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Malika Biochem MCAT > Chapter 11 > Flashcards

Chapter 11 Flashcards

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MCAT flashcards
1
Q

Differentiate between micelles and chylomicrons in lipid digestion

A
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2
Q

Function of hormone-sensitive lipase

A

Stimulated by catabolic hormone release in adipose tissues such as (ACTH, epinephrine and glucagon); hydrolyzes triacylglycerols into fatty acids and glycerol (promotes lipolysis)

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3
Q

What are lipoproteins?

A

Carrier proteins for lipids in the blood

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4
Q

Different types of lipoproteins

A

Chylomicrons - they assemble in intestinal lining, carry triacylglycerols and cholesterol esters
VLDL - they are produced/assembled in the liver, transport triacylglycerols to tissues
IDL - exists as a transition particle and can become either HDL or LDL depending on what it picks up (either cholesterol or triacylglycerol
LDL - MAIN lipoproteins which carries cholesterol to deliver to tissues
HDL - cleans up excess cholesterol from tissues to excrete

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5
Q

What is the purpose of creating fatty acids in our body?

A

Firstly, the purpose is when we eat a heavy meal, insulin is released and allows us to break glucose down to supply our body with ATP. However, we don’t need all the energy that is produced, some is sufficient. The rest is utilized to make fatty acids which can be stored in adipose tissue, to utilize later on for our body.

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6
Q

How does our body create fatty acids de novo?

A

It utilizes citrate that is transported from the mitochondria through the citrate shuttle into the cytosol where the citrate goes through a series of 3 steps:
1. Citrate is split into OAA and acetyl-CoA by the enzyme citrate lyase
2. Acetyl-CoA carboxylase adds CO2 to to acetyl-CoA using 1 ATP and forms malonyl-CoA
3. Malonyl-CoA is transformed into the fatty acid “palmitate”by the enzyme palmitate synthase –> this reactions requires 2 NADPH

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7
Q

Inputs and outputs of FA synthesis

A
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8
Q

What is the rate-limiting step/enzyme of fatty acid synthesis?

A

Enzyme is Acetyl-CoA carboxylase which converts Acetyl-CoA into Malonyl-CoA.
In order to function, the enzyme requires ATP and is stimulated by insulin and citrate. INHIBITED BY GLUCAGON.

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9
Q

Once fatty acids are made, where are they packed to be stored in the body?

A

In the liver, 3 fatty acids are attached to glycerol, they are packaged in VLDL proteins and sent to the adipose tissue where they are stored as triacylglycerol.

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10
Q

Explain how insulin and glucagon relate to fatty acid synthesis and fatty acid beta-oxidation.

A

Insulin - Insulin decreases fatty acid oxidation, increases fatty acid synthesis/re-esterification
Glucagon - increases fatty acid oxidation (because fatty acids need to be broke down for energy), decreases fatty acid synthesis

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11
Q

Where does beta-oxidation primarily occur? What is the 2nd place it can occur at? What is the purpose of fatty acid oxidation in general?

A

Primarily in the mitochondria; then in peroxisomes
Fatty acid oxidation allows for the break down of fatty acids into acetyl-CoA and ATP that can serve as fuel for the body when glucose is low.

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12
Q

What is the rate-limiting enzyme/step of fatty acid oxidation?

A

Cartnitine acyl-transferase I –> attaches a carnitine group to the acyl-CoA (displacing the CoA group) –> this allows acyl carnitine to travel to the mitochondria ; otherwise it can’t cross the inner membrane
Inhibited by malonyl-CoA (intermediate of fatty acid synthesis).

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13
Q

What molecules/products inhibit fatty acid oxidation? What molecules inhibit fatty acid synthesis?

A

Long chain FA oxidation is inhibited by malonyl-CoA which is a product of fatty acid synthesis.

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14
Q

What is the only fatty acid humans can synthesize de novo?

A

Palmitate, 16 carbon carboxylic acid

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15
Q

What kind of oxidation do branched fatty acids undergo?

A

alpha-oxidation

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16
Q

How are short and medium chain fatty acids oxidized?

A

They travel straight through the mitochondrial membranes UNLIKE long chain fatty acids.

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17
Q

In order for LONG-CHAIN fatty acids to enter the mitochondria, they have to undergo a series of steps to be able to cross the membranes. What are these steps?

