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Biochemistry 1

The document discusses various metabolic pathways including glycolysis, the TCA cycle, and the HMP shunt, detailing the biochemical processes involved in energy production and regulation. It highlights the roles of enzymes, substrates, and coenzymes in these pathways, as well as the effects of insulin and glucagon on metabolism. Additionally, it addresses the implications of metabolic disorders and the importance of NADPH in cellular functions and detoxification processes.

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moryadhiraj21
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0% found this document useful (0 votes)
70 views23 pages

Biochemistry 1

The document discusses various metabolic pathways including glycolysis, the TCA cycle, and the HMP shunt, detailing the biochemical processes involved in energy production and regulation. It highlights the roles of enzymes, substrates, and coenzymes in these pathways, as well as the effects of insulin and glucagon on metabolism. Additionally, it addresses the implications of metabolic disorders and the importance of NADPH in cellular functions and detoxification processes.

Uploaded by

moryadhiraj21
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

Couloohylroe metabc0sm.

ineipee mono Sacahanle Gut pru t gola to


diet Stel, leete) Betee
Sueroe
|igemon in intesttne

L aboptiou
(epcte portat nin)
to exra hupotie
hup tiu
20gemioy mtaboicme
Cota bo i y Qnab oisu ot metatli

yel
9gogenes
H MA lotone Syntesis pathwy
7ygenoyais (energy reqie)
nelea se)
Cemrg
beakduon
fach cides
(Catabe We pqth
Tyogenoy[is
(anabbie) Cyopas m)
Iggenesis qluose é ANABOLJc v latose
ytoptasm
gtolysis (catabaie patway)
I ytoptasm
guomo gcnesiswa Pyrurate
canabotapatn LDH
Lactce

AcelyleoA oatab are atwaz


TCA
e
citocomdria)
HNPhunt
Rinoe| A1P
guuone (Catas eie)
Da

Net Xn
guoe Insutiy
AT
ADP aKNADt
-gucagon 9AP+ 9NADHt
Lauuoscbphosphate
phospho guuoe energgHo
kinase
Frutose B6 phophte inculin, ADP guokinase 4KTP ’ (ADP
phosphotnto hocpno fmuo kinae IAP
kinare |NDP
ADe gucagou, ATP
Pràctae ,6 biphosphote cisate
AldoeA 9geeratdahgsphoptte
dahy cnagenae
DHAP
phosphotioxlomorats phosphogyero n a ADP
Pyruvae kina
gycerateodaADt 4Stonsevaic
enerom n &ADp ATP
3-pnosphe NADH HT
denydye nac'
,3 biphb &phogycerate glyceradehyde 8 hosphate
phospho ADP X2
9yiero ATPX2
dunyo genone
’NAD H+H*
inase
ax 3 pho $phogyrate OXPHOS
phopho ‘
re 6 A7P
aeo bic ondn
8xa phophog'ycerake luicde &AP |0A1P
enot and energ Nt gatn- 8AP.
X pho gphwphen pyruvaeinsulin, ADP
P9ware ADPX2 kurose h6 biphosphate
kinael ATPX2
gucago, ATP
Pyruate hypetíc condh
anaeo b'e ond
reguuaroy enemymes Chaletel mus les
with ofew mibcuoneln'a
lo guo hinae RBC, renal med ulla ) cenea , lens.
2. Phocphotuoki nane clticieny 4
hemo yhe anaemian RBc
3. Pyvveke knase yurohe hin
euercibce mtn n guomo genesis .
obe oncliioy
4ruveke LDH lautoe (Cybso1)
tay ate ehydnogcnne
NAPH
yeq ci es
Net eae gain
net neaho
+ AADP t aNApt +2Pi ’ py ruvate t NADHt2H* t
LDH
Pyruvte +NADH la tc aud t 2NAD

anaero bi'e .Oxiolohon , geS lgy o ye6


BMS
- RBCs, Rena nedlutl tosneo ) lns lert Aherobic
gyolyss
Qkeletae mue les moder hy poxta
toudiae museles unoer loo 0) ’ Myocarollal ImcH Ou
alchono)
pyruvate Qutaleenyc dewy drgvorehan)
Pnvte C<yeant)
deeasboXy ue (beewers yeara)
aud
Pyevete tooct patetes in teotu hy oyse ho lautte
anaero ace condn lead ho tooth lecy
Muonce inhibi tor o anolare henee pienert gycolyss
Sodium huomole s added o blood cample betore

