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Biochemistry > Exam 3 Lipid Metabolism II > Flashcards

Exam 3 Lipid Metabolism II Flashcards

1
Q

where are TAGs stored?

A

adipocytes/adipose tisse; infinite capacity

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2
Q

what are the 3 major lipases

A
  1. HSL (hormone sensitive)
  2. LPL (lipoprotein lipase)
  3. MAG Lipase
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3
Q

what stimulate HSLs

A

HORMONES

insulin, epi/noriepnephrine, glucagon

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4
Q

lipases do what

A

chip off FAs from glycerol, release FAs, and transport of FAs

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5
Q

how do short chain FAs get transporoted?

A

are soluble so transport by themselves

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6
Q

how do long chain FAs get transported?

A

complexed with albumin for transport

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7
Q

if long chain FAs were not complexed with albumin, what would happen?

A

would stick to blood vessels and form plaque

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8
Q

where does degradation of FAs begin?

A

Adipocytes

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9
Q

after action of HSL, what is the product

A

DAG

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10
Q

after action of LSL, what is the product

A

MAG

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11
Q

after the action of MAG lipase, what is the product

A

free glycerol and free FAs

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12
Q

what is the revised breakdown of TAGs

A

includes 4 major lipases now. 4th lipase is from -/- mice experiments.

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13
Q

what is the 4th lipase? and what does it do?

A

ATGL breaks TAGs into DAGs (same as HSL)

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14
Q

what are the ligands for GPCR?

A

glucagon, epinephrine

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15
Q

what stimulates glucagon and epinephrine release

A

hunger (glucagon) and exercise (epinephrine) = promote lipolysis in adipoctyes

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16
Q

what do GPCRs do?

A

activate protein kinase A

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17
Q

what does protein kinase A do

A

phosphorylates perilipin and HS lipase

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18
Q

phosphorylated perilipin is able to do what

A

associate with HSL/ATGL

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19
Q

what does glucagon and epinephrine release do to ATGL

A

hormones release an activator that binds to ATGL

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20
Q

what stimulates release of insulin

A

the fed state; a large meat

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21
Q

what is the receptor for insulin

A

insulin receptor RTK

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22
Q

what does insulin receptor RTK do

A

activates protein phosphatase (PP1)

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23
Q

what does PP1 do?

A

dephosphorylates; inactivates HSL

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24
Q

what does free glycerol go on to do

A

can be a source for new glucose (gluconeogenesis) or become pyruvate (glycolysis)

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25
Q

what organ takes up free glycerol?

A

hepatocytes; liver cell

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26
Q

free FAs are taken up by whom

A

other tissues that need them; muscle

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27
Q

what happens to free FAs when they are taken up

A

enter cell’s mito matrix to under go beta oxidation to make acetyl coA which enters CAC cycle to make energy

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28
Q

what do perlipins function to do?

A

proteins that surround lipid droplets in adipocytes and muscle cells containing TAGS to regulate physical access to HSL (regulate lipolysis)

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29
Q

overexpression of perlipin causes?

A

inhibits lipolysis as there is no access to TAGs

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30
Q

-/- of perilipin causes?

A

no perilipin = lots of breakdown and is now a target for obesity treatment

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31
Q

what is the order of a free FAs enter the mito matrix of a cell?

A

the cell’s membrane, the outer mito membrane, the inner mito membrane, and then the mito matrix

32
Q

what occurs in the mito matrix when FAs reach there

A

beta-oxidation

33
Q

free FAs are formed in the _ -> released into the _ -> taken up by various _ types

A

formed in adipocytes
released into blood stream
various cell types

34
Q

what happens in phase I of FA breakdown

A

activation and transport to mito matrix

35
Q

how does the FA get passed the outer mito membrane

A

the FA is activated by addition of coA (occurs in the cytosol)

36
Q

how does FA-coA get passed the inner mito mem

A

carnitine displaces the coA to make permeable (happens in inter mem space)

37
Q

outer mito mem is not permeable to

A

FA

38
Q

inner mito mem is not permeable to

A

FACoA

39
Q

what happens of phase II of FA breakdown

A

carnitine is lost and coA is added again undergoes beta oxidation

40
Q

what are the products of beta oxidation

A

FADH2, NADH, and acetyl coA

41
Q

what is the fate of acetyl coA

A

taken up by liver to make ketone bodies or enter TCA cycle to make energy

42
Q

by using ATP, the carboxyl group of a FA when added with coA undergoes

A

FA activation via a thioester bond to make Fatty Acyl CoA

43
Q

to get FAs into mito matrix, what must occur?