A
  1. Attachment of a Co-A to the fatty acid (CoA makes a good leaving group) –> forming acyl-CoA
  2. CoA is displaced by a carnitine group
  3. Acyl-carnitine travels through the double membranes into the mitochondrial matrix
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18
Q

Describe the 1/4 step of beta oxidation in the mitochondrial matrix.

A
  1. First oxidation
    Oxidation of the fatty acid by FAD - Formation of a double bond between the alpha & beta carbons, electrons travel to FAD to form FADH2.
    Reaction is catalyzed by acyl-CoA dehydrogenase.
    FADH2 then enters the electron transport chain to eventually produce 1.5 ATP molecules through oxidative phosphorylation.
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19
Q

Describe the 2/4 step of beta oxidation in the mitochondrial matrix.

A
  1. Hydration
    H2O reacts w/ the beta position of the double bond on the fatty acid by the enzyme enoylCoA hydrolase.
    This adds an OH group on the 3rd carbon.
    If the fatty acid is trans before –> it forms the L isomer. Cis –> D isomer
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20
Q

Describe the 3/4 step of beta oxidation in the mitochondrial matrix.

A
  1. Second oxidation
    The OH group of C3 is oxidized to a ketone by the enzyme L-3-hydroxyacyl-CoA dehydrogenase.
    Simultaneously an NAD+ is reduced to NADH.
21
Q

Describe the 4/4 step of beta oxidation in the mitochondrial matrix.

A
  1. Thiolytic cleavage by coenzyme A
    Another acetyl-CoA molecule which has a thiol (–SH) group nucleophilically attacks the newly oxidized C3 carbonyl and the acetyl-CoA leaving group leaves.
    Beta-ketothiolase catalyzes this reaction.
22
Q

How many ATPs are used per synthesis of palmitic acid?

A

7 ATP

23
Q

Are even-numbered and odd-numbered fatty acids oxidized the same way?

A

Yes they are, except the last oxidation of an odd-numbered fatty acid yields an acetyl-CoA & a propionyl-CoA instead of regularly two acetyl-CoAs.
Propionyl-CoA is converted into a TCA cycle intermediate.

24
Q

Calculating how many acetyl-CoA’s are produced per n-carbon fatty acid and how many ATPs.

A

For n = a random even number, divide it by 2 and that will be your # of acetyl-CoAs
ATP = # of acetyl-CoA - 1

25
Q

Calculating how many NADH and FADH2 are produced from beta-oxidation of n-carbon fatty acid.

A

n is your length of carbons in the fatty acid
(n/2) - 1

26
Q

What are ketone bodies and where are they produced?

A

Ketone bodies, acetoacetate and 3-hydroxybutyrate are produced in mitochondria of the liver when the body is in a fasting state because there is an excess buildup of acetyl-CoA from beta-oxidation of fatty acids.

27
Q

Why do ketone bodies get produced?

A

Ketone bodies are produced because the body isn’t getting its energy from glucose, so it resorts to fatty acid oxidation which causes too much acetyl-CoA. FA oxidation has no negative feedback mechanism, so acetyl-CoA keeps accumulating.
Therefore, to counteract this buildup, the liver converts acetyl-CoA into ketone bodies.

28
Q

True or false:
Ketone bodies are utilized in all tissues as a source of energy.

A

False, ketones aren’t used by the liver as a source of energy. This is because the enzyme which catabolizes ketones, thiophorase, is present only in tissues outside of the liver.

29
Q

During prolonged starvation, the brain starts to utilize (fatty acids/ketones) as its main energy source.

A

Ketones

30
Q

Process of ketone formation/ketogenesis:

A
  1. HMG-CoA synthase catalyzes the reaction of Acetyl-CoA to HMG-CoA.
  2. HMG-CoA is converted into acetoacetate by enzyme HMG-CoA lyase.
  3. Acetoacetate îs reduced to 3-hydroxybutyrate.
  4. Acetoacetate & 3-hydroxybutyrate enter the bloodstream and travel to various tissues
31
Q

What is a byproduct of ketogenesis?

A

Acetone

32
Q

How does alcoholism affect the metabolic processes in the body?