manig btevd gueee Sammple o pevent g4colyss


POH Comples
C oxiautine decosb oxyeahom
wnde aeroc conc
ln mochom dna mohi

by Pyuvale ae hydrogenone cometey,


H(autne auetate)
Pyrurae bxidised i nro
ane nequinep
enyme
|. TPP - Thiami ne pyrvphophete iole
FAD blavn adenne imualeo
2. upoic aud
hicoh na mide aclenin dinu cleoble
y. NAD- A
co enyme
ugh Cs in mio ohond aa
NADH Ht lc poduee Oicle t
Domverted nto 3r1P.
PDH & a mutienyme lomplex
has 2 eny mo
Pysuvake duhydrgenae (29)
di hy doe li°y dahy drg enae(s)
lyuate + coA 1e,fAD, upoie aud
NAD'
NADH Ht
Requtation (louo onargy ckehu)
3ATP ADP
ATP
Pi
( dephocpherglated pOH)
tDH phosphato PPH Kinase

Hoo.
inautraed PDH-0 ADP

insuin adipocyres) (phosphey lcsed POH)


,aLtylot
Catt n musees ADP
atradeg toom cephospnea laey NADH1
guuogon
t PDH omple inauhvated fom (phoiphoglaea) NAp
PDH hinae
a. deponde em fwo enyme
enyms
areI
ten wit inbht
NADH Acyl co Wgh
NAO hinone
omples and aeti rateg fDH
POH nacirtcot PDH
atiraed pDH nb dibeles meliho
9 eene
Acety toA
n aipoytea to releae
releone
CASET
usiu tead o Dyposis n
and NADH
nreond lene
omples and atinhon B PDy
fo nibihon & PDH
kinase adiocytes
releae , Incuin in
CASE
IIT ceLe
low energy ctas o hene Quhvciou 0
acivaion 5 PDH omp lex and
PDHpuophauta

PDH phopetac
BMS. (3

PYevae and tauric aud lead o CNS disoesi


TCACyce
(eads oxidehon 4 auhy coA
ouus ln mib cuon dnal na hir
aero bie tondihou n pesene %O
a b knoon as krebs cy cle calikco nared by Hans kab)
TCA
4
åic açd y
cee pdt is me ald whicu ts
AkA
biçaboyic aid nt
ah'on
Oxid hon NADH, PAD
onieRme nergy as 7eduoing powers
7. TCA ycle chondnal orstae COn nert
ooug ETS vta mo
Ohich
AP tnis ts hhown as bxicl outiMe Pho sproylab'ou
ADP In
hu hmaws
6. TA Quowmls 2 9 AP hodueen u
Ho
NAD 00A( )
NAD

OXalaacLtate
syntmauy
irohe
Knaare
dthydogenny auonitax
Malare
AP, NAD
ADP so cihroeAD
NADH 02
fumana
(isoarolk dehydge
HoFumarate nar)
suejnate Kelo glutarae
duhydnogenne
(akasoguarak dehydr
PADH
genae co mple
Suinate
Suinyl COA+ NAD+
none
OA
mioki gueinye
Co A
NADH con

ADRSL
guo Oridaion
way path ncthie lei at .
cesotble for quycoysis
and
gnd
1CA gyc0ysis o
bo
TCApathwag ipman wacbung
phospuoguiomase
phospnote pente
Meo Aka
monopnorphole
ghunt Shunt HMP
(NADt) miain
tunic Pamto
(PAD)
A)(co aud wiamin
ba
CHhiami vitamine,
TPP
[Link], casbs, too
BMS
kelo O
NADPH,
Su ATP, etaegnné g
coA uiny cagenane dehy relle ei(to
ADP,NAD
1a ouion Regul
NAD P AP
NADPH ATe,ciree,
7CA
AbXPHOS
0XPHOS) I6A7P
C6-
2Pyuvae
cye OxPHOS) Yl6- ’gP
(2^1P aerobic
4NADH gonohe duhy Maleue
1PADH2 enow olog dehy Suinae
tniokinme Rucçnate
INADH
’ dnogno cale
duhy Kehoguton N
genone duhya rase 0so
ci
ANADH yele 11CA
PApt 3NAD+ cOA
.
J e mot porioe energy NADPH. for
ng po uu
Eh pocluee nel
Kain &unchonmdnal
mib cho Sy ntheis S fA.,Sferoids. syntheb's
Rboe fo nueleohole
HMP Shunt þoviclus Hsuas, laetai gan, eoeo,
Operetto in eine, ddipene syntnn't oq eA.
6 nany- uti ey (nuetued In

