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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
Q

Beta oxidation

A

4 steps

acyl-CoA –> Acetyl-CoA

26
Q

Beta oxidation mnemonic

A

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
Q

Why is beta oxidation called spiral pathway?

A

2 less C per round

28
Q

Where does beta oxidation occur?

A

Matrix, but also…

C3 (two carbons from carbonyl carbon)

29
Q

Where are acetyl units lost from in beta oxidation?

A

activated CoA end (not methyl end)

30
Q

Why does beta oxidation happen?

A

Source of free energy when CH2O unavailable (especially during fast, when no carbs)

31
Q

Total ATP from beta oxidation

A

14 ATP (10 per acetyl –> 3 NADH, 1 QH2, 1 GTP)

  1. 5 = QH2
  2. 5 = NADH
32
Q

Regulation of Beta oxidation depends on availability of free CoA as well as

A

NAD+/NADH

Q/QH2

33
Q

Cis Fatty acids: Beta oxidation

Where is problem?

A

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
Q

Why do unsaturated fatty acids yield less energy than saturated fatty acids?

A

need isomerases for beta oxidation
QH2 bypass =1.5
NAPH reduction =2.5

Total 4 ATP lost

35
Q

Propinyl-CoA to Acetyl-CoA

A

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
Q

Why must propionyl-CoA be fully converted to pyruvate to enter CAC as acetyl-CoA?

A

to utilize energy in thioester bond

37
Q

What’s weird about Methylmalonyl-CoA Mutase?

A

Prosthetic group derived from cobalamin

Obtained from B12

38
Q

Peroxisome fatty acid oxidation: what’s so special about that?

A

Where it happens in all plants
Step 1 is special: acyl-CoA OXIDASE

FAD FAH2
O2 –> H2O2

39
Q

Peroxisomes are a chain shortening system: why?

A

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
Q

Beta oxidation summary:

1) Location
2) Acyl-group attached to what?
3) Where does it funnel e-?
4) ATP involved?

A

1) M. Matrix
2) Coenzyme A
3) Q and NAD+
4) 2x ATP to activate

41
Q

Fatty acid synthesis:

1) Location
2) Fatty acid chain attached to what?
3) Reducing agent
4) ATP involved?

A

1) Cytosol
2) acyl-carrier protein (ACP)
3) NADPH
4) Consumes 1 ATP for every 2C incorporated

42
Q

How do we get acetyl-CoA to cytosol for fatty acid synthesis

A

CITRATE transporter

43
Q

How does citrate transporter regenerate pyruvate?

A

Malic enzyme

44
Q

What is the main regulatory step of fatty acid synthesis?

A

Acetyl-CoA Carboxylase

45
Q

Acetyl-CoA Carboxylase

A

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
Q

Fatty acid synthesis: enzyme

A

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
Q

First two reactions of fatty acid synthesis

A

Transacylations
prime/load the enzyme with reactants for condensation reaction

MAT

48
Q

Condensation (KS) reaction of Fatty acid synthesis (step 3)

A

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
Q

Fatty acid synthesis step 4

A

KR

Reduction (NADPH –> NADP+)

50
Q

Fatty acid synthesis step 5

A

DH
H2O released
Dehydration

51
Q

Fatty acid synthesis step 6

A

ER
NADPH –> NADP+
Reduction

52
Q

Fatty acid synthesis step 7

A

acyl group transferred from ACP to enzyme Cys group

Another malonyl loaded onto free ACP for another condensation reaction

53
Q

1 malonyl-CoA per round of fa synthesis costs 1 ATP per molecule

How much for 7 rounds for palmitate?

A

42 ATP

7 ATP + 35 ATP from the 14 NADH

54
Q

Why is using multienzyme protein advantage?

A

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
Q

Where does elongation occur?

A

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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