BIOC2300 > Lecture 25 > Flashcards

Lecture 25 Flashcards

FAS part 1 (90 cards)

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1
Q

What is Madelung’s disease?

A

Madelung’s disease is a rare disorder of fat metabolism that results in an unusually high accumulation of subcutaneous fat deposits.

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2
Q

Where are the fat deposits located in Madelung’s disease?

A

The deposits occur directly under the skin around the neck, shoulders, trunk, hips, upper arms, and thighs.

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3
Q

Why is Madelung’s disease often mistaken for obesity?

A

Because of the totally symmetrical deposition of fat.

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4
Q

What functional symptoms can patients with Madelung’s disease experience?

A

Although painless, the fatty tumors can compromise function of other structures in the affected area, resulting in difficulty swallowing, speaking, and breathing.

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5
Q

How does Madelung’s disease affect quality of life?

A

It can very much limit the quality of life of these patients due to the functional compromise of affected areas.

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6
Q

Which demographic is most often affected by Madelung’s disease?

A

Adult males between ages 30 to 70 with a history of excessive drinking (chronic alcoholism).

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7
Q

Can women or non-drinkers get Madelung’s disease?

A

Yes, women and those who do not drink alcohol can also get Madelung’s disease.

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8
Q

In which populations is Madelung’s disease more common?

A

It is more common in Mediterranean and European populations.

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9
Q

In which populations is Madelung’s disease less frequent?

A

It is less frequent in Asian populations.

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10
Q

What is known about the underlying causes and treatment of Madelung’s disease?

A

The underlying causes aren’t fully understood, which can lead to limitations in treatment options.

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11
Q

Why do adult humans generally have little need for fatty acid synthesis?

A

Because our diet meets our physiological needs for fats and lipids.

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12
Q

In which tissues does de novo fatty acid synthesis primarily occur in adults?

A

Primarily in the liver and lactating mammary glands and, to a lesser extent, in adipose tissue.

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13
Q

When is fatty acid synthesis physiologically required?

A

Under certain physiological conditions, such as embryonic development and lactation.

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14
Q

What can result from too much fatty acid synthesis?

A

It can lead to pathological conditions and diseases such as fatty liver diseases (alcoholic and non-alcoholic).

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15
Q

What distinguishes Alcoholic from Non-alcoholic fatty liver disease?

A

Alcoholic liver disease is due to high alcohol consumption. Non-alcoholic is most often due to metabolic disease, including obesity and type two diabetes.

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16
Q

What happens to the liver’s appearance in fatty liver disease?

A

Fatty deposits result in a discoloration of the liver lobes, giving it a more pale-like color (compared to the healthy maroon color).

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17
Q

What are the potential progressions of fatty liver disease?

A

It can give rise to inflammation and hepatitis, as well as progress to overt liver cirrhosis and liver failure.

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18
Q

What is the first biochemical hurdle in fatty acid synthesis?

A

Synthesis takes place in the cytoplasm, but acetyl CoA (the raw material) is formed in the mitochondria, which are not permeable to acetyl CoA.

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19
Q

How does the cell solve the Acetyl-CoA mitochondrial permeability problem?

A

Citrate, synthesized in the mitochondria, is transported to the cytoplasm and cleaved by ATP-citrate lyase to generate acetyl CoA.

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20
Q

What does Citrate carry across the mitochondrial membrane?

A

It carries acetyl groups.

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21
Q

What is the reaction catalyzed by ATP-citrate lyase?

A

Citrate + ATP + Coenzyme A + Water ? Acetyl CoA + ADP + Phosphate + Oxaloacetate.

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22
Q

Is the ATP-citrate lyase reaction energy consuming?

A

Yes, it is an ATP consuming reaction.

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23
Q

What metabolic pathway does Citrate inhibit?

A

Citrate inhibits phosphofructokinase, thus shutting down glycolysis.

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24
Q

What does Citrate accumulation signal?

A

It is considered a signal of an energy-rich status of the cell.

