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BISC 330 > JAGGERS EXAM 3 > Flashcards

JAGGERS EXAM 3 Flashcards

1
Q

triose phosphate isomerase

A

converts DHAP to GAP
central core of 8 B strands surrounded by 8 a helices (aB barrel)
active site: Glu 165 and His 95, form enediol intermediate
kinetically perfect enzyme

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2
Q

stage 1 of glycolysis

A

trapping and priming of glucose
glucose > G6P > F6P > F16BP > DHAP & GAP (2 3C fragments, interconvert with TPI, worth using ATP instead of having a 2C and a 4C)

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3
Q

stage 2 glycolysis

A

GAP > 13BPG > 3PG > 2PG > phosphoenol-pyruvate > pyruvate

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4
Q

GAP to 13BPG

A

oxidation
dehydration via GAP dehydrogenase
2 rxns COUPLED to occur
formation of thioester intermediate (high energy) which captures energy released from oxidation to drive dehydration

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5
Q

how is redox maintained in glycolysis?

A

NAD+ lost from GAP > 13BPG is replenished when pyruvate is converted into ethanol

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6
Q

pyruvate to ethanol

A

1) decarboxylation of pyruvate to acetaldehyde
2) reduction of acetaldehyde to ethanol –> regenerates NAD+ for glycolysis

glucose > 2 ethanol + 2 ATP + 2 CO2

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7
Q

lactic acid fermentation

A

pyruvate is produced faster than it can be oxidized in CAC, but NAD+ must be recycled
glucose > 2 lactate + 2 ATP

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8
Q

fructose 1-phosphate pathway

A

fructose > F1P > glyceraldehyde + DHAP > GAP (enters at GAP)

1 fructose = 2 ATP

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9
Q

galactose processing in glycolysis

A

galactose > galactose 1P
galactose 1P + UDP-glucose > G1P + UDP-gal

G1P to G6P by phosphoglucomutase (enters glycolysis at G6P)
UDP-gal > UDP-glu via epimerase

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10
Q

regulation of glycolysis in muscle

A

high ATP inhibits phosphofructokinase by binding to regulatory sites
G6P inhibits hexokinase
pyruvate kinase is inhibited by ATP and activated by F16BP

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11
Q

fructose 2,6 BP in the liver

A

excess F6P forms F2,6BP via PFK2
F26BP is an activator of phosphofructokinase, accelerates glycolysis
PFK2 activity regulated by phosphorylation

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12
Q

glucokinase and hexokinase activity

A

glucokinase is an enzyme in the liver that produces G6P for glycogen synthesis
glucose has lower affinity for glucokinase than hexokinase
glucose inhibits hexokinase but not glucokinase, when glucose is abundant hexokinase is inhibited and glucokinase activity occurs

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13
Q

forms of pyruvate kinase

A

L-form in liver, M-form in muscle and brain
only L-form subject to regulation by phosphorylation
when blood glucose is low, its more urgently needed in muscle and brain

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14
Q

glycolysis regulation in the liver (3)

A

pyruvate kinase regulated by phosphorylation
glucokinase activity based on affinity of hexokinase
PFK activated by F26BP

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15
Q

when blood glucose levels are low, pyruvate kinase…

A

is mostly in M-form (muscle and brain), L-form is inhibited by glucagon

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16
Q

what are the major non-carb precursors?

A

lactate
amino acids
glycerol

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17
Q

gluconeogenesis

A

noncarb precursors (AAs, lactate, glycerol) are converted to pyruvate > glucose
pyruvate > oxaloacetate > PEP > 2 PG > 3PG > 13BPG > GAP > F16BP > F6P

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18
Q

lactase dehydrogenase reaction

A

L-lactate to pyruvate (and vice versa), promoted by low glucose and therefore low pyruvate

low glucose causes L-lactate to make pyruvate

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19
Q

what determines glycolysis vs glucogenesis occuring?