kegulalioM
ene is guatoyenyme
agulatoy
otvog
gual 6phoiphle dehy
inbibik ati viy
NADQt
the 46Pp
NADPH J actiahes
NADPt
wLeleked state
phosphog uomcale ctehy
plt G6PD 2
nsulin
dogenae ete& mellitu .
/dlab
inhibitegucyon/ shavh'on sunt byy 96pp
" HMe Shml aleo Hp
Hue
thy otd her moneg o e Bphospne
mer ase
hoheko iSo
Phosp
icomerase 1
phesphoguco fructoe 6 phosphate
phoyphogrutokinase

bi pnosphcte
Pructo l,6 aldolae A

r0se iconera
phospho DHAP

cdehy droycenafe
gse6 phosphote

nsutinithynoid NADPH J starvahon,


NADP 4 hogmones NADP iabetes
NADPH melitus.
HMP chunt in
abpD cat atys as 19 shep o HMP 2hunt
e NADPH
tedued gutotuione lenels
AlNOPH mai nt ains piculion 4 Hio
sod 4or datoxi
recdusdAlutatnione is rocq ui PBc trom oxidah ne do da mage
4. NADPH Oes a.s proleeion tes
aye deloxy Ho by
glutathion puorid
e. gtudat hienk
O
proleshng ABe tom
it \nio Ho amd
hacmolyhe anaemio
Hamoeyte anaemia
o RBC desnuuhon
hamog ubi numo
" kaemog lolbi e mia
9, Ho
lonals
b low Benene hatmogtels.
Symphoms ftaiure to gh
" ranal
1. pale foa
n
leat haumolytie jaundia
A. eho charolie.
ely
3. ra bocly uuaknenCentargemenr 4pley
geu
4. migaty Centagem
s spleeuo
heuo
Senene c e
it can
daprome j suljoramidy
(kuraxony
i maquçn)
Animalautc
(aspins
kniipyo
inteiu Csenere bava beAw

Heloiades
HMPghunt g utahiore
J4SH
NADPt
s s4
NADPHtT fultatnion
oridahe
perovidoe dlamae
phosphogutanolacone anul
huemalya
anaeiua.
HMP Shunt
NADPH
b.
RXhramiocuondnal
and chole Qhol
moe bþorak d dde movo
in celle Involned n at ne

0 wanes.
pres ervahou 4
mnsp
HMÝ aeny o lens and onea
Shuunt NADPH dued glutatuione
’ roded

enentou
Reoed
glutatione amd
amd RBC
gutamae dehy dro genaso
NADPH deroxi ticahon XenobioHs
6. NADPt
haem broakdoon
HMP Shunt gen nboe suga
g. NADPH-phayo 8oms kili ng s baterio cimp)
9. HMPgnt oxidires pentos. (yeeecrida) Cystem
gluconengenuss
guose tom mon Cantbohydrote soure %energ
Bue as Pyruvote,
Jactote
Intemediaeo TCA
integmeolicteo 9,gy0s5
source tmat leads ho toomah
non canbeyroe
a e tknown guuo eo gouic preee
newgue animals
bn n mo st
quuoneogcueic
in
enul c0Ytex

