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Cellular Biochemistry > Chapter 17 > Flashcards

Chapter 17 Flashcards

1
Q

Atherosclerosis

A

Lipid accumulation in vessel walls = inflammation/recruit WBC (macrophages)

Macrophage- consume lipids, recruit more macrophages

Plaque forms- cholesterol/dead macrophages, SMCs, this could lead to calcification

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2
Q

Function of lipoproteins

A

transport dietary triacylglycerols to adipose tissue

and cholesterol to the liver

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3
Q

Chylomicrons

A

Intestine –> Other tissues
TAGs –> Adipose
Cholesterol –> Liver

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4
Q

How does liver repackage cholesterol/lipids?

A

As VLDL

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5
Q

VDLD

A

Release TAGs and become LDL

50-65% TAG

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6
Q

LDL

A

Circulating Lipoprotein, “bad”
Taken up by adipose tissue/liver
45-50% cholesterol

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7
Q

HDL

A

Transport extra cholesterol from tissue back to the liver

40-55% protein

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8
Q

How LDL gives cell cholesterol

A

Receptor mediated endocytosis

LDL receptor recycled, but LDL protein degraded

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9
Q

How HDL removes excess cholesterol from adipose tissue

A

Flippase (ABC)

Tangier disease- defect in transporter gene = accumulation in tissues

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10
Q

Familial hypercholesterolemia

A

Genetic defect in LDL receptor

Causes rise in serum levels, atherosclerosis, early death

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11
Q

Nonfamilial hypercholesterolemia

A

Treated with PCSK9 inhibitor leads to increased recycling of LDL receptor to cell surface (PCSK9 causes degradation of LDL receptor)

More LDL receptor = increased uptake of circulating LDL

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12
Q

What is the primary source of fatty acids used as metabolic fuel?

A

Dietary triacylglycerols

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13
Q

Triacylglycerol —-> glycerol and 3x fatty acyl groups by

A

lipoprotein lipase (extracellular peripheral)

add 3H2O

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14
Q

Hydrolysis of triacylglycerols occurs

A

extracellularly

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15
Q

Why is the concentration of free fatty acids in body very low?

A

These molecules are detergents and could disrupt cell membranes

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16
Q

How are TAGs mobilized?

How do released TAGS travel?

A

Mobilized: via intracellular hormone-sensitive lipase

Travel: albumin carrier

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17
Q

Where are free fatty acids taken to?

A

Liver/muscles (especially heart muscle)

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18
Q

To be degraded, first, fatty acid must be…

A

activated

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19
Q

How are fatty acids activated?

A

2 steps by acyl-CoA synthetase

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20
Q

Fatty acid 2 step activation

A

1) F.a. displaces diphosphate group of ATP. This creates an acyladenylate
2) HSCoA displaces AMP from acyladenylate froming acyl-CoA

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21
Q

Why is fatty acid synthesis spontaneous and irreversible?

A

the hydrolysis of PPi is highly exergonic

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22
Q

Synthases are specific depending on

A

length of fatty acids

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23
Q

Fatty acid activation occurs

A

in the cytosol

then use carnitine system to get out

24
Q

Carnitine shuttle

A

carnitine acyltransferase: transfers acyl group to carnitine

In mitochondria: carnitine acyltransferase acyl group to HSCoA

Carnitine returns to cytosol via transporter; acyl group remains in matrix for oxidation