A

high energy levels > glycolysis inhibited, glucogenesis promoted
in liver, determined by blood glucose level

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20
Q

why is acetyl CoA an activated carrier

A

hydrolysis is highly exergonic due to thioester linkage

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21
Q

pyruvate to acetyl CoA net reaction

A

pyruvate + CoA-SH + NAD+ –> acetyl CoA + CO2 + NADH + H+

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22
Q

pyruvate to acetyl CoA mechanism

A

TPP coenzyme becomes a carbanion (highly acidic, pKa 10)
carbanion attacks pyruvate carbonyl
joined complex decarboxylates and releases CO2, forming hydroxyethyl-TPP

hydroxyethyl-TPP and lipoamide form TPP carbanion and acetyllipoamide (thioester bond)
acetyllipoamide + CoA > acetyl CoA + dihydrolipoamide (which is then oxidized to form NADH)

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23
Q

transacetylase

A

enzyme for pyruvate to acetyl CoA
has 3 distinct active sites (E1, E2, E3)
lipoamide group in E2 extends away and can swing around

1) lipoamide collects acetyl group from E1
2) transfers acetyl to CoA to form acetyl CoA in E2
3) E3 to get reoxidized

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24
Q

citrate synthase reaction

A

acetyl CoA + oxaloacetate forms Citroyl CoA
CoA cleaved by hydrolysis, citroyl leaves
energy from thioester is used to synthesize a larger molecule

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25
Q

citrate synthase

A

catalyzes acetyl CoA and oxaloacetate to form citrate, uses induced fit
binding of oxaloacetate causes CC to form acetyl CoA active site, prevents wasteful hydrolysis because citroyl CoA is made before hydrolysis

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26
Q

how do amino acids enter glycolysis?

A

turned into oxaloacetate > PEP

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27
Q

how does glycerol enter glycolysis?

A

converted to G3P > DHAP

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27
Q

how does lactate enter glycolysis?

A

turns into pyruvate via lactase dehydrogenase reaction

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28
Q

what hormone activates glycolysis and inhibits gluconeogenesis?

A

insulin

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29
Q

what hormone inhibits glycolysis and activates gluconeogenesis?

A

glucagon

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30
Q

what is special about 1,3-BPG?

A

high energy compound
can make ADP into ATP

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31
Q

The formation of what intermediate allows the oxidation of GAP to 1,3-BPG, and the addition of a phosphate, to be coupled by GAP dehydrogenase?

A

thioester intermediate

cleavage of thioester bond provides energy needed for the formation of high phosphoryl transfer compound

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32
Q

What intermediate is galactose converted to in order to feed into glycolysis? What other molecule is necessary for this process?

A

G-6P, UDP glucose

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32
Q

Describe how the carbons from glucose get fed into the Citric Acid Cycle

A

glycolysis: glucose to pyruvate
pyruvate dehydrogenase: pyruvate to acetyl CoA
CAC: acetyl CoA + oxaloacatete > citrate

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33
Q

Describe the negative regulation of alpha-ketoglutarate dehydrogenase and isocitrate dehydrogenase
in the Citric Acid Cycle

A

both experience negative feedback
alpha-ketoglutarate dehydrogenase: inhibited by succinyl CoA and NADH
isocitrate dehydrogenase: NADH

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34
Q

3 enzymes for the 3 irreversible steps of glycolysis

A

hexokinase: glucose > G6P
phosphofructokinase: F6P > F16BP
pyruvate kinase: PEP > pyruvate

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35
Q

pyruvate dehydrogenase complex, 5 cofactors

A

converts pyruvate to acetyl CoA
3 enzyme components (E1, E2, E3)
5 cofactors: TPP, lipoamide, CoA, FAD, NAD+
CO2 released

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36
Q

aconitase

A

isomerizes citrate to isocitrate, moves hydroxyl group

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37
Q

isocitrate dehydrogenase

A

isocitrate > oxalosuccinate > a-Ketogluterate

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38
Q

a-ketoglutarate dehydrogenase

A

a-ketoglutarate > succinyl CoA
mechanistically similar to pyruvate dehydrogenase complex

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39
Q

pyruvate dehydrogenase - 3 enzymatic active sites

A

lipoamide group (E2) can swing around and interact with E1 to collect acetyl group, transfers acetyl to CoA, E3 to get reoxidized

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40
Q

succinyl CoA synthetase

A

succinyl CoA to succinate
generates GTP
only CAC step that produces a high-phosphoryl-transfer potential

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41
Q

citric acid cycle

A

CIKSSFMO

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42
Q

why is FAD the electron acceptor when succinate is converted to fumerate?

A

the free-energy change is not sufficient to reduce NAD to NADH

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43
Q

3 reactions of succinate to oxaloacete

A

oxidation, hydration, oxidation

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44
Q

which reaction in the CAC has a large positive free energy charge? how is it driven?