mitonedomdn a ana y tonl


o [Link]
most s reps in ytosol
4 speutic oeaions.
LL ysurae casbovy lane
phosphopend pyruvaue canbo ny kinane
Ls phogpholase
Ls thutose, b6 bi
Ly glwt kphospralosu
Fusotions
I. ubncahou
dinphagm ngaine tnhc
maintalve 4inhrapleu
Arenia [Link] within
ideel Ino phars (1o
PEP
Pyev Pyuvale ree
PER
-gluose (Ge)
gusk6phoqpnatase
notATP
guucokinase
9luoe 6phophdle
phosphohKO truchoxh6biphospnataie
0so erase
tuto bhophehe m ot A
phospho huutokinase JG, 6bphocphale
koutoe e Ho
Atdolase A 1
phosphoiot
1°erlysphosphad cNADÍSOMerai Net ATÝconsumd
corsumte

bijphosphog ycurale t2A7P


+247PJ
ADP
phosphoglyekinaf C
2A7P
pmoipnegyenmutace
&phosphog ycerale (9930)
Pybs enolase sHo X2Pyruvale(3)
Phosp hophont
2NADH Hrt)t24Dp
ADp
4A7P247TPt>gucoe
ATP
Phu vae PyruvaleX2
kinare
Pypwatet +2Pit 2 #PP
+4Po 42NApf

Pyrurake Ge coubawylase)
Pyuvote
phosphopheno
D Pgttae eeor
Pyuvae
Oxaloetate e)
Cautony
kins ADP
Malate
NADHtH olehydrgenae
NADt
Malae
(1en)

NADH9TNAD

denydrogenare
Malate

on't yele
luose' g
Pi
. phorp
gluepe
sphte guore
eeaev ban syl guco So
phee qlueoe 4.
ddebran
ngchi 3.
emyme
glucsPnopho oo l:.
mutase
v hato phop 6gluco
gycog
enYmes. requine
S
liny debra Dnergt
glyco oloon becak
ogox inb geu gyo o I
ovtole lo ysie geno yyco
Soure Steuvaiou
ry enerty gluey a
total
(2S0g) toge ettng
Muswla
iver. utçted
by be
anna analaLtvihes ntoining s
cecut musShenous
gyogcn
wal for
blool hepatte
poy Sortgemupcles in
slored
lants sacelroele
(n dautt abun
Anmaa
hb lo0. Ne below t uoraabho
8 PAGT

Anemia
dlinical conditiow ueue oxy ge cauying capauy 4
blad is ALdued

<I2mg ldl
qAadi ng Haemogobtn lontent
Mild anmia: 8-12 wgldl
Senee aneia ! (Smgldl

clam cation
ETIbLOUlCAL
due to blood lo
2. DIETARY DEPICENCIES ! de to ULOu, Vit betu n
3. DYSHAeMOPOESiS : olukeut in eythiopetsis Higin aplothe
aneia

Xhay uadiaion
Traysiadiaton
wypeusens hvity bone manew to dngs
4. HAEMO YTI ANEMIA deto exem ne olsrehon
RBLs
MORPHOLOqICAL WNTROBES LABIF{CATIDN
conntration
Bad sn ie and hamgobin
NowMOytie kyprchsoie
Neochomje
Aute hammonhege chloie hammohage
haemoytic anenmias
aptom an
Mauocytic
Nemochomie hypochuomie
yitby dy koic aud
GOGD wRITE
[Link]

NeMocsont
Mivoyti
yppcuomie croie epeetion
Thalaema

PERNICIOUs ANEMIAJ ADDISONS ANEMIA


destuctine linjuious
Cauuss.
lalk 1F
fa'ue q aboo pen vit Bz
muita whie
imay Oxynti
containo cells.
charateic eatuo.
BONE MARROU
Aneoia podud nypoxia
ythropoens in bone n ous witn mnatusation ren
bone muso buone hypuptomhb
naivis hone mauow - megaloblenie hypeplona 4bone
mauo.
BOD CHAN QES
Roe mauo cytic -henocsomie
ount< lmillion
amete =&.2Mm CN= 7.2Mm)
RBes wita poikiloytenis
Rei euloya cemt ^ amituyors
25/ CN- /)
twee and platele
Changes in 97
atopuy / cestuction 4
garmee muera Cont oini ng
Cels
GOOD WRIrE 0xyutie
wRITE GOOD
abxeytien
oli_eae buene 4.
nm cluleacd
py Yomale ingany demanel lnueand &
loo btd tnal men od ,inu ply ay
hago haeme chonic a.
haemnechege auue
ntt in; mll ke- jnta deueene
yalent (omyney Mert
anenmia dehiceny son
LKgo) demant ineacd
intake dietoy tew
Caus
dshicienyt vtBu anemiat galoblonte
0E£ICIENCY ACID FOuc
cemind Rbaute
cbd. pual dguadatien4
aycdadvance
SUSTCM VOUs NER
masheA.
laie) ontal patny
inglammalon
teg and Soeews
|DAIl
PAE
ushlogc al feaheles

