✗

✗
✗

✗
pyruvate Dehydrogenase BAN
Citric Acid Cycle pyruvate complex pentose phosphate pathway (by converting f- 6- p
GI -

nFDE°
①A
'

Phase # 1 : oxidative to make NADPH into ribose -

5- phosphate) purines pyrimidines

ATP I -1 n= # Ote
-

AUM ' -10A Atp (e) ADP ( t ) Phase # non oxidative

citrate 2 :
to make 5- ( sugars HAM aud MMMM)
-

H2o '
used in anabolic
acetyl coat) 96,485J / MOI

"""""""""
- .

H H
Nappy, f- =

" " " "" "

•

1ˢᵗ step -

dehydration of glucose 6- phosphate -

"" " " DE°= Tea

◦

citrate " " " " " " " "" " " " " " """ " H F-
-
F- ox
" H
Most important factor :
NADP
regulating
'

isocitrate It
H①+ NADH
-1 OXAIOAUTAH Nap
-1 4 Distinct MOMS
'

.
H H

1. Ribose 5- phosphate needs > NADPH needs H

r
Isocitrate
-

3
NHZ

N
g. malate
phosphate
.

NAD
-1
dᵈMdW%ⁿᵈ " .
F- 6- p and f3p used to generate ribose -5 -

NHZ
dehydrogenate > NADH + coz
activated
"
-

glycolysis H at }
malate regulatory steps d- ketoglutarate A -1pct 2. Ribose NADPH
phase / →
for biosynthesis
phosphate 5-
Roslglutathione
=
-

µ
reduce )
succinyl COAT)
-

oxidative phase of Ppp activated H

'
H H
phase 2- nucleotide synthesis N N
O N O N
d- ketoglutarate NADA " 3. Ribose 5- phosphate needs NADPH needs <
fumarate 4.
-

7. NAD
"

dehydrogenase -
Ribose -

5- phosphate produced feeds back

H H H
IOMPUX NADPH Adenine Cytosine Thymine
to generate
Hzo > NADH +
Oz .

allows for complete oxidation to 102

+
active pathways Hzo
fumarate
→
A G- 6- P 2 NADP
10AM"Mt
+ 0
-

+
0
6. succinate 5. succinyl - -

oxidative phase of ppp

ribulose 5 - -

p +
coz -1 2 NADPH -1 2 Ht
"
non oxidative
"
phase of ppp

①
dehydrogenate synthase "
-
.

gluconeogenesis µ
/ DNA )
tRNA )
succinate
ADP + Pi 4 . NADPH 31 ATP required " 2N
"
N
° N H
products -

active pathways
N
Adenine Uracil Thymine
,
FABHZ ATP 3 NADH H
oxidative phase of PPP H
•

GTP / ATP )
-

FAD I
-

glycolysis
-

I FADHZ Guanine uracil cytosine

-

" Wahine
Acetyl -
10A -13 NAH + FAD +
ADP + pit a Hzo Fatty Acid Degradation
→ 2602-1 3 NADH + FADH , + ATP Degradation 1. of tri acyl glyceride to release

fatty acids 31 glycerol into the blood for transport

drive to energy
requiring tissues
Transaminases lswaps amine group out for carbonyl group )
Electron Transport Chain goal to ATP synthesis
-

→
is
2. Activation and transportation of FFA into mitochondria •

these enzymes help convert amino acids into glutamate so

intermembrane space *
+ cytc FFA needs to be activated ( tatty acyl 10A ) then to get
-

through around
1++11--1 H+ carries one e-
into the mitochondria It has to be glutamate can carry urea
•

④ H+ -1 converted to
Fest Fez
#
reduction
→
H⊕ of
1-1-10 *+

Htp H+
1++1+-1
'
It
fatty allll carnitine
e-
↑ accepts up
-

Mom Degradation of fatty

Examples : alanine transaminase
H+ #
Ubiquinone to Ze 3. acids acetyl CoA processing
+
" to for
'

AE
_ .

-1
.

it
- -

It
-

# ◦a ←
_

.
. complex I and I by the CAC alanine + d-
ketoglutarate glutamate +
pyruvate
,

T AITNK ( mitochondrial
T Hydwphlc freely MMM
→
,,, w can
oxidation
-
.
,
, , Beta -

°" M """ Md " " fatty acyl CoA

amino acid transaminase
É " Mdb " " aspartate
'

_
FAD QHZ
e- e- , e- mpmnfno.ge acyl-coa
] 1. Oxidation aspartate + a- ketoglutarate = glutamate
+ oxaloacetate
FADHZ FAD
'

dehydrogenase ,
FADA , Q

É
+
*

" ADP
'
ATP
Transportation of nitrogen into liver
NADH NAD enoyl COA for B- oxidation the
-

