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Biochemistry II > Ch. 21 Fatty Acid Synthesis > Flashcards

Ch. 21 Fatty Acid Synthesis Flashcards

1
Q

Where does fatty acid synthesis occur?

A

Fatty acid synthesis happens in the cytosol.

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2
Q

Where do the carbons for fatty acid synthesis come from?

A

Carbons come from acetyl-CoA, but most are made into malonyl-CoA.

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3
Q

What is malonyl-CoA?

A

A three carbon molecule that is linked to acetyl-CoA via a high energy thioester bond.

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4
Q

How is malonyl-CoA made?

A

It is made by condensing acetyl-CoA and CO₂ via acetyl-CoA carboxylase.

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5
Q

What is acetyl-CoA carboxylase?

A

It is an enzyme with two active sites and a biotin group (B vitimin) that brings CO₂ into the reaction. It requires an input of 1 ATP.

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6
Q

What is fatty acid synthase?

A

A multifunctional enzyme made of multiple active sites in one big complex. It produces palmitate (16:0).

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7
Q

How many carbons does fatty acid synthase add at a time?

A

It ALWAYS adds two carbons at a time, which is why most fatty acids are even numbered.

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8
Q

What is acyl carrier protein?

A

ACP is one subunit of fatty acid synthase that is loosely tethered to the other subunits of fatty acid synthase.

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9
Q

What does ACP allow to happen?

A

It allows reactants to go into different active sites within fatty acid synthase.

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10
Q

What is the pathway of fatty acid synthesis via fatty acid synthase? (9)

A
  1. acetyl-CoA covalently bonded to a subunit of fatty acid synthase. (ONLY first two carbons come from acetyl-CoA)
  2. malonyl-CoA covalently bonded to ACP
  3. malonyl-CoA decarboxylated and condensed with first two carbons from acetyl-CoA (now 4C on ACP), breaking acetyl-CoA’s bond to the enzyme
  4. outermost carbonyl group is reduced using NADPH
  5. ACP swings molecule to next subunit where dehydration reaction produces C=C
  6. double bond is reduced using NADPH
  7. 4C fatty acid is transferred from ACP to the subunit where the original acetyl-CoA was bonded
  8. repeat process until a 16C fatty acid is achieved
  9. release fatty acid from ACP and diffuse away
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11
Q

What is the net reaction of fatty acid synthase?

A

acetyl-CoA + 7 malonyl-CoA + 14 NADPH + 14 H⁺ → palmitate + 7 CO₂ + 8 CoA + 14 NADP⁺ + 6 H₂O

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12
Q

Why is the use of 14 NADPH and 7 ATP during fatty acid synthesis okay?

A

The cell is in a high energy state so the energy use is okay.

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13
Q

What will the fatty acids produced become? (2)

A

They will become a phospholipid or a TAG.

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14
Q

What do you need lots of in the cytosol for fatty acid synthesis and where does it come from (2)?

A

Cells need LOTS of NADPH in the cytosol. It comes from the pentose phosphate pathway and from the conversion of malate to pyruvate via malic enzyme in the cytosol (most comes from this one!)

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15
Q

Where does the acetyl-CoA used in fatty acid synthesis come from?

A

It DOESN’T come from β Oxidation (futile cycle). Carbohydrate metabolism produces acetyl-CoA, and amino acids can feedstock anapleurotic reactions to keep CA cycle running.

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16
Q

How does acetyl-CoA get out of the mitochondrial matrix and into the cytosol? (5)

A
  1. citrate synthase combines oxaloacetate and acetyl-CoA to make citrate
  2. citrate transporter moves citrate out of the mitochondrial matrix into the cytosol
  3. citrate lyase breaks citrate into acetyl-CoA and oxaloacetate using ATP (bcs. of thioester bond formation)
  4. oxaloacetate in cytosol will be converted to malate, which can either be transported back into the mitochondrial matrix or oxidized to pyruvate by malic enzyme (producing NADPH)
  5. if pyruvate enters mitochondrial matrix, it will be converted to oxaloacetate, using another ATP, to start again
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17
Q

What is fatty acid synthesis? (ana. or cata.)?

A

Fatty acid synthesis is anabolism so the cell must be in a high energy state.

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18
Q

What inhibits acetyl-CoA carboxylase?

A

Palmatyl-CoA inhibits it via feedback inhibition.

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19
Q

What activates acetyl-CoA carboxylase?

A

Citrate activates it because if citrate is high, carbon must flow somewhere. That somewhere is fatty acid synthesis. (get fat because FA’s are stored in TAG)

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20
Q

When will citrate build up?

A

When succinyl-CoA and high energy molecules are plentiful, the citric acid cycle is dammed and therefore citrate will build up.

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21
Q

What else is citrate?

A

Citrate is a precursor to acetyl-CoA, so when it is in high concentration, fatty acid synthesis will occur.

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22
Q

What happens to acetyl-CoA carboxylase when it is phosphorylated?

