You are on page 1of 4

Test 3 Learning Objectives

Chapter 17
1. Describe the rationale for the reciprocal regulation of
gluconeogenesis and glycolysis.
Achieved by both allosteric and endocrine mechanisms. Allosteric effectors
(F2,6BP) alter enzyme activity, while endocrine mediators may also alter gene
expression. They are not simultaneously degrading or synthesizing glucose.
2. List the regulatory enzymes of glycolysis and gluconeogenesis.
Glycolysis HK, PFK, PK
Gluconeogensis FBPase, PEPCK, PyrCarb, G6P
3. Describe the allosteric effects of AMP, citrate, and fructose 2, 6bisphosphate on the regulatory enzymes of gluconeogenesis and
glycolysis providing a biochemical explanation for each.
AMP (+) PFK and (-) F1,6BP
Citrate
(-) PFK
F2,6BP
(+) PFK and (-) FBPase
4. A. Describe how F6P affects the activity of the bifunctional enzyme
(PFK2).
B. Describe how glucagon changes the activity of PFK2 through
covalent modification.
A. PFK2 is allosterically activated by F6P.
B. Glucagon indirectly activates protein kinase A leading to the phosphorylation
and inhibition of PFK2.
5. Evaluate the effects of named hormones on the synthesis of the
regulatory enzymes of glycolysis and gluconeogenesis.
Insulin (+) glycolytic enzymes and (-) gluconeogenic enzymes. Glucagon is
opposite.
Glucocorticoids (+) gluconeogenic enzymes promoting protein breakdown.
6. Describe the mechanism for glucagon-mediated covalent
modification of pyruvate kinase.
When blood sugar is low, PK is phosphorylated and inactivated.
take note)

(See pg. 108 of

When blood sugar is high, PK is dephosphorylated and activated.


Chapter 18
1. Describe the pathways of glycogen synthesis and degredation.
Synthesis:
G6P G1P by phosphoglucomutase
G1P UDP-g
by UDP-glucose pyrophosporylase
UDP-g adds to growing glycogen polymer
Glycogen has many branches
Degredation:
Glycogen phosphorylase breaks -1,4 bonds 4 residues from an -1,6 branch point.
-1,6 branches are removed by one enzyme with two activities, Dglucanotranferase and amylo--1,6 glucosidase.
The -1,4 glycosidic bonds degraded by phosphorylysis G1P
catalyzed by
glycogen phosphorylase.
2. Explain how glycogen synthesis is initiated and terminated.
Glycogen synthase requires a polymer.
Glycogen synthase cannot simply add a UDP-glucose to a single glucose molecule
within the cell to initiateglycogen synthesis.
Primer is the tyrosine residue on glycogenin, the self-glucosylating enzyme and
protein scaffold.
UDP-glucose is added to the glycosylated glycogenin.
Glycogen exerts a negative feedback effect on glycogen synthase promoting a b
transition.
3. Appraise the role of the branching enzyme in glycogen synthesis.
Good job branching enzyme! j/k. This enzyme relocates a section of approximately
7 glucose residues from the end of a branch (at least 11 residues long) onto the C6
hydroxyl of an adjacent glucose monomer. The monomer must be at least 4
residues away from the nearest branching point. The creation of the highly
branched glycogen requires both synthase and the branching enzyme.
4. Outline the role of the various enzymes in glycogen degradation.
See question 1
5. Differentiate between glycolysis and glycogenolysis in terms of ATP
production.
When G1P G6P and enters glycolysis, 3 molecules of ATP are produced. It skips
HK ATP input.

Chapter 19
1. Explain why the regulation of glycogen metabolism is different in liver and
muscle tissue.
Muscle, glycogen functions as an energy store for the synthesis of ATP
Liver, glycogen functions as a glucose reserve to maintain blood sugar levels.
2. Evaluate 2 mechanisms that enable glycogen synthase and glycogen
phosphorylase to be reciprocally coordinated.
Active form (a)

Inactive form (b)

Glycogen synthase

-OH

-P

Glycogen Phosphorylase

-P

-OH

3. Describe the effect of AMP, ATP, and G6P on muscle glycogen


phosphorylase.
AMP
ATP
G6P

active b form,
Maintain b in its less active state, ba
Maintain b in its less active state, ba
4. Review the effect of glucagon and epinephrine on glycogen metabolism
and describe how the effect of these hormones varies between liver and
muscle tissue.

Epinephrine promotes glycogen degredation in muscle and a little effect on


hepatocytes.
Glucagon, when BSL is low, promotes glycogenolysis in the liver. Both inhibit
glycogen synthesis.
5. Appraise the enzyme deficiency in four genetic disorders of glycogen
metabolism
Disease

Deficiency

Type

Tissue

Von Gierkes

G6P

Liver

Pompes

-1,4-glucosidase

II

Liver

Coris

Debranching enzyme

III

All lysosomes

Andersens

Branching enzyme

IV

All organs

McArdles

Glycogen
Phosphorylase

Muscle

Hers

Glycogen
Phosphorylase

VI

Liver