SYLLABUS FOR FST 861; WINTER 1998
HIERARCHY OF DIETARY AND HORMONAL CONTROL MECHANISMS
Call No. 08146-4, 3 credit hours, Tues. and Thurs. 2PM in 123 Vivian Hall.
Instructor: Dr. Karla Roehrig; 292-7706, 292-1090 or e-mail at roehrig.1@osu.edu
Office hours:9-11AM Tues. in 225 Howlett
Hall or by appt.
Purpose: This course examines the
means by which organisms maintain a homeostatic environment in
the face of intermittent food supplies and demand on energy
reserves. The approach is species independent and focuses on
cellular and subcellular mechanisms by which various forms of
regulation are achieved. Students will expand their basic
knowledge of biochemical pathways and mechanisms and gain a
broader perspective of metabolic regulation by examining a series
of physiologic systems in considerable detail. The overall
objectives for each topic of discussion are given in the course
outline below. Individuals with advanced degrees are expected to
be able to communicate their ideas clearly and concisely and to
back them up with appropriate supporting evidence. Consequently,
there will be numerous opportunities for class discussion and
participation. Involvement in these discussion is both desired
and required.
Objectives: The successful student in this course will be able to
* identify the likely control mechanisms for any physiological system
* relate established data about given systems to potential control points
* evaluate the relevance of current literature concerning regulatory systems
* integrate new material with long held physiological paradigms
* focus on pathway interactions that maintain homeostasis
* design experiments to test hypotheses
relating to metabolic regulation
Evaluation: The extent to which
objectives are met will be measured several ways. The first
midterm (100 points) will be closed book, in class and will
measure mostly objective information about regulatory systems.
The second midterm and the final (each worth 100 points) will be
take home exams. Any source of information including discussions
with each other are acceptable. You are encouraged to interact
with others as much as possible. Finally, there will be biweekly
in class exercise, sometimes written and sometimes oral or group
exercises. They will be restricted to 10 minutes and will count
20 points each for a total of 100 points. The exercises will be
based on class discussions occurring that week. Required reading
is included in a course packet available from Grade A Notes. You
are encouraged to read the assigned material ahead of each
class period so that you are able to participate fully in class
discussions.
Day Date Topic and Objectives
Unit 1. Types of Regulation
T 1/6 Course introduction and outline of 10 forms of regulation
A. Outline the procedures and expectations for the course
B. List the 10 forms of regulation to produce a homeostatic environment
C. Discuss the advantages and disadvantages of each type of regulation
No outside reading
Th 1/8 Regulation by compartmentation, substrates, products and metabolic
effectors
A. Evaluate the requirements and outcomes of these 4 types of regulation
B. Cite examples of each
C. Determine the speed, regional impact and communication potential of
of these control mechanisms
D. Discuss the methodology for studying them.
Required reading: D. Bray (1997) Reductionism for biochemists: how to
survive the protein jungle. TIBS 22, 325-326.
T 1/13 Regulation by synthesis, degradation and ambiquity
A. Identify the elements involved in the regulation of protein synthesis
B. Identify the elements involved in the regulation of protein degradation
C. Compare the energy costs of synthesis and degradation to other forms
of control
D. Debate the advantages of ambiquity in various physiological conditions
Required reading: A. Haas and T. Siepmann (1997) Pathways of ubiquitin
conjugation. FASEB J. 11, 1257-1268.
10 Minute in class exercise
Th 1/15 Covalent modification
A. List the known types of covalent modification
B. Examine the G protein based systems
C. Outline energy requirements for each type
D. Identify appropriate controls for each system
Required reading: M. Gelb (1997) Protein prenylation, etc.: signal
transduction in two dimensions. Science 275, 1750-1751.
T 1/20 Regulation of hormones and neural effectors
A. Compare and contrast these two types of regulation
B. Assess the action of hormones acting in endocrine, paracrine or
autocrine fashions
C. Discuss the concept of a second messenger and the mobile receptor
hypothesis
D. Identify control systems that operate on more than one level
E. Debate the advantages of multicellularity
Required reading: M. Cobb and E. Goldsmith (1995) How MAP kinases
are regulated. J. Biol. Chem. 270,
14843-14846.
Th 1/22 In class exam, closed book, two
hours
1/23 Last day to audit and last day to
drop w/o a W.
Unit 2. Specific Regulatory Pathways
T 1/27 Peptide Hormones I.
