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Exam 1 Lipid synthesis Flashcards

1
Q

fatty acid synthesis occurs in

A

cytosol

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2
Q

hormone that stimulates fatty acid synthesis

A

insulin

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3
Q

prostethic group of ACC

A

biotin

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4
Q

substrates that ACC needs to make malonyl coa

A

Acetyl coa , bicarbonate and ATP

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5
Q

what happens when you eat raw eggs*

A

white stuff has avidin which steals biotin, ACC wont work so it would affect conversion of Acetylcoa into malonyl coa

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6
Q

how is mitochondrial Coa available in cytosol

A

Acetyl coa cant cross membrane
Citrate synthase converts OAA and Acetyl coa— citrate
citrate has transporter that takes it from mitochondria to cytosol
cytrate lyase- – citrate=== OAA and Acetyl coa
malate dehydrogenase– oAA– malate
malic enzyme—- malate ==== pyruvate Co2 NADPH

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7
Q

what happens when citrate is in excess

A

Citrate is transported via carrier from matrix into citosol and it can be used as precursor for acetyl coa synthesis

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8
Q

Name the reductant that is required for the fatty acid synthesis.

A

NADPH

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9
Q

substrate and product for malic enzyme

A

malate=== pyruvate co2 and NADPH

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10
Q

ACP vitamin derivative

A

phosphopantetheine
■ derivative of vitamin pantothenate (Vit B5)
■ a prosthetic group that a​nchors t​he growing fatty acid chain during
fatty acid synthesis

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11
Q

during palmitic acid synthesis what is used 7 times

A

Malonyl Coa

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12
Q

Name the enzyme domain that releases palmitate from the fatty acid synthase complex.

A

thioesterase I

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13
Q

Name the enzyme that is expressed during lactation in mammary gland that is relevant
to fatty acid synthesis.

A

Thioesterase II

causes premature release of shorter chain fatty acids

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14
Q

Fatty acids released by thioesterase II

A

Capric acid​(C­10)
○ Lauric acid (C­12)
○ Myristic acid (C­14)

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15
Q

two essential fatty acids

A

linoleic, linolenic

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16
Q

All naturally occurring double bonds of fatty acids are of cis­configuration.

A

true?

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17
Q

linoleic acid is precursor for

A

arachidonic acid

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18
Q

storage form of fatty acid

A

tryglyceride

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19
Q

tryglycerides stored

A

adipose tissue

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20
Q

Name the precursors for the synthesis of triglyceride.

A

fatty acids
○ CoA (coenzyme A)
○ Glycerol 3­phosphate

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21
Q

tryglycerides- fatty acids sterified to

A

glycerol backbone

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22
Q

Fatty acid synthesis occurs in ?

A

cytosol

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23
Q

in beta oxidation fatty, activted fatty acids are esterified to

A

carnitine

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24
Q

fatty acid breakdown occurs in

A

mitochondria

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25
Q

3 energy related compounds in produced in beta ox

A

NADH
FADH2
Acetyl coa

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26
Q
  1. Name an enzyme that is located in the mitochondrial matrix that cleaves fatty acyl-
    carnitine.
A

carnitine acyltransferase II

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27
Q

Name a methylated fatty acid that is derived from dairy products.

A

phytanic acid

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28
Q

enzyme that uses cobalamin as coenzyme

A

methyl malonyl Coa mutase– odd chain fatty acid metabolism

methionine synthase– aAA metabolism

29
Q

Name a three carbon compound that is formed from the oxidation of odd chain fatty acid.

A

propionly COA

30
Q

Name two enzymes that convert propionyl CoA into succinyl CoA.

A

Propionyl CoA carboxylase (​has biotin as a prosthetic group)
○ Methyl malonyl CoA mutase (​has cobalamin as a prosthetic group)

31
Q
  1. Name two carboxylases that require biotin as a coenzyme.
A

acetyl CoA carboxylase ​(pg. 50)

○ propionyl CoA carboxylase (​pg. 60)

32
Q

compound catabolized by alpha oxidation

A

phytanic acid

33
Q

why is phytanic acid NOT a substrate for ACC?

A

because it is substituted at the BETA carbon– so it cant undergo beta oxidation

34
Q

allosteric activator of ACC

35
Q

allosteric inhibitor of ACC

A

fatty acyl coa ( product)

36
Q

Carnitine acyl­transferase is inhibited by

A

malonyl coa

37
Q

hormone that triggers catabolism of fats

38
Q

T/ F Phosphorylation of acetyl CoA carboxylase by protein kinase A
inactivates the enzyme.

