transport Processes
(a) Beta cell at rest. The KATP channel is open and the
cell is at its resting membrane potential.
1
2
Low glucose
levels in blood
Metabolism
slows.
3
4
KATP
ATP
decreases. channels open.
K+
Glucose
Metabolism
5
K+ leaks
out
of cell
Cell at resting
membrane potential;
no insulin is released.
Voltage-gated
Ca2+ channel
closed
ATP
GLUT
transporter
No insulin
secretion
Insulin in
secretory vesicles
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Figure 5-38a
Insulin Secretion and
Membrane Transport Processes
(a) Beta cell at rest. The KATP channel is open and the
cell is at its resting membrane potential.
1
Low glucose
levels in blood
Glucose
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Figure 5-38a, step 1
Insulin Secretion and
Membrane Transport Processes
(a) Beta cell at rest. The KATP channel is open and the
cell is at its resting membrane potential.
1
2
Low glucose
levels in blood
Glucose
Metabolism
slows.
Metabolism
GLUT
transporter
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Figure 5-38a, steps 1–2
Insulin Secretion and
Membrane Transport Processes
(a) Beta cell at rest. The KATP channel is open and the
cell is at its resting membrane potential.
1
2
Low glucose
levels in blood
Glucose
Metabolism
slows.
Metabolism
3
ATP
decreases.
ATP
GLUT
transporter
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Figure 5-38a, steps 1–3
Insulin Secretion and
Membrane Transport Processes
(a) Beta cell at rest. The KATP channel is open and the
cell is at its resting membrane potential.
1
2
Low glucose
levels in blood
Metabolism
slows.
3
4
KATP
ATP
decreases. channels open.
K+
Glucose
Metabolism
K+ leaks
out
of cell
ATP
GLUT
transporter
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 5-38a, steps 1–4
Insulin Secretion and
Membrane Transport Processes
(a) Beta cell at rest. The KATP channel is open and the
cell is at its resting membrane potential.
1
2
Low glucose
levels in blood
Metabolism
slows.
3
4
KATP
ATP
decreases. channels open.
K+
Glucose
Metabolism
5
K+ leaks
out
of cell
Cell at resting
membrane potential;
no insulin is released.
Voltage-gated
Ca2+ channel
closed
ATP
GLUT
transporter
No insulin
secretion
Insulin in
secretory vesicles
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Figure 5-38a, steps 1–5
Insulin Secretion and
Membrane Transport Processes
(b) Beta cell secreting insulin. Closure of the KATP channel
depolarizes the cell, triggering exocytosis of insulin.
1
2
High glucose
levels in blood
Metabolism
increases.
3
ATP
increases.
4
KATP channels
close.
5
Cell depolarizes and
calcium channels
open.
6
Ca2+ entry
acts as an
intracellular
signal.
Ca2+
Glucose
Glycolysis
and citric
acid cycle
ATP
GLUT
transporter
Ca2+
7
Ca2+ signal
triggers
exocytosis,
and insulin
is secreted.
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Figure 5-38b
Insulin Secretion and
Membrane Transport Processes
(b) Beta cell secreting insulin. Closure of the KATP channel
depolarizes the cell, triggering exocytosis of insulin.
1
High glucose
levels in blood
Glucose
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 5-38b, step 1
Insulin Secretion and
Membrane Transport Processes
(b) Beta cell secreting insulin. Closure of the KATP channel
depolarizes the cell, triggering exocytosis of insulin.
1
2
High glucose
levels in blood
Glucose
Metabolism
increases.
Glycolysis
and citric
acid cycle
GLUT
transporter
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 5-38b, steps 1–2
Insulin Secretion and
Membrane Transport Processes
(b) Beta cell secreting insulin. Closure of the KATP channel
depolarizes the cell, triggering exocytosis of insulin.
1
2
High glucose
levels in blood
Glucose
3
Metabolism
increases.
ATP
increases.
Glycolysis
and citric
acid cycle
ATP
GLUT
transporter
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 5-38b, steps 1–3
Insulin Secretion and
Membrane Transport Processes
(b) Beta cell secreting insulin. Closure of the KATP channel
depolarizes the cell, triggering exocytosis of insulin.
1
2
High glucose
levels in blood
Glucose
3
Metabolism
increases.
ATP
increases.
Glycolysis
and citric
acid cycle
ATP
4
KATP channels
close.
GLUT
transporter
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 5-38b, steps 1–4
Insulin Secretion and
Membrane Transport Processes
(b) Beta cell secreting insulin. Closure of the KATP channel
depolarizes the cell, triggering exocytosis of insulin.
1
2
High glucose
levels in blood
Glucose
3
Metabolism
increases.
ATP
increases.
Glycolysis
and citric
acid cycle
ATP
4
KATP channels
close.
5
Cell depolarizes and
calcium channels
open.
GLUT
transporter
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 5-38b, steps 1–5
Insulin Secretion and
Membrane Transport Processes
(b) Beta cell secreting insulin. Closure of the KATP channel
depolarizes the cell, triggering exocytosis of insulin.
1
2
High glucose
levels in blood
Metabolism
increases.
3
ATP
increases.
4
KATP channels
close.
5
Cell depolarizes and
calcium channels
open.
6
Ca2+ entry
acts as an
intracellular
signal.
Ca2+
Glucose
Glycolysis
and citric
acid cycle
ATP
Ca2+
GLUT
transporter
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 5-38b, steps 1–6
Insulin Secretion and
Membrane Transport Processes
(b) Beta cell secreting insulin. Closure of the KATP channel
depolarizes the cell, triggering exocytosis of insulin.
1
2
High glucose
levels in blood
Metabolism
increases.
3
ATP
increases.
4
KATP channels
close.
5
Cell depolarizes and
calcium channels
open.
6
Ca2+ entry
acts as an
intracellular
signal.
Ca2+
Glucose
Glycolysis
and citric
acid cycle
ATP
GLUT
transporter
Ca2+
7
Ca2+ signal
triggers
exocytosis,
and insulin
is secreted.
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Figure 5-38b, steps 1–7
Summary
 Mass balance and homeostasis
 Law of mass balance
 Excretion
 Metabolism
 Clearance
 Chemical disequilibrium
 Electrical disequilibrium
 Osmotic equilibrium
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Summary
 Diffusion
 Protein-mediated transport
 Roles of membrane proteins
 Channel proteins
 Carrier proteins
 Active transport
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Summary
 Vesicular transport
 Phagocytosis
 Endocytosis
 Exocytosis
 Transepithelial transport
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Summary
 Osmosis and tonicity
 Osmolarity
 Nonpenetrating solutes
 Tonicity
 The resting membrane potential
 Insulin secretion
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings