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FHB - GI/Metabolism - Exam 3 > Metabolism Lecture 4 - 5 - Glycogen regulation & Fatty Acid > Flashcards

Metabolism Lecture 4 - 5 - Glycogen regulation & Fatty Acid Flashcards

1
Q

What can store more glucose, liver or muscle?

What is the key enzyme that add glucose-1 - phosphate to growing glycogen chains?

What enzyme makes glucose from glycogen?

A

MUSCLE (400g)

Glycogen Synthase

Glycogen Phosphorylate

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2
Q

Which tissue directly contributes to blood glucose levels

Liver or Muscle

WHy?

A

Liver

  • has G-6- Phosphotase enzyme to convert G-6-P to Glucose and thus release it to the blood
    (found in the ER)

Muscle cannot release G-6-P since it does not have this enzyme, thus its main function is to generate ATP in the form of energy by going through glycolysis and the Krebb’s cycle

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3
Q

What is G-6- P converted to before it is stored as glycogen?

A

G-1-P!

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4
Q

After a meal, hepatic glycogen _____ and it ____ between meals.

A
  1. INCREASES

2. DECREASES

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5
Q

What is the purpose of the glycogen stores in muscle and liver?

A
  1. Muscle:
    - glycogen stored for the production of ATP within the tissue
  2. Liver: glucose reserve for the maintenance of blood glucose
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6
Q

What 2 enzymes are required for glycogen synthesis?

A
  1. Glycogen Synthase
    - adds glycosyl units in an alpha -1,4 - linkage
  2. Branching enzyme
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7
Q

What 3 enzymes does Glycogen BREAKDOWN require?

What are the 2 functions of the deb ranching enzyme?

A
  1. Glycogen Phosphorylase
  2. Debranching enzyme
  3. Additional phosphorylating enzymes (Phosphorylase Kinase)

Debranching enzyme:

  • 4:6 transferase activity
  • alpha 1,6- glucosidase
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8
Q

How do high levels of the following affect glycogen synthesis/breakdown:

  1. AMP
  2. Calcium
  3. Insulin
A
  1. AMP - can bind to the B form of Glycogen phosphorylase and convert it to the A form to facilitate Glycogen breakdown
  2. Calcium binds to Calmodulin complex and phosphorylates PHOSPHORYLASE KINASE (activates) which leads to activation of Glycogen Phosphorylase via phosphorylation (b to a)
  3. Insulin inhibits GLYCOGEN PHOSPHORYLASE (with phosphatase/inhibitory activity) to remove Pi and inactive (a to b)
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9
Q

Phosphorylation of the following results in activation or inactivation?

  1. Glycogen Synthase
  2. Glycogen Phosphorylase
A
  1. Inactive (bform)

2. Active (a form)

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10
Q

How do the following affect glycogen storage:
1. Insulin

  1. G- 6 - P**
  2. Glucose
  3. ATP
A
  1. Increases storage by activating phosphorprotein PHOSPHOTASE and dephosphorylating glycogen synthase (while also dephosphorylating and inactivating phosphorylase)
  2. G - 6 - P
    - ALLOSTERIC ACTIVATOR (functions regardless of phosphorylation status)
    - activates the B form of glycogen synthase !
  • storage occurs!
  1. More glucose ALLOSTERICALLY INHIBITS phosphorylase A (binds to it)
    - promotes glycogen storage
  2. More ATP ALLOSTERICALLY inhibits Phosphorylase A (binds to it)
    - promotes glycogen storage
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11
Q

Glucagon and epinephrine stimulate both LIVER and MUSCLE tissue.

True or False

A

FALSE

  • Glucagon does NOT stimulate muscle cells (only liver cells)
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12
Q

How does cAMP affect the muscle and liver differently?

In the Liver it performs the following functions:
> Promotes
Glycogen
Degradation

> Inhibits
Glycolysis

> Inhibits
Glycogen
Synthesis

A

ALL the same except muscle STIMULATES glycolysis

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13
Q

What do IP3 and Calcium stimulate via ALPHA -AGONISTS?

A

GLycogenolysis (glycogen degradation)

    1. IP3 increases Ca
      1. Ca activates Calcium dependent PK
      2. DAG (diacylglycerol) activates PKC

IN LIVER

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14
Q

What is Von GIerke disease or Type I GSD?

A

lack of enzyme G-6-Phosphotase

  • enlarged liver
  • failure to thrive
  • severe hypoglycemia
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15
Q

What is the overall effect of Glucagon?