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25
How is Citrate formed in the mitochondria?
By the condensation of acetyl CoA with Oxaloacetate (OAA) in the TCA cycle.
26
How is ATP-citrate lyase regulated by insulin?
Insulin stimulates the enzyme by initiating a signal transduction pathway that results in phosphorylation and activation of the lyase by protein kinase B (Akt).
27
What happens to the Oxaloacetate (OAA) formed in the cytoplasm?
Since the inner mitochondrial membrane is impermeable to OAA, it undergoes a series of bypass reactions to return to the mitochondria.
28
What is the first bypass reaction for Oxaloacetate in the cytoplasm?
Oxaloacetate is converted to Malate by malate dehydrogenase.
29
What is the second bypass reaction for Oxaloacetate in the cytoplasm?
Malate is converted to Pyruvate by malic enzyme.
30
How does Pyruvate re-enter the cycle from the cytoplasm?
Pyruvate readily enters mitochondria, where it is carboxylated back to Oxaloacetate by pyruvate carboxylase.
31
What is the balanced equation for the Pyruvate Carboxylase reaction?
Pyruvate + CO2 + ATP + H2O ? OAA + ADP + Pi + 2 H+.
32
What is the significance of the Malate to Pyruvate conversion for NADPH?
The reducing potential of NADH is converted into that of NADPH. One molecule of NADPH is generated for each molecule of acetyl CoA transferred.
33
How much NADPH is generated by the citrate/pyruvate shuttle for palmitate synthesis?
Eight molecules of NADPH are formed when eight molecules of acetyl CoA are transferred (required for palmitate synthesis).
34
Where do the additional molecules of NADPH needed for palmitate synthesis come from?
The additional six molecules come from the pentose phosphate pathway.
35
What does fatty acid synthesis require regarding metabolic coordination?
It requires the cooperation of various metabolic pathways located in different cellular compartments.
36
What does the Pentose Phosphate Pathway provide for fatty acid synthesis?
It provides NADPH (reducing equivalents).
37
What does Glycolysis provide for fatty acid synthesis?
It provides ATP.
38
What does the TCA cycle provide for fatty acid synthesis?
It provides Citrate (carbon atoms).
39
What is the 2nd step of fatty acid synthesis?
Activation.
40
What supplies the energy for the carbon-to-carbon condensations in fatty acid synthesis?
The carboxylation and subsequent decarboxylation of acyl groups in the cytosol.
41
What reaction starts fatty acid synthesis?
The carboxylation of acetyl CoA to malonyl CoA.
42
What is Malonyl CoA?
The activated form of acetyl CoA.
43
Which enzyme catalyzes the formation of Malonyl CoA?
Acetyl CoA carboxylase I (ACC).
44
What cofactor and substrates does Acetyl CoA carboxylase require?
It operates with a biotin cofactor and transfers carbon dioxide from bicarbonate in an ATP-requiring reaction.
45
Is Malonyl CoA synthesis reversible?
No, it is an irreversible process.
46
How does Malonyl CoA regulate fatty acid oxidation?
Malonyl CoA inhibits carnitine palmitoyltransferase I (CPT1), preventing fatty acid entry into mitochondria and thus inhibiting beta-oxidation.
47
Why is the inhibition of CPT1 by Malonyl CoA important?
It ensures that fat synthesis and fat oxidation are coordinated and do not operate at full speed simultaneously (preventing a futile cycle).
48
What is the rate-limiting and regulated step in fatty acid synthesis?
Acetyl CoA carboxylation (catalyzed by ACC).
49
How does Citrate allosterically regulate Acetyl CoA Carboxylase (ACC)?
Citrate activates ACC by causing polymerization into active filaments (signaling high energy/abundance).
50
How does Palmitoyl CoA allosterically regulate Acetyl CoA Carboxylase (ACC)?
Palmitoyl CoA (the end product) inactivates ACC by causing depolymerization (feedback inhibition).
51
How does AMPK regulate Acetyl CoA Carboxylase (ACC)?
AMPK phosphorylates and inactivates ACC. AMPK is active when energy is low (activated by AMP, inhibited by ATP).
52
How does Insulin regulate Acetyl CoA Carboxylase (ACC)?
In the presence of insulin, ACC is dephosphorylated and active (signaling nutrient-rich status).
53
How does long-term diet affect ACC levels?
High-carbohydrate/low-fat diets increase ACC synthesis. Low-calorie/ketogenic diets decrease ACC synthesis.
54
What is the 3rd step of fatty acid synthesis?
Carrier transfer.
55
What carrier is used in fatty acid synthesis instead of CoA?
Acyl carrier protein (ACP), which is part of the fatty acid synthase complex.
56
Describe the structure and function of Acyl Carrier Protein (ACP).
A single polypeptide chain of 77 residues that acts as a giant prosthetic group or 'macro CoA'.