A

malate to oxaloacetate, driven bc NADH is consumed and it is produced from the reaction

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45
Q

CAC net reaction

A

Acetyl CoA + 3 NAD+ + FAD + ADP + Pi + 2 H20 > 2 CO2 + 3 NADH + FADH2 + ATP + 3 H+ + CoA—SH

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46
Q

regulation of pyruvate dehydrogenase complex (PDH)

A

(1) feedback inhibition: inhibited by pyruvate and acetyl CoA (accumulation)
(2) covalent modification of E1: phosphatase turns PDH on in response to insulin/muscle contractions/epinephrine, kinase turns PDH off

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47
Q

Isocitrate dehydrogenase regulation

A

stimulated by ADP, inhibited by ATP and NADH

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48
Q

a-ketoglutarate dehydrogenase

A

inhibited by energy charge (ATP, NADH) and reaction products (succinyl CoA and NADH)

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49
Q

If oxaloacetate is pulled from the cycle by a cell’s demand for
biosynthesis, how is it replenished so that energy demand is also accommodated?

A

Oxaloacetate can be synthesized directly from pyruvate

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50
Q

complex I of ETC

A

Goal: transfer e- from NADH (from CAC) to CoQ
NADH reduces FMN > FMNH2 > [Fe-S] > Q > QH2 leaves to Q pool
4 H+ pumped from matrix to IM space
1 NADH + 5H(matrix) + Q = QH2 + 4H(IM space)

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51
Q

where do the protons to reduce Q to QH2 come from?

A

FADH2 from CAC in matrix (complex II) or NADH + H+ (complex I)

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52
Q

NADH-Q oxidoreductase

A

transfer electrons in NADH to CoQ

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53
Q

complex II of ETC

A

Goal: feed the Q pool
feeds the Q pool (H+), FADH2 from CAC reduces Q to QH2

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54
Q

complex III of ETC

A

Goal: Q cycle
1) QH2 enters complex III and gives 2 e-: 1 to cyt c, other to distal Q > semiquinone
2) another QH2 enters complex II and gives 2 e-: 1 to cyt c, other to complete reduction of semiquinone > QH2
during reduction of distal Q, H+ pulled from matrix

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55
Q

how many net cyt c reduced per QH2

A

2 reduced cyt c per QH2

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56
Q

how does the Q cycle contribute to the proton gradient?

A

they become reduced (Q>QH2) via protons from the matrix, and release into IM space during oxidation

57
Q

complex IV of ETC

A

CuA/CuA > Heme a > Heme a3 > CuB
1) 2 cyt c transfer e- to heme a3 and CuB
2) reduced CuB and Fe in Heme a3 bind O2 to form peroxide bridge
3) 2 H(matrix) and 2e- cleaves bridge
4) another 2H(matrix) releases water

4 H(matrix) end up in water

58
Q

where does glycolysis take place?

A

cytoplasm

59
Q

where does CAC take place?

A

mitochondrial matrix

60
Q

where does ETC/ox phosphorylation take place?

A

inner membrane of mitochondria, protons are pumped from matrix to IM space to create gradient

61
Q

what is needed to reduce molecular oxygen?

A

2 NADH = 4 cyt c = 4 e-

62
Q

2 main units of ATP synthase

A

F0: sits in membrane, forms proton channel
10-14 c subunits form a c ring

F1: catalytic activity, protrudes in matrix

62
Q

why can O2 as an electron acceptor have adverse consequences? how is it prevented?

A

partial reduction yields peroxide / ROS (reactive oxygen species) which cause oxidative damage
complex IV holds it tightly until fully reduced, but sometimes ROS released
If ROS released, there are defense systems - Super Oxide Dismutase

63
Q

5 subunits of F1 ATP synthase

A

α3, β3, γ, δ, ε
α and β subunits arranged alternately in hexameric ring
γ and ε form the central stock
γ makes different contacts with each β unit (different conformational states)

64
Q

3 conformational states of β-subunit

A

L: loose, binds ADP and Pi loosely
T: tight, forms ATP from bound ADP + Pi
O: open, ATP is released and new ADP + Pi can enter

65
Q

rotation of c-subunit

A

aspartic acid residue in c subunit can be -/0 if deprot/prot
1) IM channel is H+ rich so Asp protonated
2) protonation causes entire ring to turn so Asp is in hydrophobic environment
3) another c subunit is positioned next to matrix half channel (H+ poor) and deprotonated