craratesti keatro
nemal
4 peipral sne a- aniso oytens, poikiloyto SiS.
S. Bone
Ponu m
manO w hemublenhe hypeplano
WBe ad platllete- neYmal
1. Diinabin e0.4 m¡l dl
8 Nail t dy s~eu» Mhapd, dengitenal Shmahon
tonge -ngy ad.
buathtenno, paypiYatitny Apatd eut ie
9. cus egira toxy - comubrat on, headaelu
yne aitetibiy bo

GOOD WRITE
Lid htebeim
pe vi de en ential F.A
74>q0' te hotal dletay eipids. coarue fa fat olubleut.
bile salt
gyem, FA 7ic necyheiad
paneuah wene ls
bile salts Cayl cod
aymthae)
dylomino
cetles) abioed in inleatinal
mucosa

adipeu isee
reentei fied wie

e FuEL RESERVE
Dictany iplds Cmain'y T4) satk
pasand ile
(aigation)
FA + mono auyt yel
gycenol+Fe
tn inetnal muosa
esgntnik T4s
inteatinat muora
Fomahoy & chyowmions in
cells.
lyjingl ate duuk tren ditcharged
into
duyomi aons nto blavd.

chylomion in yatomahe oulation


daylomions hydroyed Ace owed bodyt
om FfAtgycu TOs are kydwyed
In adipone ti ssue
(poploteln ipales( not heenone auorrdingy
Censiti ne) uijsgenesis
FEA
PA
VLDL
adipoe tiegyeud-tphophae
tFM 14s (6uel reseme) endogenous to
khahepahc teus.
Hho hophuto aipo
ate) ( (inactie)
A
ipax fa epaseb T4
ADP (inactia)
cactine) kinav ProBein
Proleinkinae
+Pi CAMP Te
qyolase
adenylate homor gow
euiho diabky
AaH
cotcotda
Apace T9
Homo.
[SH
Ah, epinep
phm horepi FAt inb T9down4 Pak
ttpentent honnone gycenol
hp lycis Lio
HwSensi
Joxidahoy
[Link]üe
k Cnnt
tackig
eugy
wn lie uti can
phorace. taio RB) ulla med renalChrain,
exp ie vanous kinae
toneys ,Kidgyeqlandswhe
amen todue
eamnt bet Mmmay tiome
hy
utiuit autily
.odue inw hy eids phopo
daenev
enoy albuminyel
lbumiueld ptama aeau FAguux, T4,
exkahpahiy eningo Syntheis
hiue
heois) (Kuto bociu kutona Stinauvahou
J oxidahn B
uatliuet
t A lineu In Melihu diahedea
baties ketone oxiQxcemn
. p
glucocortioids. tA(4yauol
) + Kto
by epinaphri gucagouj
Sensih owhan
bakdoipolysis lysis. Lipo
Insutin
14ine Censi hormoe oene ful
upae
Hesunone Senu ne T4 lipase c1SH,Ty quuoctti wds, qutagow)
. hemmonw at adipouyto auirating ogme adang late cydace
Adnylate cyelae autinele eaye ATP ’ CAMP
3. CAMP auiraleu eAMP clepen dent protein kinape
mtein kin ate phophoryate inattve homone sen citne
Actne 14 ipe a.
T4 ipae b to homone genei ti ne
a stimutale pelysis.
utirated cphosphongatecl T4 Lipasenhibit
tivatu phosphodliestea
Cattiene md top hytline
wyme Shulatng polycis.