57
Which enzyme attaches Acetyl CoA to the ACP?
Acetyl transacylase (forming Acetyl ACP + CoA).
58
Which enzyme attaches Malonyl CoA to the ACP?
Malonyl transacylase (forming Malonyl ACP + CoA).
59
What are the four steps of the first elongation cycle (Steps 4-7)?
1. Condensation 2. Reduction 3. Dehydration 4. Reduction.
60
Describe the Condensation step (Step 4).
Acetyl ACP and Malonyl ACP react to form Acetoacetyl ACP + CO2. Catalyzed by Beta-ketoacyl synthase (condensing enzyme).
61
Describe the 1st Reduction step (Step 5).
Acetoacetyl ACP is reduced to D-3-hydroxybutyryl ACP by Beta-ketoacyl reductase (uses NADPH).
62
Describe the Dehydration step (Step 6).
D-3-hydroxybutyryl ACP is dehydrated to form Crotonyl ACP by 3-hydroxyacyl dehydratase (releases water).
63
Describe the 2nd Reduction step (Step 7).
Crotonyl ACP is reduced to Butyryl ACP by Enoyl reductase (uses NADPH).
64
What happens in the second round of fatty acid synthesis?
Butyryl ACP condenses with Malonyl ACP to form a C6-beta-ketoacyl ACP, followed by reduction, dehydration, and reduction.
65
How long do the elongation cycles continue?
Until a full C16 acyl ACP (Palmitoyl ACP) is formed.
66
How is the fatty acid chain length determined and released?
The Thioesterase enzyme acts as a ruler. It hydrolyzes C16-acyl ACP to yield palmitate and ACP.
67
How does the Bacterial Fatty Acid Synthase differ from the Mammalian one?
Bacteria use the same mechanism, but the complex dissociates upon cell lysis (distinct enzymes). Mammals have a single large super-complex.
68
How does the synthesis of odd-numbered fatty acids begin?
It starts with Propionyl ACP (instead of Acetyl ACP), which is formed from Propionyl CoA.
69
Which enzyme is responsible for forming Propionyl ACP?
Acetyl transacylase. Unlike Malonyl transacylase (specific), Acetyl transacylase is promiscuous and can transfer groups other than acetyl, though slower.
70
Do humans synthesize short chain fatty acids (2-6C)?
No, short chain fatty acids are produced by intestinal bacteria.
71
Where are medium chain fatty acids (7-12C) typically made in animals?
In the mammary gland.
72
How are fatty acids longer than C16 synthesized?
By Elongase enzymes attached to the endoplasmic reticulum.
73
How are unsaturated fatty acids formed?
By Desaturase enzymes bound to the endoplasmic reticulum, which introduce double bonds.
74
Why are Linoleate and Linolenate considered essential fatty acids?
Because mammals lack the enzymes to introduce double bonds beyond carbon 9.
75
Describe the synthesis of Oleic Acid (C18:1).
Palmitate (C16) -> Stearate (C18) via Elongase -> Oleic Acid via Delta-9 Desaturase.
76
Who can perform Delta-12 desaturation to form Linoleic acid?
Only plants! Animals cannot desaturate beyond C9.
77
What is the notation for Linoleic acid?
C18:2 n-6 Delta 9, 12.
78
What is Arachidonic acid synthesized from?
It is synthesized from Linoleic acid via Delta-6 desaturation and subsequent elongation/desaturation steps.
79
What is the structure of Arachidonic acid?
C20:4 n-6 Delta 5, 8, 11, 14.
80
What are Omega-3 fatty acids like EPA and DHA made from?
Alpha-linolenic acid (C18:3 n-3).
81
What does the Lipoatrophy case study in mice demonstrate?
That fat synthesis is not always bad. Mice without fat had diabetes/growth issues; transplanting fat reversed these conditions, normalizing glucose and insulin.
82
How does Triclosan act as an antibiotic?
It targets Enoyl-ACP reductase, an enzyme in bacterial fatty acid synthesis (specific target, not a general microbicide).
83
How does Isoniazid (TB drug) work?
It also inhibits Enoyl ACP reductase.
84
What is the stoichiometry for Malonyl CoA synthesis (preceding step)?
7 Acetyl CoA + 7 CO2 + 7 ATP ? 7 Malonyl CoA + 7 ADP + 7 Pi + 14 H+.
85
What is the overall stoichiometry for Palmitate synthesis (Inputs)?
8 Acetyl CoA + 7 ATP + 14 NADPH + 6 H+.
86
What is the overall stoichiometry for Palmitate synthesis (Outputs)?
Palmitate + 14 NADP+ + 8 CoA + 6 H2O + 7 ADP + 7 Pi.
87
Compare the carrier molecule in FA Degradation vs Synthesis.
Degradation uses Coenzyme A (CoA). Synthesis uses Acyl Carrier Protein (ACP).
88
Compare the redox cofactors in FA Degradation vs Synthesis.
Degradation uses NAD+ and FAD (oxidants). Synthesis uses NADPH (reductant).
89
Compare the chemistry steps in FA Degradation vs Synthesis.
Degradation: Oxidation, Hydration, Oxidation, Cleavage. Synthesis: Condensation, Reduction, Dehydration, Reduction.
90
Compare the location of FA Degradation vs Synthesis.
Degradation occurs in the Mitochondria. Synthesis occurs in the Cytoplasm.
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