66
Q

malate dehydrogenase

A

oxaloacetate to malate, reduces malate (can then act as an electron carrier in malate shuttle)

67
Q

malate-aspartate shuttle

A

1) in cytoplasm: oxaoloacetate to malate via malate dehydrogenase, malate carries electrons
2) malate shuttle moves across inner m membrane
3) malate reoxidized to oxaloacetate by malate dehydrogenase, mitrochondrial NAD is reduced to NADH + H
4) oxaloacetate converted to aspartate, which can cross back to cytoplasm
5) aspartate converted back to oxaloacetate

68
Q

glycerol 3-phosphate shuttle

A

DHAP to Glycerol 3P, glycerol 3P takes electrons from NADH
glycerol 3P donates e- to E-FAD on inner mitochondrial membrane
E-FADH2 used to oxidize Q

69
Q

ATP-ADP translocase

A

allows a 1:1 exchange of ADP for ATP
ADP from cytoplasm to matrix, ATP from matrix to cytoplasm
energetically expensive, dampens membrane potential

70
Q

complete oxidation of 1 glucose molecule yields how much ATP?

A

30-32 depending on transport system from cytoplasm
(30 for glycerol, 32 for malate)

71
Q

net ATP / NADH in glycolysis

A

2 ATP, 2 NADH (cytoplasmic)
(2 ATP used then 4 ATP made)

72
Q

how do electrons enter ETC via glycerol 3P shuttle?

A

electrons transferred to FAD which are then transferred to Q, bypassing complex I

73
Q

how do electrons enter ETC via malate aspartate shuttle?

A

e- transferred to NAD which transfers e- to complex I

74
Q

what energy is produced from pyruvate dehydrogenase?

A

2 NADH (mitochondrial)

(per glucose)

75
Q

how many protons are pumped per 1NADH in ETC?

A

complex I, III, IV: 4, 4, 2 = 10 protons/NADH

76
Q

what energy carriers are produced in the CAC (1 glucose = 2 cycles)

A

2 GTP = 2 ATP, 6 NADH, 2 FADH2

77
Q

how many protons per ATP produced in ATP synthase?

A

4 H+ / ATP
About 3 H+ per ATP in oxidative phosphorylation, plus calculating for offsetting the dampening of membrane potential

78
Q

1 NADH yields how much ATP?

A

2.5
10 H+ / 4 used per ATP

79
Q

hibernation & ETC

A

electron transport can be uncoupled from ATP production, no H+ gradient, energy released as heat, keeps animal warm

80
Q

how many protons are pumped per 1 FADH2 in ETC?

A

complex III, IV: 4, 2 = 6 H+/FADH2
bypasses complex I

81
Q

how does low [ADP] affect the CAC?

A

less NADH is consumed > NAD+ levels drop > slows CAC

82
Q

porphyrins

A

central N binds metal ion - Fe in heme, Mg in chlorophyll a
planar and aromatic - absorbs visible light

83
Q

light rxn in photosynthetic bacterium

A

photoexcitation in special pair (P960)
electron transferred to BPh
BPh transferred to QA
QA transfers to QB to form semiquinone intermediate
after 2nd cycle, fully reduced to QBH2
QBH2 > QB > cyt bc1 > cyt c2 > P960
electrons from QBH2 contribute to proton motive force

84
Q

PSII goal & electron flow

A

P680, catalyzes transfer of e- from water to plastoquinone
reduction of Q + water splitting help establish H+ gradient

H2O → photoexcitation in P680 → Ph → QA → QB → QBH2 → cyt bf → plastocyanin (Pc)

85
Q

how does plastocyanin contribute to the proton gradient

A

via electron carrier QBH2, protons are transferred from stroma to thylakoid lumen

86
Q

how does electron transfer from water to P680 work?

A

coordinated by manganese (Mn) center of PSII

87
Q

how many electrons are needed for 1 oxygen acceptor? how many water molecules?

A

4e- from 2 H2O = 2QH2 = 1 O2

88
Q

how many protons are moved into the thylakoid space from 2 H2O?

A

4H+ from 2H2O, 8H+ from stroma via Q cycle = 12H+

89
Q

PSI

A

P700, uses high energy e- to produce reducing power in the form of NADPH

e- transfer through a series of intermediates to ferredoxin

90
Q

ferredoxin-NADP+ reductase

A

uses 1 FAD to collect 2 e- from 2 ferredoxin and catalyzes transfer of NADP+ > NADPH

91
Q

how much ATP is produced as a result of oxidizing 2 water molecules
in photosynthesis?