25
Beta oxidation
4 steps | acyl-CoA --> Acetyl-CoA
26
Beta oxidation mnemonic
Fatty acyl-CoA, Enoyl-CoA, 3-hydroxyacyl-CoA, ketoacyl-CoA, 2C shorter fatty acyl-CoA and acetyl-CoA (F.A. E HOA K) dehydrogenase, hydratase, dehydrogenase, thiolase DHDT
27
Why is beta oxidation called spiral pathway?
2 less C per round
28
Where does beta oxidation occur?
Matrix, but also... | C3 (two carbons from carbonyl carbon)
29
Where are acetyl units lost from in beta oxidation?
activated CoA end (not methyl end)
30
Why does beta oxidation happen?
Source of free energy when CH2O unavailable (especially during fast, when no carbs)
31
Total ATP from beta oxidation
14 ATP (10 per acetyl --> 3 NADH, 1 QH2, 1 GTP) 1. 5 = QH2 2. 5 = NADH
32
Regulation of Beta oxidation depends on availability of free CoA as well as
NAD+/NADH | Q/QH2
33
Cis Fatty acids: Beta oxidation | Where is problem?
Problem is in second step of round 4: 3,4 DB Solution: enoyl-CoA isomerase cis 3,4 --> Trans 2,3 But for linoleate, 2x DB? Round 5: reductase uses NADPH to convert trans 2,3 & cis 4,5 ---> Trans 3,4 Then, isomerase trans 3,4 --> trans 2,3
34
Why do unsaturated fatty acids yield less energy than saturated fatty acids?
need isomerases for beta oxidation QH2 bypass =1.5 NAPH reduction =2.5 Total 4 ATP lost
35
Propinyl-CoA to Acetyl-CoA
Please, may Mary sell seashells for money, please ``` Propinyl-CoA CARBOXYLASE Methylmalonyl-CoA RACEMASE Methylmalonyl-CoA MUTASE Succinyl-CoA SYNTHETASE Succinate DEHYDROGENASE Fumarase Malic Enzyme Pyruvate DEHYDROGENASE ```
36
Why must propionyl-CoA be fully converted to pyruvate to enter CAC as acetyl-CoA?
to utilize energy in thioester bond
37
What's weird about Methylmalonyl-CoA Mutase?
Prosthetic group derived from cobalamin Obtained from B12
38
Peroxisome fatty acid oxidation: what's so special about that?
Where it happens in all plants Step 1 is special: acyl-CoA OXIDASE FAD FAH2 O2 --> H2O2
39
Peroxisomes are a chain shortening system: why?
Peroxisomal enzymes specific for very long chain fatty acids. Branched chains not recognized by mitochondrial enzymes; peroxisomes compensate for lack of recognition due to branched methyl groups
40
Beta oxidation summary: 1) Location 2) Acyl-group attached to what? 3) Where does it funnel e-? 4) ATP involved?
1) M. Matrix 2) Coenzyme A 3) Q and NAD+ 4) 2x ATP to activate
41
Fatty acid synthesis: 1) Location 2) Fatty acid chain attached to what? 3) Reducing agent 4) ATP involved?
1) Cytosol 2) acyl-carrier protein (ACP) 3) NADPH 4) Consumes 1 ATP for every 2C incorporated
42
How do we get acetyl-CoA to cytosol for fatty acid synthesis
CITRATE transporter
43
How does citrate transporter regenerate pyruvate?
Malic enzyme
44
What is the main regulatory step of fatty acid synthesis?
Acetyl-CoA Carboxylase
45
Acetyl-CoA Carboxylase
Similar to propionyl-CoA/pyruvate carboxylase Co2 activated by biotin (consumes ATP) carboxylate transferred to acetyl-coA Malonyl-CoA donates 2-carbon acetyl unit to build FA
46
Fatty acid synthesis: enzyme
multifunctional, 7 catalytic reactions Pantothenate arm in ACP swings 6 active sites MAT, KS, KR, DH, ER, TE (Married Kangaroos Kick Dirty Elves Tirelessly)
47
First two reactions of fatty acid synthesis
Transacylations prime/load the enzyme with reactants for condensation reaction MAT
48
Condensation (KS) reaction of Fatty acid synthesis (step 3)
decarboxylates malonyl-ACP, which allows C2 to attack acetyl thioester to form acetoacetyl-ACP Product similar to product of step 2 beta-oxidation, but for this it’s in the D configuration Growth of acyl chain occurs at thioester end
49
Fatty acid synthesis step 4
KR | Reduction (NADPH --> NADP+)
50
Fatty acid synthesis step 5
DH H2O released Dehydration
51
Fatty acid synthesis step 6
ER NADPH --> NADP+ Reduction
52
Fatty acid synthesis step 7
acyl group transferred from ACP to enzyme Cys group Another malonyl loaded onto free ACP for another condensation reaction
53
1 malonyl-CoA per round of fa synthesis costs 1 ATP per molecule How much for 7 rounds for palmitate?
42 ATP 7 ATP + 35 ATP from the 14 NADH
54
Why is using multienzyme protein advantage?
Allows enzymes to be synthesized and controlled in a coordinated fashion Product of one reaction can quickly diffuse to the next active site In mammals, fatty acid synthase produces mostly 16C saturated f.a. Palmitate.
55
Where does elongation occur?
Either ER OR mitochondria ER: use malonyl-CoA as the acetyl-group donor Mitochondria: fatty acids elongated by reactions that more closely resemble the reversal of beta oxidation but use NADPH

Cellular Biochemistry (15 decks)

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