[FMS] NAM - fat as fuel

Question 1

what are the 3 biological function of lipids

Answer 1

1. Components of cell membranes - (phospholipids & cholesterol)
2. Precursors of hormones
   cholesterol → steroid hormones

arachidonic acid → prostaglandins
3. Long term fuels (triglycerides)

Question 2

how are triglycerides stored

Answer 2

triglycerides stored as large fat droplets in the fat cells of adipose tissue

Question 3

what are the common fatty acids and their ratios

Answer 3

remember ‘pimsols’ = PSOLL

Question 4

• How is stored triglyceride fat in the adipose tissue broken down?

Answer 4

remember: TAG, DAG, MAG ‘The Disgusting Man’

Question 5

How is glycerol metabolised in most tissues

Answer 5

Enters glycolysis pathway for conversion to pyruvate, then
into TCA cycle foroxidation to CO2

Question 6

How is glycerol metabolised in liver/ starvation

Answer 6

Enters glycolysis pathway and is converted to glucose by gluconeogenesis

Question 7

where does the b oxidation of fatty acids occur

Answer 7

mitochondrial matrix

Question 8

How are long chain fatty acids activated?

Answer 8

activated in the cytosol by the addition of Fatty acyl-CoA synthetase.

Question 9

Outline how fatty acyl-CoA is transported into the mitochondria?

Answer 9

CARNITINE SHUTTLE

Question 10

why is it called the b-oxidation pathway?

Answer 10

Called β-oxidation because the β-carbon undergoes oxidation to produce a carbonyl group (carbon double-bonded to oxygen).

Question 11

where is CPTI?

Answer 11

outer mitochondrial membrane

Question 12

where is CACT?

Answer 12

inner mitochondrial membrane

Question 13

where is CPTII?

Answer 13

mitochondrial matrix

Question 14

what does one round of b-oxidation produce

Answer 14

One round of β-oxidation produces acetyl-CoA and a fatty acyl-CoA that is 2 carbons shorter
- the 2 carbons are now carried by acetyl-CoA.

Question 15

what are the steps of b-oxidation including the enzymes and products lost

Answer 15

Question 16

how many repeats does a C16FA pass through and how many NADH and FAHD2, snd acetyl coA is produced in b-oxidation?

Answer 16

Fatty acid with 16 C atoms
will pass through 7 repeats
of b-oxidation pathway
producing 7 NADH, 7 FADH2, and 8 acetyl coA

REMEMBER: beta oxidation of fatty acids makes:
1 acetyl CoA
1 NADH
1 FADH2

Question 17

what is the total ATP yield from fatty acid oxidation, why is 2 subtracted from the total amount?

Answer 17

106/107

its originally 108 but -2 because 2 ATP is used in activation stage

Question 18

3 ways fat metabolism can be regulated

Answer 18

1. Release of fatty acids from adipose tissue
   (adrenaline & glucagon activate lipase enzyme)
2. Rate of entry into mitochondria via carnitine shuttle
3. Rate of reoxidation of cofactors NADH & FADH2 by Electron Transport Chain

Question 19

How are odd-numbered fatty acids metabolised?

Answer 19

• If we break down an odd numbered fatty acids we end up with 3 carbons.
• To break this down you have to use ATP so it is not as energetically favourable as breaking down an even-numbered carbon.
  – You then have to do 2 conversion reactions and you need to add carbon.
• This forms succinyl-coA which enters the TCA cycle.

Question 20

when does ketogenesis occur in fat metabolism

Answer 20

in starvation
in Type I diabetes

^ ie when fat metabolism is the main source of energy

Question 21

outline how ketone bodies are formed

Answer 21

increased fatty avid oxidation = increased acetyl CoA

increased acetyl CoA exceed the TCA cycle capacity, Excess Acetyl CoA is converted into ‘ketone bodies’ and released as acetoacetate and β hydroxybutyrate into the bloodstream

They can be taken up by cells for utilisation.

Question 22

what are 2 ketone bodies

Answer 22

acetoacetate

β hydroxybutyrate

Question 23

most cell types can use ketone bodies, what intermediates do they get converted into for TCA cycle?

Answer 23

acetyl CoA and succinate

Question 24

• what is the fuel for human brain? why?

Answer 24

glucose

Brain cannot utilise fatty acids because they can’t get across the blood brain barrier – instead it uses glucose and small amount of ketone bodies (‘emergency fuel’)

Question 25

- what are the major muscle fuels?

Answer 25

glc, FA (ketone bodies)

Question 26

- what do muscles and brain lack?