A

True- insulin activates a phostphate that DEphosphorylates ACC into itss active form

39
Q

defect in Refsum disease

A

defficiency in alpha hydroxylase enzyme-

cant degrade phytanic acid – accumulates in plasma and nerve

40
Q

SIDS deffective enzyme

A

medium chain fatty

acyl CoA dehydrogenases.​(pg. 66)

41
Q

Name the two conditions that would result in methylmalonic acidemia​.​(pg. 66)

A

methylmalonyl CoA mutase ​is missing
○ deficiency of vitamin B12 ​(deoxyadenosyl c​obalamin​) ​(or conversion of
startVitamin B12 into a coenzyme form is missing)

42
Q

what happens in methylmalonic acidemia

A

acidemia​​­ causes metabolic acidosis and mental retardation due to
the impaired metabolism of odd chain fatty acids

43
Q

define obesity

A

obesity ​­ ​BMI (body mass index) greater than 30 kg/m2

44
Q
  1. Name a natural & an artificial compound that inhibits fatty acid synthase.
A

natural inhibitor ­ cerulenin

○ artificial inhibitor ­ C75 (analog of cerulenin)

45
Q

Malonyl CoA inhibits the production of a neuropeptide hormone called ____

46
Q

T/F neuropeptide y signals inhibition of feeding?

47
Q

describe diabettic ketoacidosis

A

Occurs when blood concentrations of acetoacetic acid &
beta­hydroxybutyric acid (ketone bodies) are high.
○ These compounds are strong acids, resulting in acidosis.

48
Q

DKA conditions similar to what?

what is the ratio of glucagon insulin?

A 
the conditions are very similar to ​starvation ​because ​glucagon/insulin ratio
is high (i.e. high glucagon, or low insulin)
49
Q

Two enzymes that convert alcohol into acetate

A

alcohol dehydrogenase

○ aldehyde dehydrogenase

50
Q

Reductant produced in oxidation of alcohol

51
Q

compounds metabolised by omega oxidation pathway

A

C 6-10
capric acid (C10)
■ caprylic acid (C8)
■ caproic acid (C6)

52
Q

how many ATP used in omega oxidation

53
Q

Explain why fat storage is energetically better compared to glycogen?

A

fatty acids hold more amount of energy per storage mass because it can be stored in anhydrous environment

54
Q

Explain how ketone bodies can serve as an energy source in brain during starvation?

A

Ketone bodies are able to cross the blood­brain barrier (wikipedia)
○ This means that ketone bodies a​re a direct energy source​for the brain

55
Q

Explain why carnitine palmitoyltransferase I deficiency​leads to hypoketosis?​

A

carnitine palmitoyltransferase I (CPT I) converts palmitoyl CoA to
palmitoyl­carnitine so that it can be transported from the cytosol into the
mitochondria for oxidation.
○ Deficiency ​in carnitine ​or carnitine acyltransferase​→ can’t
metabolize long­chain fatty acids (palmitic acid) → muscle weakness and

56
Q

ketone bodies

A

acetoacetate beta hydroxy butyric acid, acetone

57
Q

hypoketosis due to

A

LOW levels of ketone bodies

58
Q

ketoacidosis due to

A

High levels of keone bodies

59
Q
  1. Is the NADH/NAD+ ratio high or low in alcoholics?

what does it do

A

high

promotes fatty liver thru inhibition of gluconeogenesis and fatty acid oxudation

60
Q

What are omega­3 and omega­6 fatty acids?

A 
Counting from the end of the carbon chain, FA with a double bond after the
3rd and 6th carbons respectively
○ Omega 3 FA = Linolenic acid
○ Omega 6 FA ​= Linoleic acid
○ essential fatty acids
61
Q

Describe the citrate lyase catalyzed reaction. (pg. 49)

A

CoA + citrate + ATP → oxaloacetate + acetyl CoA + ADP

62
Q

Can carbon skeleton from C­17 fatty acid oxidation enter gluconeogenic pathway? If yes,
explain how?

A

Yes, because oxidation of odd chain fatty acids produces 1 molecule of
propionyl CoA which is converted to succinyl CoA, so this is an
anapleurotic reaction because it generates a TCA cycle intermediate.
Succinyl CoA then eventually gets converted to oxaloacetate, which is an
intermediate in gluconeogenesis

63
Q

Can carbon skeleton from C­16 fatty acid oxidation enter gluconeogenic pathway? If yes,
explain how?

A

No, because oxidation of a C­16 fatty acid chain produces only acetyl CoA.
Acetyl CoA is then released from TCA cycle as carbon dioxide, so this
reaction is NOT anapleurotic because it does not replenish TCA cycle
intermediates. Thus, gluconeogenesis cannot occur because oxaloacetate
is not made

64
Q

Excretion of higher methylmalonic acid through urine is a sign of what vitamin
deficiency?

65
Q

compound has sweet odor in type I

A

Ketone bodies

66
Q

Explain the rationale behind the ketoacidosis in alcoholics.

A

Increased alcohol consumption will lead to conversion of ethanol to Acetyl
CoA through a series of reactions (page 66). Increased amount of acetyl
CoA will cause the liver to produce large amounts of ketone bodies which
lowers blood pH and the result is ketoacidosis.

67
Q
  1. HIgh NADH/NAD+ in alcoholics results in the production of _____
A

3­hydroxybutyrate (Beta­hydroxybutyrate)

68
Q

A person with a deficiency of vitamin B12 is recommended to avoid what type of food?

69
Q

Biotin defficiency cant metabolize?

A

odd chain fatty acids

Biochem (10 decks)

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