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FMS > [FMS] NAM - fat as fuel > Flashcards

[FMS] NAM - fat as fuel Flashcards

1
Q

what are the 3 biological function of lipids

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

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

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2
Q

how are triglycerides stored

A

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

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3
Q

what are the common fatty acids and their ratios

A

remember ‘pimsols’ = PSOLL

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4
Q
  • How is stored triglyceride fat in the adipose tissue broken down?
A

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

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5
Q

How is glycerol metabolised in most tissues

A

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

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6
Q

How is glycerol metabolised in liver/ starvation

A

Enters glycolysis pathway and is converted to glucose by gluconeogenesis

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7
Q

where does the b oxidation of fatty acids occur

A

mitochondrial matrix

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8
Q

How are long chain fatty acids activated?

A

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

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9
Q

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

A

CARNITINE SHUTTLE

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10
Q

why is it called the b-oxidation pathway?

A

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

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11
Q

where is CPTI?

A

outer mitochondrial membrane

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12
Q

where is CACT?

A

inner mitochondrial membrane

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13
Q

where is CPTII?

A

mitochondrial matrix

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14
Q

what does one round of b-oxidation produce

A

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.

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15
Q

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

A
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16
Q

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

A

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

17
Q

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

A

106/107

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

18
Q

3 ways fat metabolism can be regulated

A
  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
19
Q

How are odd-numbered fatty acids metabolised?

A
  • 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.
20
Q

when does ketogenesis occur in fat metabolism

A

in starvation
in Type I diabetes

^ ie when fat metabolism is the main source of energy

21
Q

outline how ketone bodies are formed

A

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.

22
Q

what are 2 ketone bodies

A

acetoacetate

β hydroxybutyrate

23
Q

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

A

acetyl CoA and succinate

24
Q
  • what is the fuel for human brain? why?
A

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’)

25
Q
  • what are the major muscle fuels?
A

glc, FA (ketone bodies)

26
Q
  • what do muscles and brain lack?
A

glucose-6-phosphatase

27
Q
  • what does the liver do?
A

provides brain, muscle and other organ fuel

28
Q

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

A

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

29
Q

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.
A

1

30
Q

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.
A

3

31
Q

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.
A

1

32
Q

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.
A

5

33
Q

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.
A

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.

  1. 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.
  2. 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.
  3. 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.
  4. 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).

34
Q

how are intermediates in b oxidation presented

A

CoA thioesters

35
Q

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

A

conserved via:

  • transfer of 2H atoms to the cofactors NAD+ and FAD to make NADH and FADH2
36
Q

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

A

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

37
Q

what are the stages of beta oxidation

A

activation
oxidation
hydration
oxidation
thiolysis

38
Q

what can inhibit carnitine acyltransferase

A

malonyl CoA

39
Q

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

A

Malonyl CoA

FMS (33 decks)

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