A

Alcoholism causes a high consumption of NAD+. There is not enough NAD+ for glycolysis and the TCA cycle (necessary) substrates, so the body resorts to ketogenesis. This causes alcoholic ketoacidosis which is the buildup of ketones in the bloodstream.

33
Q

Ketogenic amino acids

A

-Amino acids which can be converted into acetyl-CoA & ketone bodies
-Includes leucine, lysine, isoleucine, phenylalanine, threonine, tryptophan, and tyrosine “PITTT LL”

34
Q

Glucogenic amino acids

A

AA’s which can be converted into pyruvate/OAA to be shuttled into gluconeogenesis creating glucose
-Include all AAs except leucine and lysine

35
Q

Mnemonic for AA which are both ketogenic & glucogenic

A

“I” “P” “Triple T”
Isoleucine
Phenylalanine
Tyrosine
Tryptophan
Threonine

36
Q

Ketogenic amino acids contribute to synthesis of (glucose/fatty acids), while glucogenic amino acids contribute to synthesis of (glucose/fatty acids).

A

fatty acids, glucose

37
Q

Essential vs nonessential amino acids

A

Essential AA - amino acids which the body can’t synthesize de novo, has to come from diet
Nonessential - amino acids which the produce can produce on its own

38
Q

Steps of catabolism of amino acids.

A
  1. Transamination - amino group is removed from the amino acid and transferred to a common acceptor, called alpha-ketoglutarate.
  2. In the liver, alpha-ketoglutarate becomes glutamate and then donates the amine group as ammonia TO the urea cycle
  3. Essentially the ammonia is funneled into the urea cycle and urea is then excreted with the urine.
  4. The remaining carbon backbone becomes an alpla-keto acid & is funneled into gluconeogenesis or fatty acid oxidation.
39
Q

Question about amino acid catabolism

A
40
Q

Once fatty acid oxidation creates Acetyl-CoA, what is it used for?

A

Acetyl-CoA can be used in two different pathways.
1. IF there is enough oxaloacetate, then it is funneled into the TCA cycle to create more ATP
2. IF there is NOT enough oxaloacetate, then it can’t go through the TCA cycle –> instead acetyl-CoA is converted into ketone bodies

41
Q

What is the cori cycle?

A

A cycle which connects gluconeogenesis and glycolysis together. The cycle starts when lactate is created in the muscles due to anaerobic metabolism. Lactate travels in the blood to the liver, where it is funneled into gluconeogenesis to create glucose.
The regenerated glucose then moves via the bloodstream to the peripheral tissues where it undergoes glycolysis to provide ATP.

42
Q

What is the advantage of the Cori-cycle?

A

Lactate does not accumulate in blood as it is used by the liver for gluconeogenesis

43
Q

Everything to know about the urea cycle:

A

-Occurs in liver both in cytosol & mitochondria
-Each molecule of urea contains 2 N atoms
-Ammonia which gets its nitrogen from catabolism of amino acids, donates the nitrogen to urea

44
Q

Which of the following products of catabolism molecules can be funneled into gluconeogenesis?
Even numbered fatty acids
Odd numbered fatty acids
Glucogenic amino acids
Ketogenic amino acids

A

Even numbered fatty acids - don’t contribute
Odd numbered fatty acids - can contribute bc propionyl-CoA which is one of the products of the FA oxidation can be used an an intermediate in TCA
Glucogenic amino acids - can contribute
Ketogenic amino acids - don’t contribute because they produce acetyl-CoA which isn’t directly funneled into gluconeogenesis

45
Q

Rate-limiting enzymes for:
Fatty acid synthesis
Beta-oxidation or fatty acids
Cholesterol synthesis
Ketone body synthesis

A

Fatty acid synthesis - Acetyl-CoA carboxylase
Beta-oxidation or fatty acids - Carnitine acyl transferase
Cholesterol synthesis - HMG CoA reductase
Ketone body synthesis - HMG CoA synthase

46
Q

Give examples of intermediates from non-glycolytic pathways that can enter the TCA cycle

A

Protein catabolism = deamination of alanine forms pyruvate which is funneled into TCA cycle or gluconeogenesis

47
Q

Alanine deamination forms _______.

A

pyruvate

48
Q

Which 2 amino acids can NOT contribute to gluconeogenesis?

A

Leucine and Lysine

Malika Biochem MCAT (11 decks)

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