A

carnitine must replace coA

44
Q

what is the enzyme to get FAs into the mito matrix

A

carnitine acyltransferase I

45
Q

what is the rate limiting enzyme of FA degradation

A

carnitine acyltransferase I/CPT-1

46
Q

what does malonyl coA do?

A

inhibits the rate limiting enzyme of FA degradation

47
Q

once inside matrix, acyl carnitine (FA-carnitine) is acted upon what enzyme to do what?

A

acted upon by carnitine acyltransferase II to release FA-coA and carnitine

48
Q

what are the 4 enzymes of phase 1

A
  1. FA-coA synthase
  2. CPT-1 (carnitine palmitoyltransferase I)
  3. CACT (carnitine-acylcarnitine translocase)
  4. CPT-II (carnitine palmitoyltransferase II)
49
Q

what does FA-coA synthase do

A

activates free FAs to cross outer mito mem

50
Q

what does CPT-1 do?

A

rate limiting enzyme in FA degradation forms FA-carnitine

51
Q

what does CACT do

A

antiporter that shuttles carnitine

52
Q

CPT-II does what

A

frees carnitine and makes FA-coA available for beta oxidation

53
Q

beta oxidation cuts how many carbons at a time?

A

2

54
Q

what are the 4 steps of beta oxidation

A
  1. oxidation
  2. hydration
  3. oxidation
  4. thiolysis
55
Q

what is the enzyme responsible for the first step of beta oxidation

A

acyl coA dehydrogenase ACAD

56
Q

what do the 4 main steps of beta oxidation generate

A

FADH2, NADH, and acetyl coA

57
Q

where does FADH2 go

A

delivers e-s to CoQ of ETC

58
Q

where does NADH go

A

delivers e-s to complex I of ETC

59
Q

where does acetyl co go

A

enter TCA cycle

60
Q

C16 FA-coA + 7FAD + 7NAD + 7coA + 7H20 ->

A

7FADH2 + 7NADH + 7(H+) + 8 acetyl coA

61
Q

how much ATP did we use for activating an FA

A

2

62
Q

why do ketone bodies form?

A

form as an energy source under conditions of starvation

63
Q

ketone bodies have what properties as compounds

A

are water soluble and acidic

64
Q

ketone bodies are only produced where

A

liver

65
Q

ketone bodies provide energy for

A

peripheral tissues and brain during fasting and starvation

66
Q

how do formation of ketone bodies start

A

starts with condensation of 2 acetyl coAs and a third acetyl coA

67
Q

utilization of acetoacetate is a _ process

A

reverse

68
Q

free FAs breakdown into _

A

acetyl coA

69
Q

too much acetyl coA in the cell promotes synthesis of _

A

ketone bodies

70
Q

after a first hours of fasting, the fuel supply is

A

blood glucose followed by glycogen stored in liver and muscle

71
Q

after 1 day of fasting, fuel source is

A

TAGs in adipose tissue

72
Q

after 3 days of fasting, fuel source is

A

ketone bodies made in liver and proteins in muscles

73
Q

after 1-2 weeks of starvation, energy source is

A

brain switches to ketone body

74
Q

after 2-3 months of starvation, fuel source is

A

proteins lead to coma and death

75
Q

physiological ketosis is

A

mild to moderate increase in ketone bodies

76
Q

pathological ketoacidosis

A

occurs when glucagon/insulin ratio ratio is increased (reduced OAA)

Biochemistry (32 decks)

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