What are the direct & indirect ways that Glucagon inhibits Glycolysis?

What are the direct and indirect ways it ACTIVATES Gluconeogenesis?

How does it inhibit Glycogenesis?

How does it stimulate glycogenolysis/degradation?

A
  1. Increase blood glucose
  2. Direct: via Pyruvate Kinase inhibition
  3. Indirect - inhibits PFK-2 –> decreases F-2.6-BP and thus decreased activity of PFK-1
  4. DIrect - inhibits pyruvate kinase (inhibiting glycolysis)
  5. Indirect - Inhibits PFK - 2 leads to decrease F-2,6-BisP and thus nothing to inhibit F - 1,6,-BisPhosphoTASE
  6. Inhibits GLycogen Synthase
    • activates glycogen phosphorylase
      - activates phosphorylase kinase (to activate glycogen phosphorylase)
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16
Q

What is the rate limiting enzyme in the Pentose Phosphate Pathway?

Destructing of this enzyme can cause what clinical problem? How?

What is produced in this pathway?

A

Glucose - 6- Phosphate DEHYDROGENASE

  • lead to hemolytic anemia –> low NADPH thus not enough to keep Glutathionine (GSH) in its reduced form
  • need the reduced form of GSH for peroxide reduction
  • peroxide builds up and cells lyse
  • lead to increased BILIRUBIN
  1. NADPH
  2. Ribose 5 - Phosphate
  3. Intermediates for glycolysis
17
Q

In fed state, what drives the synthesis of cholesterol and fatty acyl-coA’s? From what?

How are fatty acids transported?

A

Insulin

  • from Acetyl Co A
    2. Transported as TAG’s on lipoproteins
18
Q

In fasting state, what drives the formation of acetyl co A and ketone bodies?

How are Fatty Acid’s transported in this state?

A

Epinephrine!

  1. WIth ALBUMIN
19
Q

What is the rate limiting enzyme in fatty acid synthesis?

What is produced from acetyl coA and malonyl-coA?

A

Acetyl CO - A Carboxylase!

Produce PALMITATE (even number of saturated fatty acids)

20
Q

What are the 6 things required for fatty acid synthesis?

A
  1. Acetyl Groups
  2. Citrate (activates acetyl co A carboxylase)
  3. Acetyl CO A Carboxylase
  4. Fatty Acid Synthase Complex
  5. NADPH
  6. Biotin
21
Q

All carbons are ultimately derived from what?

A

Acetyl CO A (acety co A’s are from carb metabolism)

22
Q

What are the 3 main functions of citrate?

A
  1. Stimulates FA synthesis
  2. Transports Acetyl Groups from mitochondria
  3. Allosterically activates Acetyl CO A Carboxylase
23
Q

What is the carrier of acetyl groups from mitochondria to cytoplasm?

A

Citrate

24
Q

What are the 3 main functions of Acetyl CO A Carboxylase?

A
  1. Rate limiting in FA synthesis
  2. Catalyzes formation of Malonyl CO A from Acetyl CoA
  3. Biotin serves as a carrier of activated CO2
25
Q

What allosterically regulates Acetyl CO A Carboxylase in FA synthesis?

A

Malonyl Co A

  • regulates(inhibits) FA degradation and ketone body formation
26
Q

State the following for Carboxylase ACC:

  1. Allosteric Activator
  2. Allosteric Inhibitor
  3. Hormonal Activator
  4. Hormonal Inhibitor

What long term effects increases enzyme synthesis?(3)

Decreases?(2)

A
  1. Citrate
  2. Palmitoyl Co A & AMP
  3. Insulin
  4. Glucagon / Epinephrine
  5. High carb
  6. Insulin
  7. Thyroid Hormone
  8. High fat diet
  9. Fasting Glucagon
27
Q

What regulates the Fatty Acid Synthase complex (7 enzyme activities found in 1 protein)
- catayzes formation of fatty acids (palmitate)

1.Allosteric Activator

What long term effects increases enzyme synthesis?(2)

Decreases?(2)

A
  1. Fructose - 1,6- Bisphosphate
  2. High Carb diet via insulin
  3. Fat free diet
  4. Glucagon
  5. High fat diet
28
Q

Fatty acids may be _____ into:

  1. TAG
  2. Phospholipids
  3. Cholesterol
A

ESTERIFIED

29
Q

How are fatty acids stored?

How are fatty acids transported? Where does this modification occur?

