Chapter 17

Question 1

Oxidation of fatty acids produces 80% of the energy for which two organs?

Answer 1

The heart and liver.

Question 2

What is Emulsification?

Answer 2

The breakdown of fats into smaller lipid droplets for transport or digestion.

Question 3

Name 3 sources of fatty acid fuels for cells.

Answer 3

1. Fats consumed in the diet.
2. Fats stored in cells as lipid droplets.
3. Fats synthesized in one organ for the use in another.

Question 4

Explain how dietary fats are processed.

Answer 4

1. Bile salts convert dietary fats in mixed micelles (bile salts and triacylglycerols).
2. Intestinal lipases convert triacylglycerols to mono- and diacylglycerols which help…
3. Diffusion into the intestinal epithelium.
4. The broken down products are reformed into triacylglycerols and packaged with cholesterol to form chylomicrons.
5. The lipids move through the intestinal epithelium to the blood.
6. Lipoprotein lipases in muscle and adipose hydrolyze triacylglycerols to fatty acids and glycerol.
7. Fatty acids enter muscle and adipose cells.
8. In muscle they are used for energy, in adipose they are reesterified for storage.

Question 5

What kind of molecule is a chylomicron?

Answer 5

Lipoprotein

Question 6

What is an apolipoprotein?

Answer 6

A lipid binding protein without a lipid.

Question 7

How are chylomicrons broken down?

Answer 7

They have cell surface receptors that identify themselves to the cell and promote uptake.

Question 8

How are stored fats mobilized?

Answer 8

Adipocytes have surface receptors for glucagon and epinephrine. When triggered it activates cAMP which activates PKA. PKA phosphorylates a lipase and perilipin. This releases fatty acids into the blood stream bound to albumin.

Question 9

What is perilipin?

Answer 9

A lipid droplet guardian protein.

Question 10

Where does the mobilized fat in blood go?

Answer 10

Myocytes

Question 11

What are the 3 enzymes that breakdown triacylglycerols?

Answer 11

1. Glycerol Kinase
2. Glycerol 3-Phosphate Dehydrogenase
3. Triose Phosphate Isomerase

Question 12

Where does fatty acid oxidation occur?

Answer 12

In the mitochondria.

Question 13

How do fatty acids get into the mitochondria?

Answer 13

12 carbons or shorter freely diffuse.

14 carbons or longer at attached to a CoA via fatty acyl-CoA synthetase which requires ATP.

Question 14

How is fatty acyl-CoA transported into the mitochondria?

Answer 14

It is attached to carnitine forming fatty acyl-carnitine by carnitine acyltransferase 1 which allows it into the intermembrane space.

Question 15

What does the acyl-carnitine transporter do?

Answer 15

Provides movement through the inner membrane with subsequent transfer back to CoA with carnitine acyltransferase 2.

Question 16

What are the 2 steps in fatty acid oxidation?

Answer 16

1. Removal of successive two- carbon units in the form of acetyl-CoA by β-oxidation.
2. The acetyl groups of each acetyl-CoA are oxidized to CO2 in the citric acid cycle yielding 3 NADH2 and 1 FADH2.

Question 17

Name the 4 enzymes in β-oxidation.

Answer 17

1. Acyl-CoA dehydrogenase
2. Enoyl-CoA hydrates
3. β-hydroxyacyl-CoAdehydrogenase
4. Acyl-CoA acetyltransferase (thiolase)

Question 18

What does Acyl-CoA dehydrogenase do?

Answer 18

Catalyzes the dehydrogenation of fatty-acyl CoA creating a trans C=C at C-2 (trans-Δ2) and passing electrons to FAD creating FADH2.

Question 19

What does Enoyl-CoA hydratase do?

Answer 19

Catalyzes the addition of water to the double bond reducing it to a alkane and adding an OH group onto the β carbon.

Question 20

What does β-hydroxyacyl-CoA dehydrogenase do?

Answer 20

Dehydrogenates the β-hydroxyacyl- CoA passing an electron to NAD+ to form NADH.

Question 21

What does Acyl-CoA acetyltransferase do?

Answer 21

Catalyzes the transfer of CoA-SH to the remaining fatty acid chain and the creation of acetyl-CoA.

Question 22

How many acetyl CoA’s are produced from a fatty acid?

Answer 22

(n/2)+1

n being the number of carbons

Question 23

What is produced in β-oxidation?

Answer 23

• 1 NADH
• 1 FADH2
• 1 H2O
• 1 Acetyl CoA for each carbon plus 1 extra

Question 24

Explain ATP priming.

