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BMSC 230 Metabolism > Roesler section post midterm > Flashcards

Roesler section post midterm Flashcards

1
Q

what are the four classes of lipids?

A

Fatty acids
triacylglycerols
phospholipids
cholesterol

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2
Q

How are fatty acids numbered? what are carbons 2 and 3 in the chain?

A

Usually numbered beginning with carboxyl terminal carbon atom
- 2 and 3 are a and b respectively

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3
Q

Why can we get so much energy out of fatty acids?

A

because it exists in a highly reduced state

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4
Q

What is the storage form of fatty acids?

A

triacylglycerol

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5
Q

Can the liver synthesize fats from carbs?

A

yes

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6
Q

How many ATP can you get from 1 fatty acid?

A

about 100

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7
Q

are fatty acids hydrophilic or hydrophobic?

A

both : amphipathic

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8
Q

How do we absorb dietary triacylglycerols?

A
  • too hydrophobic to cross biological membranes
  • degraded in small intestine and resynthesized in intestinal cells via enterocytes
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9
Q

What does an omega 3 refer to?

A

placement of the first double bond on carbon three starting from the omega (CH3 end)

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10
Q

What kind of tissue are triacylglycerols stored in?

A

Adipose tissue

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11
Q

Do saturated fatty acids have double bonds?

A

no

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12
Q

What do lipases do?

A

break down lipids and usually release a fatty acid

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13
Q

What is the result when pancreatic lipase breaks down a triacylglycerol?

A
  • cannot release all 3 FA
  • middle FA is inaccessible to active site
  • TG turns into a monoacylglycerol and 2 FA
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14
Q

What are chylomicrons?

A

type of lipoprotein
- fat shuttle
- synthesized only in intestine and released into circulation
-allow for transport of insoluble lipid (TGs) into blood stream to tissues - mainly muscle
-triacylglycerol makes up the core

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15
Q

How much energy can we get out of TG?

A

37 kJ/g or 9kCal/g

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16
Q

What form are TGs stored as?

A

anhydrous - means theres no water - way less weight than glycogen

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17
Q

What are two roles for protein components of plasma lipoproteins?

A
  • solubilize hydrophobic lipids
  • contains cell targeting signals
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18
Q

What are the 5 classes of lipoproteins? What is the distinguishing factors?

A

Chylomicron
VLDL
IDL
LDL
HDL
- different proportions of TG and cholesterol attached
- diff protein components
- made in liver - IDLs are VLDL remnants used to make LDLs

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19
Q

What are the two products when TGs are broken down?

A

fatty acid plus glycerol

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20
Q

What can glycerol made from lipolysis be used in?

A

gluconeogenesis

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21
Q

Where does fatty acid oxidation occur?

A

in the mitochondrial matrix

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22
Q

What two things need to happen to oxidize fatty acids?

A
  • needs to be activated - bound to CoA
  • needs to be transported, carnitine shuttle
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23
Q

What is the rate limiting step pf fatty acid oxidation?

A

fatty acid transport into the mitochondria
- carnitine shuttle has low activity at energy surplus
- high activity when energy deficient
- 1st step of the carnitine shuttle is regulated

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24
Q

What are the three steps in ATP production from fatty acids?

A

B oxidation - degradation of fatty acids (acyl CoA), 2 carbons at a time producing Acetyl CoA, NADH, FADH2
2. Acetyl CoA from Boxidation are oxidized to CO2 (TCA)
3. production of ATP

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25
Q

What type of reactions does B oxidation work on?

A

simple fatty acids
- saturated, no double bonds
- even number of carbons

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26
Q

What is step 1 in B oxidation?

A

Acyl CoA dehydrogenase oxidizes Acyl CoA to produced a trans double bond between C2 and C3 (making trans enoyl CoA)

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27
Q

What is step 2 in B oxidation?

A

Hydration of trans Enoyl CoA to L 3 Hydroxyacyl CoA - hydrates and removes double bond

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28
Q

What is step 3 in B oxidation?

A

Oxidation of L3 hydroxyacyl CoA via Hydroxyacyl CoA dehydrogenase to make 3 ketoacyl coa

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29
Q

What is step 4 in B oxidation?

A

Thiolase creates an acetyl CoA and an Acyl Coa with carbons 1 and 2 of a fatty acid becoming each acetyl Coa - acyl molecule is one molecule shorter

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30
Q

How many acetyl CoA are made for every two carbons removed from fatty acid?

A

1 acetyl co a

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31
Q

How do we deal with unsaturated fatty acids?

A

Enoyl CoA isomerase - moves the double bond from C 3-4 to C 2-3 and changes double bond from cis to trans - B oxidation continues as normal

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32
Q

How do we deal with odd chain fatty acids?

A
  • dont produce them but are in plants so its in our diets
  • we have enzymes to deal with it
  • early steps are dealt with by beta oxidation until 5 carbons left
  • get propionyl CoA - 3 carbons
  • above is carboxylated- converted to succinyl CoA - into TCA cycle
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33
Q

Where does B oxidation occur?

