Lecture 2 Flashcards

1
Q

How does fatty acid oxidation begin

A

with activation; due to ATP

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2
Q

How is fatty acid activated

A

the formation of a thioester bond between carboxyl group of the FA and the thiol of the CoA-SH

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3
Q

true or false; the resulting CoA ester during fatty acid activation is more soluble

A

true

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4
Q

What is the enzyme for fatty acid activation

A

acyl CoA synthetase

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5
Q

What is the role of carnitine in acyl-CoA transfer

A

acyl group is transferred to carnitine, carried across the inner mitochondrial membrane, then transferred to mitochondrial CoA

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6
Q

true or false; acyl-CoA crosses the outer mitochondrial membrane but not the inner membrane

A

true

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7
Q

What is the enzyme used for the transfer of acyl group to carnitine

A

carnitine palmitoyltransferase (CPT-1)

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8
Q

what has CPT-1 have specificity for

A

acyl groups between 14 and 18 carbons long

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9
Q

where does the breakdown of fatty acids occur

A

mitochondrial matrix and proceeds by successive removal of 2C as acetyl CoA

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10
Q

What do you call the reaction that each 2C moiety must undergo to be converted to acetyl CoA

A

B-oxidation

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11
Q

What is B-oxidation

A

a series of four reactions that cleaves carbon atoms two at a time from the carboxyl end of the fatty acid

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12
Q

What are the 4 central reactions of B oxidation

A
  1. ) dehydrogenation across a-B and C-C bond (-H2O)
  2. ) hydration of the same bond (H2O)
  3. ) second dehydrogenation yields a B-keto group
  4. ) attack by CoASH to form a new, shorter FA-CoA and acetyl CoA
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13
Q

What are the saturated FAs with even number chain length

A

C14, 16, 18 etc

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14
Q

true or false; saturated FAs with even number chain length can be completely oxidized by this route B oxidation

A

true

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15
Q

true or false; odd numbered carbon FAs can be metabolized via the B oxidation as well but a 3C unit remains

A

true

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16
Q

what is the 3C unit that remain after B oxidation of an odd numbered fatty acid

A

propionyl CoA

17
Q

what is propionyl CoA converted to

A

methylmalonyl CoA by carbon dioxide fixation; this can also enter the TCA cycle via the coversion to succinyl CoA

18
Q

What happens to unsaturated fatty acids

A

FAs containing a double bond require an additional enzyme for degradation

the cis-enoyl group is converted to the trans configuration by an ISOMERASE

19
Q

true or false; lipid oxidation generates water and CO2

A

true

20
Q

Why do ketone bodies form

A
  • surplus acetyl CoA cannot be oxidized by the TCA cycle if cellular levels of oxaloacetate are insufficient to react with; instead acetyl CoA is converted to ketone bodies
21
Q

What causes low oxaloacetate

A

diet high in lipids and low carbs
diabetes not well controlled
starvation

22
Q

what are 2 types of ketone bodies

A

acetone
B-hydroxybutyrate
acetoacetate

23
Q

where are ketone bodies formed

A

in liver mitochondria

24
Q

what uses ketone bodies

A

can be used in most tissue and organ including the brain but only after prolonged starvation

  • metabolic state called KETOSIS
25
Q

what is excess carbohydrate stored as

A

fat

26
Q

true or false; fat is a compact energy storage form, being highly reduced an anhydrous

A

true

27
Q

What are the major producers of fat

A

liver and fat cells

- mammary glands also have the ability to synthesize fat during milk production

28
Q

why cant mammals synthesize glucose from fatty acids

A

because pyruvate dehyrogenase and pyruvate kinase are irreversible

29
Q

how much energy is in 1 g of fat

A

9 kcal

30
Q

how much energy is in 1g of carbs

A

3.75kcal

31
Q

how much energy is in 1g of protein

A

4 kcal

32
Q

What is the symbol for respiratory quotient

A

RQ

33
Q

Expression of RQ

A

CO2 generated in mol/ O2 consumed in mol

34
Q

true or false; after digestion is complete the RQ is nearly 1.0

A

true

- shows that carbs (as liver glycogen) is preferentially oxidized in this state

35
Q

What is the RQ during starvation

A
  1. 71

- fats are preferentially oxidized in the starved state

36
Q

where is the chain lengthening and introduction of double bond for FA metabolism

A

ER