A

3 ATP

92
Q

For PSI cyclical electron transport, 4 photons absorbed by PSI leads to the release of ____ protons into the
thylakoid lumen, yielding ____ ATP by ATP synthase (____ photon/ATP)

A

For PSI cyclical electron transport, 4 photons absorbed by PSI leads to the release of 8 protons into the
thylakoid lumen, yielding 2 ATP by ATP synthase (2 photon/ATP)

93
Q

accessory pigments

A

ex. carotenoids
capture remaining light, transfer energy to reaction center (special pair)

94
Q

where does the calvin cycle take place?

A

stroma

95
Q

stage 1 of calvin cycle: CO2 fixation

A

rate-limiting step in hexose synthesis
ribulose 1,5 bisphosphate > + CO2 > (2) 3PG
catalyzed by rubisco

95
Q

what is the purpose of the calvin cycle?

A

ATP and NADPH from LRS are used to reduce CO2 into carbon fuel

96
Q

rubisco

A

catalyzes first step of calvin cycle
8 small regulatory subunits, 8 large catalytic subunits
required Mg2+ ion for activity
carbamate formation required to bind Mg2+ ion in enzyme active site

97
Q

How can the wasteful reaction product of rubisco be repurposed?

A

oxygenase activity forms phosphoglyolate
phosphoglycolate salvage pathway: save 3 of 4 carbon molecules by producing serine and glutamine. Wasteful because organic carbon is converted into CO2 without the production of ATP, NADPH, or another energy-rich metabolite

98
Q

stage 2 calvin cycle: reduction

A

(2) 3PG > (2) 1,3 BPG > (2) GAP > (1) F6P

99
Q

stage 3 calvin cycle: regeneration

A

GAP > F6P
F6P + 2 GAP + DHAP + 3 ATP > (3) RuBP

100
Q

how many turns of calvin cycle to make a hexose sugar?

A

6 turns

101
Q

C4 pathway

A

for tropical plants at high risk of oxygenase activity (increases w temp)
1) high CO2 exposure in mesophyll (air exposed) - malate moves CO2 to bundle sheath cells
2) malate decarboxylated to pyruvate, releasing CO2
3) pyruvate returns to mesophyll

2 ATP to transport 1 CO2

102
Q

How many ATP are needed to make 1 glucose using the Calvin Cycle? How many are needed to make 1 glucose in a C4 plant?

A

18 ATP/ glucose in the Calvin Cycle (3 ATP/CO2)
30 ATP/glucose in C4 plant (need an additional 2 ATP/CO2 to move CO2)

103
Q

why is rubisco more active during the day?

A

the stroma is more alkaline due to the light reactions, so Mg2+ is released from the thylakoid space into the stroma to compensate for increased H+ in thylakoid space
carbamate formation is favored at alkaline conditions and Mg2+ is needed to form active site

104
Q

pentose phosphate pathway

A

G6P + 2NADP+ > ribose-5P + 2 NADPH

NADPH: reducing power for biosynthesis
ribose 5P: dNTP, RNA, DNA, ATP, NADH synthesis

105
Q

how do plants make NADPH? how do organisms without photosynthesis make NADPH?

A

plants use PPP and photosynthesis
other organisms use PPP

106
Q

where does reduced ferredoxin transfer its electrons?

A

thioredoxin

107
Q

during the day, stromal ferredoxin is…

A

reduced due to PSI

108
Q

thioredoxin

A

activates many enzymes like rubisco

109
Q

where does pentose phosphate pathway occur?

A

cytoplasm

110
Q

phosphopentose isomerase

A

isomerizes between ribulose 5P (R5P) and ribose 5P and xylulose 5P (X5P)

111
Q

phase 1 PPP

A

produces NADPH and ribulose-5P
G6P > ribulose 5P

112
Q

phase 2 PPP

A

conversion of ribulose-5P into many different sugars, produces F6P and GAP via transketolase and transaldolase

113
Q

transketolase and transaldolase

A

ketose donor and aldose acceptor
transketolase moves 2C, transaldolase moves 3C

114
Q

how is phase 1 PPP controlled?