Oz removes low energy e- 31 binds-

every , MUCUS UH branched A. A. as tolls $
11 10A
hydration enoyl fatty acyl-COA shortens by
-

them wl tree Ht to
produce Hoo & 2.
use the glucose alanine you to transaminases will pull the ketone
mitochondrial matrix 2 H2O
-

maintain the CT gradient nydratase 2- carbons atoms

transport it into the liver group ottot the pyruvate to make
COQ is the common e- acceptor QHzlre%%%d% + 2 cytc / Oxidized )
-1
2HN+ 3- hydroxy acyl-CoA 16 :O →
7 cycles
room for the NHI
'
to
go into
btwn complex land 11 8 acetyl 10 As river pursue
→
Q / oxidized I -1 2 Cytclredvled ) +
4Hp+ 3- hydroxy acyl-CoA
NAB
make alanine

Ñm+y⊕
3. oxidation """ " " " ° "
synthase gauge
"

ATP "
"" ""
" " "° " " "

§
Asvbuhlt =
contains half channels that bind WI ""
" "" m ᵗ
mpg ketoacul con

§:*:B.in?:::::::::::::PdBBtormthl
- -

protons from inner membrane → matrix dehydrogenase pyruvate branched A. A .

:::::::÷ hlXaMlNC
°
4. thiolase thiolase
glutamate

(
831 Etovmthl AXU , turn in response to c- ring rotating " " "M alanine
cartoon skeletons
. fatty acyl 10A +
acetyl-COA for cellular respiration
Knob thlolase NH4⊕
p subunit contains active site that catalyzes De NOVO Pyrimidine
-
-

ketone bodies
•
*
and tllhthlslzes ATP Aceto acetyl-COA
synthesized liver transaminase enzyme will pull
in the urea a
Bicarbonate
- -

a. b. 8 subunits serve to anchor the hexamer to the C-

nng " " " "" "" " " " " " """ the Nhut Ott the alanine to
"+3
' " tamale -1mmol " ""
Binding change mechanism -
HMG-CoA Men " " "" "
'

-1
-

010pm ) form : nucleotides can bind or be released +

the WHY will go onto to an

L HOOK ) form : nucleotides trapped

-
" +
NADH
acetoacetate
d- MMMMM " carbarn 041 phosphate
-11179kt ) form : ATP is synthesized from ADP + pi NAb+
-

carnitine -
c - Aspartate
Glycogen Degradation ( cytosol ) acetone
-

cytosol → mitochondrial matrix

µ c

- -

Fatty Acid synthesis

3- hydroxy
( releases the most
butyrate
energy )
citrate { É
outer cytosol
- - - - -
-

matrix n
-
→
inner -
-

d- 1,6
-

linkage d- 1,4 linkage

Acetyl ACP acetyl-CoA
citrate
pyrimidine ring
- - - -

CORE > away

phosphate )
-
-
-

Can work UP to 4 glucose acetyl-COA PRPP / nbote

•
citrate >
8 Pi groups before branch point
synthase
phosphorylate -

removes 1 unit at a time

v

ACP
phosphate reducing end
Malonyl oxaloacetate oxaloacetate UTP CTP to RNA
glucose 1- →
8
-
-
works from non -

NADH
- - -

GIP → b- 6P na pnosphogwctomutasl TTP ↓ ↓

Acp ( Oz condensation 1- -1
unique to only DNA
glycolysis , Ppp
+
Nab TTP dctp DNA
-

C- 6P can then go into ✓ to

CORE gluconeogenesis etc Aceto acetyl Malak

-

ACP
- - -
-
-
-

Pyruvate
.

,
NOVO
.

De purine
-
-

the branch NADPH pyruvate

removes 3 glucose monomers from
ring structure
'

Transferase $ put it on the straight chain -1L

Reduction 2 Nappy
NADP purine
NADP
.

tatty acid synthase cannot generate ↓

b- 3- hydro ✗ BVTYRYI ACP
fatty acids longer than 46 palmitate IMP / MOLINAR monophosphate )
CORE Acetyl 10A malonyl-COA VIA Acetyl-CoA carboxylase 1
-

→
- - - - -

y
- -

1.
-

Dehydration
-
-

3
malonyl-COA IS transferred to an ACP by malonyl transalylafl
.

removes the last g. Nose monomer from the µ, <

2.
tho
branch to yield GNIOR 3. acetyl-COA IS transferred to an ACP by acetyl transaiylase ATP GTP to RNA
crotonyl ACP
d- 1,6 -

glucosidase ( glucose ) - Gap via hlxoklnak NADPH

4. keto allll synthase condenses acetyl ACP and malonyl ACP - -

↓ ↓
to form auto acetyl ACP + coz
Reduction 4- AATP DGTP to DNA
Nabptc 5. ketoacyl reductase then uses NADPH to reduce Fluorouracil
CORE
- - - - -
- - -
-
-