A

It will be inactive/inhibited. Kinases (and epi) will inactivate it because of this.

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23
Q

What non-chemical regulation mechanism does fatty acid synthesis (acetyl-CoA carboxylase) use?

A

Changes in gene expression can regulate this enzyme and therefore the process.

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24
Q

What is reciprocal regulation of fatty acid synthesis?

A

Malonyl-CoA inhibits fatty acid import into the mitochondria.

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25
What does reciprocal regulation with malonyl-CoA ensure?
It is one of the many ways to ensure fatty acid synthesis and β oxidation don't occur at the same time.
26
Does fatty acid synthase produce anything other than palmitate?
No. It only produces palmitate, but it can be unsaturated, elongated, or both.
27
What are all fatty acids other than palmitate made from?
All other fatty acids start with palmitate as a precursor.
28
What is the fatty acid elongation system?
It elongates palmitate to other fatty acids. It is very similar to fatty acid synthase.
29
Where is the fatty acid elongation system found? (2)
It is in the ER and mitochondria.
30
What are eicosanoids?
Lipid based signaling molecules.
31
What do all eicosanoids start as?
All start as arachadonic acid (20:4) that come from a phospholipid via lipases.
32
What is arachadonic acid converted to?
Prostaglandin H2
33
What is prostaglandin H2 converted to? (2)
Prostaglandin H2 is converted to other prostaglandins and thromboxanes which are signaling molecules involved in immune response and inflammation.
34
How can inflammation be limited?
Cyclooxygenase (COX) levels can be kept low by COX inhibitors to limit inflammation. COX is an enzyme.
35
What are common COX inhibitors?
Aspirin and Ibuprofen
36
Where are the vast majority of fatty acids stored? Define them.
In triacylglygerides which have three carbons, 2 hydroxyl groups, and a fatty acid at each carbon.
37
What are TAGs a source of?
There is LOTS of energy stored in TAGs.
38
What is glycerol-3-phosphate?
(NOT G3P!) It is the starting point for all TAGs
39
How is glycerol-3-phosphate produced?
DHAP from glycolysis is reduced to glycerol-3-phosphate.
40
How are TAGs made from glycerol-3-phosphate? (3)
1. glycerol-3-phosphate can be acetylated at each carbon producing phosphatidic acid 2. phosphatidic acid phosphotase can remove phosphate head group 3. fatty acid is attached to the third carbon producing a TAG
41
Where are TAGs stored? Where can they go from there?
Can be stored in adipocytes and converted to fatty acids by lipases. Fatty acids can be secreted into the blood stream and bound to serum albumen.
42
Where do 75% of fatty acids go once released from adipose tissue?
75% of fatty acids released from adipose tissue make it back to adipose tissue as TAGs.
43
What does insulin do in fatty acid synthesis?
Insulin stimulates carbohydrate conversion to fatty acids, and therefore TAGs. (signal to use or store energy)
44
Where does phospholipid synthesis occur?
Phospholipid synthesis happens in the ER. ER blebs to Golgi → Golgi blebs and ships to the desired location.
45
How are all phospholipids made, generally?
Specific head groups are added to phosphatidic acid to make all other phospholipids.
46
What is cholesterol?
A very hydrophobic molecule with a slight hydrophilic head that is a precursor to bile salts and steroids.
47
Where is cholesterol found?
Cholesterol is found in all animal membranes making them slightly more rigid.
48
Do plants have cholesterol?
No. Plants do not make cholesterol.
49
Where else is cholesterol found in animals?
Some cholesterol also circulates in the bloodstream.
50
What feedstocks cholesterol synthesis?
Acetyl-CoA feedstocks cholesterol synthesis. (It takes a lot of acetyl-CoA)
51
What is the key enzyme in cholesterol synthesis?
HMG-CoA Reductase is the main enzyme of cholesterol synthesis. (It is the regulatory enzyme of the pathway)
52
What are cholesterol statins?
Drugs that target HMG-CoA reductase to block cholesterol production.
53
Is cholesterol synthesis catabolic or anabolic?
Anabolic. It costs lots of energy to make acetyl-CoA and then to make cholesterol. High energy stimulates, low energy inhibits.
54
How is cholesterol transported in the bloodstream?
Cholesterol needs to be transported in the bloodstream. cholesterol → cholesterol esters (more hydrophobic) → packaged in chylomicrons
55
What are chylomicrons?
A phospholipid MONOlayer with a hydrophobic interior that packages cholesterol and TAGs. A type of lipoprotein.
56
What is a lipoprotein?
Lipoproteins transport lipids in the bloodstream.
57
What do lipoproteins have on their surface? Define them.
They have apolipoproteins. They are embedded on the surface of lipoproteins, and therefore are on the surface of chylomicrons.
58
What does the type of chylomicron tell you?
Type of chylomicron determines what kind of particle it is... VLDL, LDL, HDL
59
What is the function of apolipoproteins?