A

G6P + 2NADP+ > ribulose5P + 2NADPH
only occurs if [NADPH] is low

115
Q

how are dNTP, RNA, DNA, ATP, NADH synthesized

A

via PPP, G6P > ribulose 5P, isomerized to ribose 5P. ribose 5P is used for synthesis

116
Q

[NADPH] is adequate

A

glycolysis is favored over PPP

117
Q

[R5P] low
[NADPH] adequate

A

G6P converted to F6P and GAP by glycolysis. transaldolase and transketolase convert these products to ribose 5P (needed for synthesis)

118
Q

NADPH and R5P balanced

A

PPP favored since it produces both

119
Q

[NADPH] low
[R5P] adequate

A

3 separate reaction schemes
1) PPP Phase 1: G6P to ribose 5P and NADPH
2) ribose 5P to F6P and GAP by transketolase/transaldolase
3) G6P is synthesized from F6P and GAP by gluconeogenesis pathway

glucose 6-phosphate + 12 NADP+ + 7 H2O 12 NADPH + 12H+ + 6 CO2 +Pi

120
Q

NADPH and ATP are needed

A

PPP phase 1 (produce NADPH)
R5P to glycolysis (produce ATP)

121
Q

glycogen linkages

A

a-1,4 linkages lends helical structure
a-1,6 linkages allow for branching
many non-reducing ends for quick degredation

122
Q

cellulose linkages

A

B-1,4 linkages

123
Q

glycogen phosphorylase

A

catalyzes the phosphorolytic cleavage of glycogen (a 1,4 linkages)nto release glucose 1-P

124
Q

how is glycogen remodeled for cleavage?

A

a 1,4 linkages cannot be cleaved within 4 residues of branching
transferase transfers 3 glucose units between branches
a-1,6-glucosidase removes final glucose from branch (a 1,6 linkage)

124
Q

glycogen metabolism (3 steps)

A

1) a-1,4-linkage cleavage
2) remodel for cleavage
3) phosphorylation

125
Q

phosphorylation of glucose after glycogen metabolism

A

phosphoglucomutase: G1P to G6P
hexokinase: phosphorylates free glucose to G6P for glycolysis

126
Q

phosphoglucomutase

A

G1P to G6P

127
Q

how is G6P released from the liver?

A

glucose-6-phosphomutase converts G6P to glucose to be released into the bloodstream

128
Q

glycogen phosphorylase forms

A

a form: usually active R state, phosphorylated, liver
b form: usually inactive T state, not phosphorylated, muscle

can interconvert by serine phosphorylation

129
Q

how is Phosphorylase b regulated?

A

regulated allosterically by the cell’s energy charge (inhibited by ATP)
resting muscle = high ATP = ATP binding = inhibited T state
stimulated muscle = increasing AMP, decreasing ATP = AMP binding = R state
phosphorylase kinase converts to a form

130
Q

how is Phosphorylase a regulated?

A

glucose binding converts R state to T state (no glycogen metabolism needed if glucose is present)

131
Q

how is glycogen branching helpful?

A

increase solubility, compact the structure, increase the number of non-reducing ends available for glycogen breakdown (faster metabolism)

132
Q

biosynthesis of glycogen

A

glucose > G6P > G1P > UDP glucose
UDP glucose adds to existing glycogen primer at non-reducing end
Branching enzymes transfer 6-7 residue terminal chains to a hydroxyl group at 6-position, forming a 1,6 linkage and adding a new nonreducing end

133
Q

why is most energy stored as fat instead of glycogen?

A

fatty acids are more reduced = more energy
less hydrated because they are hydrophobic = lighter in weight

134
Q

bile acids

A

secreted as bile salts by gallbladder, insert into TG droplets to make them more accessible to digestion by lipases

135
Q

lipases

A

secreted by pancreas
convert TGs into 2 fatty acids and monoacylglycerol

136
Q

chylomicrons

A

lipoprotein aggregates that have a hydrophilic surface and hydrophobic interior
transports triacylglycerols through the body for storage and breakdown

137
Q

hydrolysis of TGs

A

glycerol (taken up mostly by liver for glucogenesis > GAP and DHAP) + fatty acids (enter bloodstream, binds to serum albumin, taken up by tissues)

138
Q

What fuel is used by the brain during starvation?

A

ketone bodies (formed from excess acetyl CoA, can’t be processed by TCA)

139
Q

diabetic ketoacidosis

A

no insulin > glucose cannot enter cells > all energy from fats > production of acetyl CoA, builds up > ketone bodies

BISC 330 (3 decks)

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