A. Establish common regulatory points
B. Speculate on important regulatory steps in the serum
C. Analyze global factors which affect hormone sensitivity
Required reading: K. Tronheim (1997) Are metabolic oscillations
responsible for normal oscillatory insulin secretion? Diabetes
46, 1375-1380.
10 minute in class exercise
Th 1/29 Peptide Hormones II.
A. Differentiate between single receptors and the mobile receptor
hypothesis
B. Outline steps in hormone receptor binding and 2nd messenger
generation
C. Design experiments to elucidate changes at the
hormone/receptor/messenger level.
Required reading: I. Macara et al (1996) The ras superfamily of GTPases
FASEB J. 10, 625-630
T 2/3 Non-peptide Hormone systems
A. Discuss alternative receptor sites for non-peptide hormones
B. Determine commonalities in signal generation
C. Design experiments to focus on agonist and antagonist functions
Required reading: N. Weigel (1996) Steroid hormone receptors and their
regulation by phosphorylation. Biochem. J. 319,
657-667.
Th 2/5 Calcium based signal systems I.
A. Identify elements allowing calcium to be a good signal
B. Evaluate relative roles of calmodulin and calcium dependent kinases
C. Describe calcium binding systems
Required reading: M. Komatsu et al. (1997) Augmentation of insulin
release by glucose in the absence of extracellular Ca++. Diabetes
46, 1928-1938.
T 2/10 Calcium based signal systems II.
A. Explore whole body calcium homeostasis
B. Compare calcium uptake and efflux systems for cells and sub-
cellular compartments
C. Evaluate drugs that interfere with calcium signalling
10 minute in class exercise
No required reading
Th 2/12 Sphingomyelin cycle signalling
A. Outline the elements of the sphingomyelin cycle
B. Identify the coupling to various cytokines
C. Discuss the regulatory implications for this cycle
Required reading: L. Martins and W. Earnshaw (1997) Apoptosis: alive
and kicking in 1997. Trends in Cell Biol. 7,
111-114.
T 2/17 Circadian rhythms
A. Compare regulatory systems for rhythms with different timing
B. Evaluate several systems for studying chronobiology
C. Explore impact of circadian rhythms on interpretation of data
Required reading: B.C. Johnson (1992) Nutrient intake as a time cycle for
circadian rhythm. J. Nutr. 122,
1753-1759.
Unit 3. How diet and hormones interact
to regulate physiological processes
Th 2/19 Regulation of appetite Exam II. Take-home due at beginning of class
A. Compare central and peripheral appetite regulatory cues
B. Assess impact of specific nutrient on appetite
C. Identify various methodological problems in appetite experiments
Required reading: Q. Wang et al (1997) Interactions between leptin and
hypothalamic neuropeptide Y neurons in the control of food intake
and energy homeostasis in the rat. Diabetes 46, 335-341.
T 2/24 Regulation of body composition
A. Describe embryological impact on tissue distribution and body comp.
B. Evaluate external parameters such as diet and exercise
C. Examine influence of genetic parameters
D. Explore aberrant states and body composition
Required reading: R. Rubenoff (1997) Inflammatory and hormonal
mediators of cachexia. J. Nutr. 127, 1014S-1016S.
10 minute in class exercise
Th 2/26 Regulation of body fat I.
A. Determine the origin of body fat
B. Consider the implications in studies with fat cells
C. Evaluate whole body effects on fat deposition
Required reading: G. Bray (1997) Progress in understanding the genetics
of obesity. J. Nutr. 127, 940S-942S.
T 3/3 Regulation of body fat II.
A. Compare regulation of various lipogenic enzymes
B. Establish regulatory events that result from functional needs
C. Identify potential sites for intervention in lipogenic regulation
Required reading: V. Zammit (1996) Role of insulin in hepatic fatty acid
partitioning: emerging concepts. Biochem.
J. 314, 1-14.
Th 3/5 Regulation of carbohydrate stores
A. Delineate the regulatory features of the glucose transporters
B. Account for the disaccharide effect
C. integrate control systems regulating glycogen levels
Required reading: J. Lawrence and P. Roach (1997) New insights into the
role and mechanism of glycogen synthetase activation by insulin.
Diabetes 46, 541-547.
T 3/10 Alterations to regulation to accommodate stress
A. Define hormones associated with stress
B. Explore the positive and negative consequences of stress for an
organism
C. Identify the environmental triggers that stimulate stress mechanisms
Required reading: S. Hand and I. Hardewig (1996) Down regulation of
cellular metabolism during environmental stress. Ann. Rev. Physiol.