Function is to let a receptor bind to the surface of that specific particle.
60
How/where do chylomicrons move?
Chylomicrons are transported from the intestine to target cells with specific apolipoproteins (e.g. liver and muscle).
61
What happens to chylomicrons after the cargo is delivered?
The remnants of the chylomicron go to the liver where they are degraded.
62
What is VLDL?
Very low density lipoprotein: a phospholipid MONOlayer with a cholesterol and TAG interior.
63
Where is VLDL synthesized?
VLDL is synthesized and secreted by the liver.
64
What is the purpose of VLDL?
VLDL is how the liver supplies cholesterol not acquired from diet.
65
How would chylomicron and VLDL transport/secretion be described?
Exocytosis.
66
What does endocytosos of fatty acids require?
It must have a specific receptor for the apolipoprotein; needs a recognition event. (Often the receptors are in lipid rafts)
67
What is an endosome?
A phospholipid bilayer with an aqueous interior containing whatever was captured by receptors.
68
How is an endosome formed? (3)
1. receptor binds to ligand 2. membrane invaginates 3. p.m. seals itself producing a vesicle in the cell (endosome)
69
What do endosomes contain?
They have proton pumps (like F₀F₁ ATPase working in reverse) that pump protons against the gradient using ATP hydrolysis.
70
What do these proton pumps in endosomes cause? (2)
They will decrease pH leading to conformation change. The conformation change will cause the receptors bound to ligand to release ligands (CURLS).
71
What is CURLs?
Compartment of uncoupling of receptor and ligand.
72
What happens to receptors upon the pH decreasing?
Receptors will bleb off of the CURL and go back to the plasma membrane to be recycled.
73
What happens to the cargo when the pH decreases?
The cargo will fuse with a lysozyme.
74
What is a lysozyme?
A compartment with low pH, proteases, and lipases that digest molecules down to free fatty acids and amino acids.
75
What is HDL?
High density lipoprotein that is synthesized in the liver and circulates in the bloodstream.
76
Why is HDL the most dense?
It is the most dense because it has the lease amount of lipid cargo.
77
What is the role of HDL?
"Reverse Cholesterol Transport" HDL scavenges excess cholesterol and TAGs from the vascular system and returns them to the liver to be used in bile salt production. (cholesterol doesn't get catabolized for energy, so it goes to bile salts)
78
What happens if HMG-CoA reductase is phosphorylated?
It is inactive.
79
What causes phosphorylation HMG-CoA reductase? (2)
1. AMP-dependent Protein Kinases which are active when the cell is in a low energy state (not making cholesterol) 2. Glucagon causes phosphorylation (low blood sugar = low energy = not making cholesterol)
80
What happens when HMG-CoA reductase is unphosphorylated?
It is active.
81
What causes unphosphorylation HMG-CoA reductase? (1)
Insulin signaling turns on a phosphotase. (high blood glucose = high energy = making cholesterol)
82
How is HMG-CoA reductase regulated by copy number? (2)
1. can be targeted by ubiquitin protein degradation 2. gene expression is regulated
83
What is the fate of cholesterol, generally? (3)
Cholesterol cannot be catabolized, so it is either excreted, converted to bile salts, or converted to steroids/hormones.
84
What are high levels of circulating cholesterol associated with?
High levels of circulating cholesterol are associated with atherosclerosis, which is associated with MI, stroke, heart failure, etc.
85
What is "good" cholesterol?
HDL; the more HDL, the less likely you are to have poor vascular health.
86
What is "bad" cholesterol?
LDL; the more LDL, the more likely you are to have poor vascular health.
87
Where do monocytes tend to bind?
Monocytes tend to bind in areas where LDL is high and STICK there, differentiating into a macrophage (still stuck to vessel wall)
88
What do macrophages have the ability to do?
Macrophages have a massive ability to internalize LDL and keep filling up to become foam cells.
89
How do foam cells die and why is that a slight issue?
Foam cells die via apoptosis (programmed cell death). The remnants, TAG and cholesterol, remain behind.
90
Why does HDL help fix the slight issue of foam cell death?
HDL can scavenge the cholesterol and TAGs within reason.
91
What happens if enough macrophages bind and HDL can't keep up with the TAGs and cholesterol?
Now you have the formation of plaque which will constrict blood flow or break off and cause embolism, stroke, MI...
92
What is familial hypercholesterolemia?
People with genetically high levels of LDL due to a mutation in the LDL receptors.
93
How does familial hypercholesterolemia work? (6)
1. mutation in LDL receptors 2. no target cells 3. cholesterol not taken up 4. massively high levels of LDL 5. HDL is overwhelmed and can't scavenge it all 6. huge risk of MI, stroke. PE...
94
What is cholesterol a precursor for?
Hormones, notably sex hormones like cortisol, aldosterone, testosterone, estrogens, and progesterone.

Biochemistry II (11 decks)

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