A

mitochondrial matrix

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34
Q

What are Ketone bodies

A

alternative to glucose as fuel or energy for the brain
- formed by ketogenesis
- usually produced at low rate
- only formed in liver
- synthesis rate increases with starvation

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35
Q

Where are ketone bodies formed?

A

mitochondrial matrix of liver where acetyl coa is produced -

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36
Q

How are ketone bodies produced

A
  • condensation of 3 acetyl coa to form acetoacetate
  • acetoacetate is converted to 3 hydroxybutyrate and acetone
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37
Q

What are the three ketone bodies?

A

acetoacetate
B hydroxybutyrate
acetone (cant be used for fuel)

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38
Q

How are ketone bodies used as fuel?

A

all converted to acetoacetate - products are 2 acetyl coa - goes into TCA cycle

39
Q

Do all ketone bodies produce the same amount of energy when oxidized?

A

No, because we get an NADH from the conversion of 3 hydroxybutyrate to acetoacetate

39
Q

is fatty acid synthesis the reversal of B oxidation?

A

no

40
Q

Where does FAS occur?

A

cytosol in liver cells, some adipose tissue

41
Q

How are fatty acids synthesized?

A

Fatty acid synthase (FAS)
sequential addition of 2 carbon units derived from acetyl CoA
- stops with formation of palmitate (C16)

42
Q

When will fatty acids be synthesized from citrate?

A

When TCA cycle is inhibited - high levels of NADH FADH2 ATP - inhibit Aketoglutarate complex - increase citrate concentration

43
Q

How do we get citrate out of the mitochondria and into the cytosol for fatty acid synthesis?

A

Citrate shuttle - moves from mito to cytoplasm
- will generate oxaloacetate and acetylcoa via citrate lyase
- oxaloacetate will go to malate and pyruvate to regenerate oxaloacetate for TCA

44
Q

What two enzymes are unique to citrate shuttle?

A

citrate lyase and malic enzyme

45
Q

What are the two sources of NADPH for fatty acid biosynthesis?

A

malic enzyme acting on malate in the citrate shuttle
PPP - many more NADPH

46
Q

What is the first AND rate limiting step in FA synthesis?

A

Acetyl CoA to Malonyl CoA catalyzed by Acetyl CoA carboxylase - via a carboxyl group transfer

  • uses ATP - not reversible
47
Q

What is Malonyl CoA?

A

Activated donor for adding fatty acid molecules

48
Q

What is ACP?

A

Acyl Carrier protein - has phosphopantetheine group that tethers growing fatty acid chain to FA synthase
(same group as CoA)

49
Q

How does FAS get loaded with substrates (step 2)

A

Acetyl CoA turns into Bketoacyl synthase - acetyl via acetyl transacylase
- Acetyl CoA gets added to an SH group
- only Acetyl CoA group - every other one is Malonyl CoA

50
Q

How does malonyl CoA load FAS with substrates in step 3?

A

Malonyl transacylase turns it into malonyl ACP - joins with the FAS

51
Q

What is step 4 condensation in fatty acid synthesis?

A

B ketoacyl synthase (KS)
- loss of CO2 from malonyl ACP
- transfers 2C from acetyl CoA to malonyl ACP
- makes B ketobutryl ACP
- trying to reduce to make fatty chain

52
Q

What is step 5 reduction in fatty acid synthesis?

A

Carbonyl group at C3 is reduced - electron donor is NADPH

53
Q

What is step 6 dehydration in fatty acid synthesis?

A

B hydroxyacyl dehydratase
- dehydration reaction
- introduces double bind
- trans butenoyl ACP

54
Q

What is step 7 reduction in fatty acid synthesis?

A

Enoyl reductase
- double bond is reduced
- electron donor is NADPH
- forms butryl acp - 4C fatty acid
- completes one round of fatty acid synthesis

55
Q

What is step 8 in fatty acid synthesis?

A

translocation
- moves 4C back to starting point
- transfer of butyryl group from ACP to KS - catalyzed by acetyl transacylase

  • repeats the other steps to add more
56
Q

How many cycles does it take to make palmitate?

A

7 cycles

57
Q

How many NADPH does fatty acid synthesis need to add 2 carbons?

A

2 so 14 for the whole thing

58
Q

Can humans synthesize odd chain fatty acids?

A

NOOOOOOOOO MOTHER FUCKA

59
Q

Where does elongation of fatty acid chains occur?

A

ER - 2 carbons are added at a time - from malonyl CoA

60
Q

What is desaturation in fatty acid synthesis?

A

the introduction of cis double bonds - catalyzed by desaturase enzymes (ER)
- location of double bond is specific for each desaturase

61
Q

humans cannot introduce carbons bonds past carbon ___

A

NINE

62
Q

Which two desaturases do humans lack?

A

12 and 15 desaturases - must be consumed in the diet (linoleate)

63
Q

How is fatty acid synthesis - acetyl CoA carboxylase - regulated?