58, 539-563.
10 minute in class exercise
Th 3/12 Final exam, in class, closed book
T 1/6 Course introduction and outline of 10
forms of regulation
A. Outline the procedures and expectations for the course
See syllabus
B. List the 10 forms of regulation to produce a homeostatic environment
1. Compartmentation
2. Substrate
3. Product
4. Metabolic effector
5. Synthesis
6. Degradation
7. Ambiquity
8. Covalent modification
9. Neural
10. Hormonal
C. Discuss the advantages and disadvantages of each type of regulation
1. Short term mechanisms offer speed, flexibility and low energy costs
2. They operate in a narrow range, however, so synthesis and degradation
offer the opportunity to increase/decrease activity many fold though at
high energy cost.
Required reading: None
Review Questions:
1. What are the 10 forms of regulation and give an example of each?
2. Calculate the relative energy cost of regulating a protein by synthesis and degradation vs covalent modification.
3. How would you determine whether an enzyme was ambiquitous?
4.What advantages do neural and hormonal regulation offer an organism?
5. What is homeostasis?
Th 1/8 Regulation by compartmentation, substrates, products and metabolic
effectors
A. Evaluate the requirements and outcomes of these 4 types of regulation
1. Oldest types of regulation
2. Substrate- usually but not always positive
3. Product- usually but not always negative
4. Metabolic effector- binds at a site
different that the active site of enzyme
B. Cite examples of each
1. Compartmentation- prokaryotic vs eukaryotic and mechanisms involved
2. Substrate- operations above or below the Km
3. Product- ability to prevent blockages in pathways
4. Metabolic effectors- primitive means to communication between pathways,
often a secondary form of control, not
synonymous with allosteric effector
C. Determine the speed, regional impact and communication potential of
of these control mechanisms
1. Substrates, products and metabolic effectors work over narrow kinetic
ranges but are immediate and short-lived.
2. Effectors provide an analog range of
regulation at low cost.
D. Discuss the methodology for studying
them.
Required reading: B. Bray (1997) Reductionism for biochemists: how to survive the
protein jungle. TIBS 22, 325-326.
Review Questions:
1. When is change in substrate concentration an effective regulator?
2. If a pathway is blocked at a step remote from a particular enzyme, what mechanisms are available to communicate the blockage?
3. How do metabolic effectors change Michaelis-Menton kinetics?
4. Under what conditions might a substrate be inhibitory?
5. How would you determine a metabolic effector was involved in a reaction?
T 1/13 Regulation by synthesis, degradation and ambiquity
A. Identify the elements involved in the regulation of protein synthesis
1. Places where nutrients alter protein synthesis
2. Elements of synthesis
3. Likely levels of regulation
B. Identify the elements involved in the regulation of protein degradation
1. Marking proteins for degradation
2. Degradation systems
3. Role of ubiquitin in protein degradation
C. Compare the energy costs of synthesis and degradation to other forms
of control
1. Comparison of energy costs over a 24 hour cycle
2. Ultimate control of protein turnover
D. Debate the advantages of ambiquity in various physiological conditions
1. Hexokinase as a prototype enzyme
2. Types of binding to cell membranes
Required reading: A. Haas and T. Siepmann (1997) Pathways of ubiquitin
conjugation. FASEB J. 11, 1257-1268.
10 Minute in class exercise
Review questions:
1. How do nutrients alter protein synthesis beyond availability of amino acids?
2. How is ubiquitin involved in regulating protein degradation?
3. What advantages to the liver cell does ambiquity of ATP citrate lyase offer?
4. How could you determine whether an enzyme is ambiquitous?
5. For a 100,000 MW enzyme that is .01% of the cellular protein (200mg protein/gm of tissue) and its turnover is once every 24 hours, compare the cost in terms of ATP to one on/off cycle by phosphorylation on one site on the enzyme.
Th 1/15 Covalent modification
A. List the known types of covalent modification
1. Phosphorylation
2. Adenylation
3. Ribosylation
4. Methylation
5. Lipidation
6. Uridylation
7. Peptidylation
B. Examine the G protein based systems
1. G protein structure
2. G protein interaction with receptors
C. Outline energy requirements for each
type
D. Identify appropriate controls for each system
1. Following covalent modification with labelled compounds
2. "Freezing" cells in the in vivo state
3. Identifying altered proteins
Required reading: M. Gelb (1997) Protein prenylation, etc.: signal transduction in two
dimensions. Science 275, 1750-1751.