A
  1. As triacylglycerols
  2. LIPOPROTEINS –> Chylomicrons
  3. the intestines
30
Q

What are the activators of Acetyl CO A Carboxylase?(2)

Inhibitors? (3)

When would you activate and inhibit this enzyme?

What pathway is this enzyme involved in?

A
  1. Citrate
  2. Insulin
  3. Glucagon
  4. Epinephrine
  5. Palmitoyl Co A

This enzyme would be activated when you need to convert acetyl co A into Fatty Acyl Co A for fatty acid synthesis

31
Q

What is the function of Acetyl Co A?

What cofactor is required?

A

Convert Acetyl CO A into Malonyl Co A

Biotin

32
Q

What is the only PHYSIOLOGIC inhibitor of Acetyl CO A Carboxylase?

A

Malonyl Co A (product)

33
Q

Define the defective enzyme in the following:

  1. Type I - Von Gierke Disease
  2. Type II - Pompe Disease
  3. Type III - Cori Disease
  4. Type IV - Anderson Disease
  5. Type V - McArdle Disease
  6. Type VI - Hers Disease
  7. Type VII - Tarui Disease
  8. Type VIII
A
  1. Type I - Von Gierke Disease = Glucose - 6- Phosphatase
  2. Type II - Pompe Disease = (1,4) alpha- Glucosidase
  3. Type III - Cori Disease = Glycogen Debranching Enzyme
  4. Type IV - Anderson Disease = Glycogen Branching Enzyme
  5. Type V - McArdle Disease = Phosphorylase
  6. Type VI - Hers Disease = Phosphorylase
  7. Type VII - Tarui Disease = PFK - 1
  8. Type VIII = Phosphorylase b Kinase
34
Q

Describe the level of glycogen in the following:

  1. Type I - Von Gierke Disease
  2. Type II - Pompe Disease
  3. Type III - Cori Disease
  4. Type IV - Anderson Disease
  5. Type V - McArdle Disease
  6. Type VI - Hers Disease
  7. Type VII - Tarui Disease
  8. Type VIII
A
  1. Type I - Von Gierke Disease = Glucose - 6- Phosphatase
    * INCREASED
  2. Type II - Pompe Disease = (1,4) alpha- Glucosidase
    * MASSIVE INCREASE**
  3. Type III - Cori Disease = Glycogen Debranching Enzyme
    * *INCREASED, shorter outer**
  4. Type IV - Anderson Disease = Glycogen Branching Enzyme
    * NORMAL**
  5. Type V - McArdle Disease = Phosphorylase
    * *MODERATE AMOUNT**
  6. Type VI - Hers Disease = Phosphorylase
    * *INCREASED AMOUNT**
  7. Type VII - Tarui Disease = PFK - 1
    * *INCREASED AMOUNT**
  8. Type VIII = Phosphorylase b Kinase
    * *INCREASED AMOUNT**
35
Q

Describe the clinical features of the following:

  1. Type I - Von Gierke Disease
  2. Type II - Pompe Disease
  3. Type III - Cori Disease
  4. Type IV - Anderson Disease
A
  1. Type I - Von Gierke Disease - Glucose - 6- Phosphotase
    - enlarged liver
    - failure to thrive
    - severe hypoglycemia
    - hyperuricemia
    - gouty arthritis
    - hyperlipidemia
    - mental retardation
    - lactic acidosis
  2. Type II - Pompe Disease - (1,4) Alpha - glucosidase
    - cardio respiratory Failure**
    - death usually before age 2
  3. Type III - Cori Disease - Glycogen Debranching Enzyme
    - like Type I, but milder
  4. Type IV - Anderson Disease - Glycogen Branching Enzyme
    - progressive cirrhosis of liver
    - liver failure causes death before age 2
36
Q

Describe the clinical features of the following:

  1. Type V - McArdle Disease
  2. Type VI - Hers Disease
  3. Type VII - Tarui Disease
  4. Type VIII
A
  1. Type V - McArdle Disease = Phosphorylase
    - limited ability to perform strenuous exercise
    - painful muscle cramps
  2. Type VI - Hers Disease = PHOSPHORYLASE
    - Like Type 1 but milder
  3. Type VII - Tarui Disease = PFK - 1
    - like type V
  4. Type VIII = Phosphorylase b Kinase
    - mild liver enlargement
    - mild hypoglycemia

FHB - GI/Metabolism - Exam 3 (21 decks)

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