A
  • AMPK inhibits synthesis - low energy = high AMPK - phosphorylates ACC - inactive
  • High energy = high ATP - AMPK inactive - ACC dephosphorylated - active

Allosterically
- citrate inhibits AMPK - ACC active
- insulin inhibits AMPK - ACC active
- epinephrine activates AMPK - ACC inactive
- glucagon activates AMPK - ACC inactive
- palmitate - inhibits end product

64
Q

Why is citrate wierd abt activating ACC?

A

its not active when citrate exists as dimers but does work when it is as a polymer or filament and can actually activate ACC

65
Q

Where is cholesterol synthesized?

A

liver

66
Q

Where does cholesterol get its carbons?, how many are there?

A

acetyl CoA - 27 carbons

67
Q

What is the purpose of cholesterol?

A
  • structural component of membranes
  • precursor of bile salts, steroid hormones, and vitamin D (not B)
68
Q

What 5 steroid hormones come from cholesterol?

A

Progesterone, cortisol, estradiol, testosterone, vitamin D

69
Q

What is the first stage in cholesterol synthesis?

A

3 acetyl CoA are used to form mevalonate - mevalonate is eventually converted to 3-isopentenyl phosphate, 6 molecules of that are used to form the precursor squalene - so 18 acetyl CoA are needed for this step for each molecule of cholesterol

70
Q

What does cholesterol do for membranes?

A

breaks up rigid structure- increases fluidity of membrane

71
Q

What is the major rate limiting enzyme in cholesterol synthesis?

A

HMG CoA reductase - its the target of statins which are competitive inhibitors

72
Q

What happens to excess cholesterol?

A

converted into bile acids and stored in the gallbladder

73
Q

Where are the three locations cholesterol can go after synthesis?

A
  • hepatocyte plasma membrane
  • bile acids
  • exported in LDLs, blood to tissues
74
Q

is there a degradation pathway for cholesterol?

A

No, can only turn till bile acids and excreted through feces

75
Q

How do three kinds of lipoproteins transport cholesterol?

A

VLDL - moves TG and cholesterol
LDL - transports cholesterol from liver to tissues (most important)
HDL - picks up cholesterol from blood and tissues

76
Q

What are the three ways cholesterol synthesis is regulated via HMG CoA reductase?

A
  • when cholesterol drops, the transcription of the gene for HMG reductase is stimulated - activates synthesis - transcription slows when cholesterol levels are high - inhibits synthesis
  • rate of translation of HMG CoA reductase mRNA is inhibited by mevalonate metabolites
  • degradation of HMG ENZYME is stimulated by elevated levels of cellular cholesterol
77
Q

How is cholesterol uptake into cells regulated by intracellular levels of cholesterol?

A

LOW cholesterol - will increase HMG, LDL, synthesis and uptake
HIGH cholesterol - will decrease HMG, LDL, synthesis and uptake

this is important for peripheral tissues

78
Q

What is familial hypercholesterolemia?

A

high circulating cholesterol levels
- severe atherosclerosis
- defective LDL receptor
- cholesterol is not properly cleared from blood

79
Q

What are the three most common membrane phospholipids?

A

Phosphatidylcholine
Phosphatidylethanolamine
Phosphatidylserine

80
Q

What is the starting substrate for both TG and PL synthesis?

A

glycerol 3 phosphate (activated form of glycerol)
-glycerol from adipose tissue goes to liver and becomes G3P via glycerol kinase
- glycerol from other tissues comes from glucose and is converted via glycolytic pathways

81
Q

What is the most abundant phospholipid?

A

phosphatidylcholine

82
Q

How is phosphatidylcholine synthesized?

A

CDP-choline pathway in all tissues
- diacylglycerol and CDP choline make phosphatidylcholine via CDP-choline diacylglycerol phosphocholine transferase

83
Q

What does acyltranferase do?

A

catalyzes sequential attachment of fatty acids to glycerol backbones (ester bond)

84
Q

What is phosphatidate?

A

important intermediate in both TG and PL synthesis
- loses phosphate group to become diacylglycerol

85
Q

What is the second pathway for synthesizing phosphatidylcholine?

A

methylation pathway in the liver
- phosphatidylethanolamine becomes phosphatidylcholine

86
Q

What phospholipid is a substrate / precursor for phosphatidylserine and phosphatidylcholine?

A

Phosphatidylethanolamine

87
Q

How do you make phosphatidylethanolamine?

A

Phosphatidylserine and PS decarboxylase makes phosphatidylethanolamine and releases a CO2

88
Q

What are all eicosanoids synthesized from?

A

arachidonate 20c(?)

89
Q

What are the major eicosanoids?

A

leukotrienes
prostaglandin

90
Q

What releases arachidonate?

A

Phospholipase A2 - released from phospholipids in the membrane

91
Q

What type of hormones are eicosanoids and what does that entail?

A

-paracrine hormines
- not stores but rapidly degraded
-send messages to nearby cells or tissues including the cell in which it was made

92
Q

PLZ RE LOOK AT THIS UNIT

A

ok

BMSC 230 Metabolism (7 decks)

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