Review questions:
1.Provide at least one example of each type of covalent modification.
2. What is the role of multiple phosphorylations?
3. How do G proteins function?
4. What advantages do covalent modifications offer?
5. Why would ATP* with the label in any phosphate provide misleading information about phosphorylation in many cases?
T 1/20 Regulation of hormones and neural
effectors
A. Compare and contrast these two types of regulation
1. Speed
2. Selectivity
3. Hormones and cytokines
B. Assess the action of hormones acting in endocrine, paracrine or
autocrine fashions
C. Discuss the concept of a second messenger and the mobile receptor
hypothesis
1. Requirements to prove second messenger status
2. Advantages of single receptors over mobile receptors
3. Various signalling systems including adenyl cyclase, phosphatidyl inositol and
sphingomyelin
D. Identify control systems that operate on
more than one level
E. Debate the advantages of
multicellularity
Required reading: M. Cobb and E. Goldsmith (1995) How Map kinases
are regulated. J. Biol. Chem. 270,
14843-14846.
Review Questions:
1. Can single cells have hormones?
2. How can you distinguish between autocrine and paracrine effects?
3. What is the evidence that hormones/cytokines that elevate cyclic AMP do so by a mobile receptor model?
4. Where are the regulatory points in the adenyl cyclase system?
5. What are the advantages and disadvantages of multicellularity?
T 1/27 Peptide Hormones I.
A. Establish common regulatory points
1. Synthesis
2. Secretion
3. Crossing the ECM and vascular
endothelial cells
B. Speculate on important regulatory steps in the serum
1. Transport of hormones in serum
2. Hormone binding proteins
C. Analyze global factors which affect hormone sensitivity
1. Analysis of hormone binding?
2. Up and down regulation
Required reading: K. Tronheim (1997) Are metabolic oscillations
responsible for normal oscillatory insulin secretion? Diabetes
46, 1375-1380.
10 minute in class exercise
Review questions:
1.How is a protein hormone targeted for export?
2. What are the advantages of secretory granules?
3. How is hormone secretion regulated?
4. What are the constraints on Scatchard analysis for hormone binding parameters?
5. What mechanisms contribute to pulsatile secretion of hormones and what extra information is conveyed?
Th 1/29 Peptide Hormones II.
A. Differentiate between single receptors and the mobile receptor
hypothesis
1. Sequence of events triggered by hormone binding to a receptor
2. Expected time course for signalling
B. Outline steps in hormone receptor binding and 2nd messenger
generation
1. H-R complex internalization
2. Studying receptor recycling
3. Duration of signal generation
4. Nature of the signals
C. Design experiments to elucidate changes at the
hormone/receptor/messenger level.
1. Modifying receptors
2. Receptor defects
3. Messenger defects
Required reading: I. Macara et al (1996) The ras superfamily of GTPases
FASEB J. 10, 625-630
Review questions:
1. What is the sequence of events from the time a hormone encounters a cell surface receptor?
2. What are the probable reasons for spare and cryptic receptors?
3. How would you determine what a hormone's second messenger system is?
4. Explain how one binding event might alter subsequent binding events and how this would appear in a kinetic analysis?
5. Explain receptor crosstalk?
T 2/3 Non-peptide Hormone systems
A. Discuss alternative receptor sites for non-peptide hormones
1. Internal receptors
2. Differences in affinity and number
B. Determine commonalities in signal generation
1. Establishing a time course for effects
2. Differences in steroid and non-steroid,
non peptide hormones
C. Design experiments to focus on agonist and antagonist functions
1. Glucocorticoid system
2. Thyroid hormone system
3. Estrogen system
Required reading: N. Weigel (1996) Steroid hormone receptors and regulation by
phosphorylation. Biochem. J. 319,
657-667.
Review questions:
1. Describe a receptor system for hormones such as glucocorticoids.
2. Why have these hormones often been called permissive.
3. What is the evidence that thyroid hormone may work both at the level of the nucleus and at the level of the mitochondria?
4. Define agonist and antagonist.
5. Why are glucocorticoids counterregulatory to insulin?
Th 2/5 Calcium based signal systems I.