Answer 26

glucose-6-phosphatase

Question 27

- what does the liver do?

Answer 27

provides brain, muscle and other organ fuel

Question 28

Red blood cells cannot utilise fatty acids or ketone bodies, use glucose only, why?

Answer 28

they don’t have mitochondria so they can’t do any of the processes.

Question 29

How are free fatty acids transported in the blood? They are:   1. carried by albumin. 2. carried by carnitine. 3. carried by chylomicrons. 4. carried by low- and high-density lipoproteins (LDLs and HDLs) 5. freely soluble and do not require a carrier.

Answer 29

1

Question 30

What are the three main biological function of lipids? 1. Components of ribosomes, precursor for steroid hormones, and long-term fuel storage. 2. Components of membranes, precursor for steroid hormones, and short-term fuel storage. 3. Components of membranes, precursor for steroid hormones, and long-term fuel storage. 4. Components of the nucleic acids, precursor for peptide hormones, and long-term fuel storage. 5. Components of membranes, precursor for peptide hormones, and long-term fuel storage.

Answer 30

3

Question 31

Fatty acids with an odd number of carbons undergo β-oxidation until three carbons of the fatty acid remain. This three-carbon unit (propionyl-CoA) is then converted to:   1. succinyl-CoA. 2. acetyl-CoA. 3. enoyl-CoA. 4. pyruvate. 5. glycerol.

Answer 31

1

Question 32

A reaction sequence that takes place in mitochondria when fatty acids are broken down for energy can be described as:   1. an oxidation followed by a hydration followed by a reduction. 2. an oxidation followed by an oxidation followed by a decarboxylation. 3. an oxidation followed by an oxidation followed by a hydrolysis. 4. an oxidation followed by a reduction followed by a hydrolysis. 5. an oxidation followed by a hydration followed by an oxidation.

Answer 32

5

Question 33

A deficiency that prevents someone from synthesising carnitine could cause:   1. Accumulation of lipid droplets in the mitochondrial matrix of liver cells 2. Accumulation of lipid droplets in the cytosol of liver cells 3. A decrease in free long chain fatty acids circulating in the blood. 4. Increased beta -oxidation and reduced storage of long chain fatty acids in liver cells 5. Increased conversion of long chain fatty acids to glucose in the liver.

Answer 33

ANSWER = 2 EXPLANATION: 1. Accumulation of lipid droplets in the mitochondrial matrix of liver cells: This is unlikely because the deficiency would hinder the transport of fatty acids into the mitochondria for beta-oxidation, leading to reduced fatty acid metabolism within the mitochondria, not accumulation of lipid droplets there. 2. Accumulation of lipid droplets in the cytosol of liver cells: This is a plausible outcome because if fatty acids cannot be transported into the mitochondria for beta-oxidation, they may accumulate in the cytosol of liver cells, leading to the formation of lipid droplets. 3. A decrease in free long-chain fatty acids circulating in the blood: This is plausible because if fatty acids are not being transported into the mitochondria for beta-oxidation, they may remain in other forms (e.g., esterified) and not circulate as free long-chain fatty acids. 4. Increased beta-oxidation and reduced storage of long-chain fatty acids in liver cells: This is unlikely because a deficiency in carnitine synthesis would hinder beta-oxidation, not increase it. 5. Increased conversion of long-chain fatty acids to glucose in the liver: This is unlikely because a deficiency in carnitine synthesis would disrupt beta-oxidation, which primarily generates energy from fatty acids rather than converting them to glucose. So, the most likely outcomes of a deficiency in synthesizing carnitine are options 2 (accumulation of lipid droplets in the cytosol of liver cells) and 3 (a decrease in free long-chain fatty acids circulating in the blood).

Question 34

how are intermediates in b oxidation presented

Answer 34

CoA thioesters

Question 35

how is the biological energy of fatty acids conserved in b oxidation

Answer 35

conserved via: - transfer of 2H atoms to the cofactors NAD+ and FAD to make NADH and FADH2

Question 36

how many enzyme reactions are involved in b oxidation and whats removed during the process?

Answer 36

4 enzyme reactions result in the removal of 2 carbon unit as acetyl CoA

Question 37

what are the stages of beta oxidation

Answer 37

activation oxidation hydration oxidation thiolysis

Question 38

what can inhibit carnitine acyltransferase

Answer 38

malonyl CoA

Question 39

which metabolic intermediate inhibits the transport system but allows newly synthesised fatty acid to enter mitochondria for oxidation

Answer 39

Malonyl CoA