Acp
Aletoacethll ACP → D- 3- hydroxy butyl ACP
bvtyryl
regulatory enzyme for glycogen degradation 6. Hydroxy acyl dehydratase is used to dehydrate
Glycogen phosphorylate Flvorodeoxyuridylak
-

Phosphorylase AIR State ) →

phosphorylated ; active site open $ accessible H2O from D- 3- hydroxy BUMI ACP → crotonyl ACP (→

Phosphorylase A IT stall ) phosphorylated ; active SIH Occluded

Tmp
•
→
7. Enoyl reductase uses NADPH to reduce cvotonyl ACP →
Bvtyryl ACP DUMP
phosphorylase BIRSTALL) → not phosphorylated ; active site open $ accessible Thymldylak
-

Phosphorylase Btstall) → not phosphorylated ; active site occluded FA synthesis Regulation synthase
-

A- B
regulated by covalent modification ACC / Acetyl Cort carboxylase)
regulated by allosteric effectors both catalyze the synthesis of malonyl 10A methylene -

Ter
-
-

tetrahydrotolak
High glucose] favors R→T
[ from acetyl COA dinyarotolate
\
-

epinephrine t) function AJ dimers glycine

-
-

] NADPH H+
+
degradation
glucagon 1+1 Muscle Phosphorylase glucagon / ) insulin ( t ) tetrahydrotolate aminoptehn
-

dinuarotoiaie
• _ -

serine
methotrexate
reductase
default state →
phosphorylate B " " " " "" c- )
epinephrine f)
-

'

Nabpt
liver Phosphorylase ( active )
.

AMP It) T→R urea MUST be Dealt with o

•

default state →
Phosphorylate A. ATPf) R - T
-

Acct / cytoplasm ) / synthesis ) wed

glucose 1- ) R→T c- 6pct k→T .

AMPKC ) -
'

Ureolltic →
convert NHy⊕ to urea TMP
specific to DNA
only nucleotide
' .

phosphorylates Allt 11hAM) -0 HZN N'+2

Glycogen synthesis ammoniolelll Tetrahydwtolale
-

excrete N.HU ( aquatic)

.

→
-

palm Hoyt coat) allows for the

the monomer that used to methyl donor →
UDP-glucose Is is extend the glycogen chalk
'
•

signals excess tatty Atlas NHy⊕ via uric and lblrdl $ lizards ) synthesis of TMP
excrete
-

uriwx.lk
-

+ →
VDP →
UDP-glucose Glycogen
+
Glycogen citrate ( )
-

• t

)
Glycogen synthase regulatory enzyme requires a primer lglycogenm signals acetyl Cort 13 ATP
→
- -_ -

synthase make a long chain of monomers ACCZ / mitochondria ) / degradation ) Urea cycle → occurs In the liver
once UDP-glucose and glycogen
•
•

comes in
prevents fatty acyl COH Into
then branching enzyme does not have
-

H2O stable molecule that can

mitochondria N group arginine %
branching enzyme will cleave about glucose units and add it via d-
-

7 1,6 linkage move around bloodstream

•

" "" " "

-

glycogen synthase inactive in phosphorylated b form " "° " """"

arglninosucclnase
"" ""

'

MSU " " 't ) activated in un phosphorylated a form

arginase
"" "

glucagon / -1 ygynpneg , , urea

lppl )
-

Protein phosphatase I phosphorylase kinase

epinephrine f) inactivates
cycle
-

'

<

shifts metabolism them

arginine succinate ornithine
ATP
'
cyclic AMP degradation to synthesis "
phosphatases
"
-

phosphorylate
de
↓
-

removes phosphoryl groups from glycogen activates g. synthetase ornithine transcarbamylatl

protein " " " " " t" "
( active /
-

←
protein kinds synthase b / inactive ) to form a -

inactivates g. phosphorylase GUNK avg.in/nossvcunaK

f) carbanion
-

kinase Insulin
A1
-

synthetase
A
protein kinase A →
phosphorylates phosphate
glycogen form B
g. synthase
to

[
-

phosphorylate phosphorylase synthase d- amino and llthlllhl

"
010
form A aspartate NHZ
14hAM g. phosphorylase to
-

kinase kinase ,

↓ , mitochondrial %
insulin activates ppl carbamoyl phosphate synthase I
914109M
-

degradation glycogen Inactivate phosphorylate kinase

a- kltoalld matrix
phosphorylate phosphorylase synthase SUNNAH
→

pyruvate cytoplasm / regulatory step )

pathway , a a b
→
inactivation of glycogen phosphorylase NH3⊕
coz -1
activates glycogen synthase glycogen synthesis
-
→
↓
insulin ↓ glycogen breakdown Immediate biochemical sources
NHz⊕
-

glycogen n glycogen n -1 comes from oxidative

↑ glycogen synthesis acetyl-COA 0tNHz④ : aspartate *
glutamate deamination of glutamate
71
glucose l
phosphate
- -

aceto acetyl-COA

✗
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✗

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