A. Identify elements allowing calcium to be a good signal
1. Insolubility of calcium phosphate
2. Measuring intra- and extracellular
calcium
B. Evaluate relative roles of calmodulin and calcium dependent kinases
1. Nature of calmodulin
2. Other Ca++ signalling systems
C. Describe calcium binding systems
1. Commonalities in Ca++ binding proteins
2. Intracellular calcium stores
Required reading: M. Komatsu et al. (1997) Augmentation of insulin
release by glucose in the absence of extracellular Ca++. Diabetes
46, 1928-1938.
Review questions:
1. How is a 3-4 order of magnitude Ca++ gradient between the inside and outside of the cell maintained?
2. What structural features allow calmodulin to bind effectively to a wide variety of proteins?
3. What is the role of protein kinase C in regulating various enzyme systems?
4. Describe other calcium binding proteins?
5. Could other ions function similar to
Ca++ as a message?
T 2/10 Calcium based signal systems II.
A. Explore whole body calcium homeostasis
1. Distribution of whole body calcium
2. Hormones involved in calcium homeostasis
B. Compare calcium uptake and efflux systems for cells and sub-
cellular compartments
1. Ca++ turnover
2. Regulation at the level of bone
C. Evaluate drugs that interfere with calcium signalling
1. Drugs to "prevent" osteoporosis
2. Impact of calcium channel blockers
10 minute in class exercise
Required reading: None
Review questions:
1. What would you expect calcium channel blockers to do to blood glucose levels and why?
2. Why is serum calcium level so tightly regulated?
3. What is the role of the kidney in calcium homeostasis?
4. What cells participate in bone calcium turnover?
5. Postulate a reason for the onset of adult respiratory distress syndrome after a severe break of a long bone.
Th 2/12 Sphingomyelin cycle signalling
A. Outline the elements of the sphingomyelin cycle
1. How is sphingosine generated?
2. What are the functions of the cylce?
B. Identify the coupling to various cytokines
1. How are cytokine receptors linked to the cycle?
2. TNF-a and the interleukins
C. Discuss the regulatory implications for this cycle
1. Coupling leading to tissue destruction
2. Nature of apoptosis
Required reading: L. Martins and W. Earnshaw (1997) Apoptosis: alive and kicking
in 1997. Trends in Cell biol. 7,
111-114.
Review questions:
1. Why does apoptosis have an advantage over necrosis?
2. How is sphingosine generated?
3. What advantage does a destructive cytokine like TNF-a confer on the host?
4. How would you determine a hormone/cytokine was linked to the sphingomyelin cycle?
5. How can you determine apoptosis is occurring?
T 2/17 Circadian rhythms
A. Compare regulatory systems for rhythms with different timing
1. Infra, ultra and circadian rhythms
2. Nature of internal clocks
B. Evaluate several systems for studying chronobiology
1. Model systems in common use
2. General features of regulatory clocks
C. Explore impact of circadian rhythms on interpretation of data
1. Controls to eliminate time of day bias
2. Why diet studies compound circadian
rhythm problems
Required reading: B.C. Johnson (1992) Nutrient intake as a time cylce for circadian
rhythms. J. Nutr. 122, 1753-1759.
Review Questions:
1. What is a free running rhythm?
2. In a meal feeding experiment, what if a treatment regimen shifts food intake times?
3. What organs/tissues regulate internal clocks?
4. What strategies alter biological clocks?
5. Design an experiment to determine
whether a particular nutrient alters biological clocks.
Th 2/19 Regulation of appetite Exam
II. Take-home due at beginning of class
A. Compare central and peripheral appetite regulatory cues
1. Historical data
2. new factors such as CCK, neuropeptide Y
and leptin
B. Assess impact of specific nutrient on appetite
1. Satiety value of nutrients
2. Mechanisms of appetite control
C. Identify various methodological problems in appetite experiments
1. Satiety vs aversion
2. Experimental models
Required reading: Q. Wang et al (1997) Interactions between leptin and
hypothalamic neuropeptide Y neurons in the control of food intake
and energy homeostasis in the rat. Diabetes
46, 335-341.
Review Questions:
1. Would you expect the same appetite mechanisms in a growing teenager compared to a 60 year old of the same gender and why?
2. What are the main theories about central regulation of appetite?
3. What are the genetics of the leptin system in animal models of obesity?
4. To what extent does a failure of satiety contribute to human obesity?
5. Are people in the USA getting fatter because they have lowered the fat content of their diets?
T 2/24 Regulation of body composition
A. Describe embryological impact on tissue distribution and body comp.
1. Adipose tissue
2. Muscle
B. Evaluate external parameters such as diet and exercise
1. Differential effects based on type of exercise
2. Short and long term implications of diet
C. Examine influence of genetic parameters
1. Twin studies
2. interpretation of body composition
D. Explore aberrant states and body composition
1. Wasting diseases
2. Hormonal treatments
Required reading: R. Rubenoff (1997) Inflammatory and hormonal
mediators of cachexia. J. Nutr. 127, 1014S-1016S.