Answer 24

2 ATP need to be removed from the net ATP production of β-oxidation because they are used to activate palmitate to palmitoyl-CoA.

Question 25

What poses a problem/stopping point for β-oxidation?

Answer 25

A double bond of a mono- or polyunsaturated fatty acid.

Question 26

What does Δ3, Δ2-enoyl-CoA isomerase do?

Answer 26

Catalyzes the isomerization of the cis-Δ3-enoyl-CoA to the trans-Δ2- enoyl-CoA which can then act as a substrate for enoyl-CoA hydrates. Trans-Δ2 can then go through β-oxidation.

Question 27

What enzymes are need to catalyze the isomerization of polyunsaturated fatty acids?

Answer 27

• 2,4-dienoyl-CoA reductase

- Δ3, Δ2-enoyl-CoA isomerase

Question 28

What does 2,4-dienoyl-CoA reductase do?

Answer 28

Catalyzes the isomerization of trans-Δ2,cis-Δ4-dienoyl-CoA to trans-Δ3-enoyl-CoA.

Requires NADPH

Question 29

What does enoyl-CoA isomerase do?

Answer 29

Moves the double bond from C3 to C2.

Question 30

How do you oxidize odd numbered fatty acids?

Answer 30

β-oxidation occurs normally until it reaches the last 3 carbons, propionyl-CoA. Then uses 3 enzymes to form succinyl-CoA.

Question 31

What enzymes are used on odd numbered fatty acids?

Answer 31

1. Propionyl-CoA carboxylase
2. methylmalonyl-CoA wpimerase
3. methyl-malonyl-CoA mutase

Question 32

What does Propionyl-CoA carboxylase do?

Answer 32

Catalyzes the carboxylation at C-2 to form D-methylmalonyl-CoA.

Uses ATP and biotin

Question 33

What does methylmalonyl-CoA epimerase do?

Answer 33

Epimerizes to the L-isomer.

Question 34

What does methyl-malonyl-CoA mutase do?

Answer 34

Catalyzes rearrangement to form succinyl-CoA via coenzyme B12,

Question 35

How is coenzyme B12 made?

Answer 35

From vitamin B12 by replacing a cyano group which is coordinated to a Co3+ coordinated to a corrin ring system with a 5’- deoxyadenosyl group.

Question 36

How does coenzyme B12 work?

Answer 36

The coordinate bond has a low bond dissociation energy facilitating the mutase reaction.

Question 37

What is the coenzyme B12 mechanism?

Answer 37

Methylmalonyl-CoA mutase breaks the Co-C bond leaving Co2+ and a 5’-deoxyadenosyl free radical.

The radical abstracts an H from methylmalonyl-CoA leaving a radical facilitating rearrangement. The H is returned to produce succinyl-CoA and the 5’- deoxyadenosyl radical is returned to regenerate Coenzyme B12.

Question 38

What are the 2 fates of fatty acyl-CoA?

Answer 38

In the liver;
1. β-oxidation in the mitochondria
2. Conversion to triacylglycerol and phospholipids in the
cytosol.

Question 39

How is β-oxidation regulated?

Answer 39

By mitochondrial transport via the carnitine shuttle which is rate-limited.

Question 40

How is the carnitine shuttle regulated?

Answer 40

High [Malonyl-CoA] builds up and inhibits when the cells have ample energy supply.

Question 41

Explain β-oxidation in peroxisomes.

Answer 41

The same as in mitochondria with 2 exceptions;

1. Acyl-CoA dehydrogenase passes its electrons directly to O2 creating H2O2 which is converted by catalase to water and O2.
2. Peroxisomes are more active on long chain (26 carbon) and branched chain fatty acids.

Question 42

Where does β-oxidation occur in plants?

Answer 42

• Peroxisomes of leaf tissues

- Glyoxysomes of the germinating seeds.

Question 43

Why is β-oxidation important in plants?

Answer 43

It produces biosynthetic precursors like oxaloacetate.

Question 44

What is a ketone body?

Answer 44

A product of acetyl-CoA or export to other tissues like skeletal and heart muscle for fuel.

Question 45

How are ketone bodies made?

Answer 45

The last step of β oxidation is reversed using 2 acetyl-CoAs to give acetoacetyl-CoA which is further acetylated and cleaved to form acetoacetate and acetyl-CoA.

Question 46

What it ketoacidosis?

Answer 46

Fatty acids are degraded to acetyl-CoA, but the acetyl-CoA can’t be used in the citric acid cycle because intermediates have been drawn off for use in gluconeogenesis. They are then converted to ketone bodies which lower blood pH causing acidosis.