10 minute in class exercise
Review questions:
1. What is the role of anabolic steroids in increasing muscle mass?
2. What are the limitations on various measures of body composition?
3. Are all adipose tissue cells regulated equally?
4. How do wasting diseases preferentially alter body composition?
5. How do nutrient partitioning agents function?
Th 2/26 Regulation of body fat I.
A. Determine the origin of body fat
1. Origin of body fat
2. Adipose tissue differentiation
B. Consider the implications in studies with fat cells
1. Pre-adipocytes vs adipocytes
2. Controlling for fat cell size in
experiments
C. Evaluate whole body effects on fat deposition
1. Hormonal control of fat deposition
2. Body fat distribution and disease
Required reading: G. Bray (1997) Progress in understanding the genetics
of obesity. J. Nutr. 127, 940S-942S.
Review questions:
1. What are the technical problems in studies with isolated adipose tissue?
2. What kind of dietary and hormonal factors influence fat cell metabolism?
3. If you successfully blocked nutrient uptake to adipocytes, what might the consequences be?
4. Are there inherent dangers in excess adiposity beyond the burden of carrying excess weight and if so, discuss them?
5. If fat cell development was blocked postnatally, would you expect to find altered metabolic regulation compared to a subject not receiving the treatment?
T 3/3 Regulation of body fat II.
A. Compare regulation of various lipogenic enzymes
1. Provision of substrate
2. Branches of the lipid pathways and their regulation
B. Establish regulatory events that result from functional needs
1. Fat for energy storage
2. Fat for regulatory compounds
C. Identify potential sites for intervention in lipogenic regulation
1. Blocking substrate availability
2. Changing ambiquity
Required reading: V. Zammitt (1996) Role of insulin in hepatic fatty acid partitioning:
emerging concepts. Biochem. J. 314,
1-14.
Review Questions:
1. What lipid compounds would you expect to be changed by administration of hydroxy citrate, an ATP citrate lyase inhibitor?
2. How can coordinate regulation of lipogenic enzymes be accomplished?
3. What regulatory mechanisms are involved in the day to day regulation of fat synthesis?
4. What might the consequences of taking an HMG CoA reductase inhibitor be beyond a reduction in cholesterol levels?
5. Would you expect all cells to make lipids and if so, would they all be the same lipids in the same proportions? Discuss.
Th 3/5 Regulation of carbohydrate stores
A. Delineate the regulatory features of the glucose transporters
1. Types of GLUT transporters
2. Regulation of glucose uptake separate
from glucose metabolism
B. Account for the disaccharide effect
1. Fructose and sucrose effects on lipogenesis
2. Coordination between carbohydrate and
lipid regulation
C. Integrate control systems regulating glycogen levels
1. Glycogen synthetase regulation in liver and muscle
2. Multiple levels of glycogen regulation
Required reading: J. Lawrence and P. Roach (1997) New insights into the
role and mechanism of glycogen synthetase activation by insulin.
Diabetes 46, 541-547.
Review Questions:
1. How do GLUT receptors help to apportion glucose to various tissues?
2. How could insulin interact with GLUT transporters separately from glucose metabolism?
3. What are the mechanisms involved in glucose transporter translocation?
4. What value is the disaccharide effect to the organism?
5. Discuss the differences in regulation of
liver and muscle glycogen systems and rationalize those
differences on a functional basis.
T 3/10 Alterations to regulation to
accommodate stress
A. Define hormones associated with stress
B. Explore the positive and negative consequences of stress for an
organism
C. Identify the environmental triggers that
stimulate stress mechanisms
10 minute in class exercise
Required reading: S. Hand and I. Hardewig (1996) Down regulation of
metabolism during environmental stress.
Ann. Rev. Physiol. 58, 539-563.
Review Questions:
1. What advantages do stress hormones confer on the organism?
2. By what mechanisms do organisms "know" whether stress (for example, fasting) will be long term or short term?
3. Design an experiment to determine the stress response to a diet imbalanced in amino acids.
4. Why should glucocorticoid levels follow a circadian rhythm?
5. Outline the response of an organism to a
wound or an invading organism.