Mal abcophien Fak fat digestioN and abovptBen je lmpai ned.


non avail abii lale
paneranh Cau s
li'seares
d'seans
SteAysin biliarycheuy hpate
(hot availale) obchu ORRHOEK 1
fasce STEA
Kus urdigered faK in
clylia chylomiuons gne milky appeasa to ymptu
emels.
aen h anorphìou in Uymp hatie
Thi's is catled dgle
3. Resen y cye
wneb
4. dne b abmomal tonnuhiou bjo ynphutie
oiabetu e takiy
S. Mio eun in patiews haning cenen
et eh oiet.
denovo
enhanug e ptake
draks chgk intakey in adipo yre.
Coubohydra gluoe
Aayt coA
ipogenesi
+ tyeaol-3-phosprae

14 clored in adipose Hseue


LIPOLYSs 14s
1. Ncipox H4ue gpei ali d
CT Aydrolyss
2 14 shred as upid duoplets yteptn
emet ‘ glored Ty hydrlysis witu ha help a homone
3. Enngy qui lipaw gine
o FFA 4qyeund. (74ipase hydolyze
enai tne 14 ester tinkages)
compey
PfA albumin Moma albumly haty ud
Nanportet to Vones tuus and organa.
S. AAain ,Md ulla, RBc oan not utiu F# 0s uree 4 n t
6. Fate 4eycel opendens ou g (erol kinase

MUSLES.
ADIPDSE
BuDOD VESs6L FA
T4
upa 3oxida hon
Omcii
BLoOp
tenergy
Plasna
A+ albumiy -FA
gyer Complex UVER
( jcerol

ddipoe Aycero inay


phoyhy

Ypath ways
Miochondmal cmatnx) majo pathway
B OxidatHon

Zellwegura syndrome Qcum long chaiy


( cenebro hepato ena)
Koxidaion endo plame retiulum Cmito somes)
+ mitochondna cinor path wa
mile hen dniat ma i
SteP1 AIVAON

9
undeigoes ovidation n vite
The tonwien 9ouin

bw-(oo A and thiol gpa oA


ThiS bond 4orm aion Mqui ra nergy andhyndud
tonva in ai tn
Ryephocphate CPP:) mutliatety phe
phe 4 inorganic Pyropophatase
pholphae bonds de bokan.

FA + [Link]

wio Gses bend


STEP2 TRANGFER OF PA1TY ACYL COA PRUM UroDL 10 MnbHSNDeIkL MASRII
|. Tran spot
maaix ts Nquined er p-oxidatHon 4P.
a. 4 is done M wih the up a carnihine and speualiud rankpost ed
ayi carrine - camiine transiocase au duivita o faty auyl teA
cannot Cros Inner milb hondnal membrane
3. Enyhhe camitne aut tranyera ce L' whid k loated en tne inre
Quta , 0ue mjtochondnal nemotane onnerr tne satbAyt
COA into hatky a Canni Hne + coA
4. This faty auyl anihne u han iporkd tron bo lnnes mlocaential
matx tou a t Camni tine- camihne trando ta
mtbouondiat
twaue 4 lnnuu
(Anitine aylleansaL II ( )

bute mitnchondI mamb dnt


undng0
4 The a yy ayl (eA ncid# ve mb thondial maiy wil
Oxilation: eimnabya nal Spau poridakey
FatyB ayl OA Conine Canittre
fatyfcy coA
Paty yl cavnit
fatitumikne
hyauy
E Camitinu auyt hanogceon I Milochendiat
(Cr 1)
t (aunithine auyt mam.
(CPI-)
tAanyuon inne mio cdhondnal wembraw
Quyl< itine - cani tine tvawlocay
BMS
cannitin duiieny Boxid aiou ,FA. ’hypegyemia
"oepet taunitin
ymtesis
Renalleakage kypglycemie
STEPS REACTIONS 6F B-OXIPAIdiasetes
wnsist q 4 Teaton' in each [Link]
. oxidation 6 Fatylacyl co
I dehy drogtnatiou reaution
Rmovdl t 2 hydrgen aloms eah hom o and po qjaty
34 Formatiou 4 doue bound b<w dc ond Be

S. FADt wdues b FAbrh which th rough mibochonduat ETU yilds 2t


6. leacs lo tormation 4 A ansenoyl co
aylco auhydegohou
fatty Quyl OA ’ hans enoyl coA
Ee aATP
PAPH)
aratioy 8 trans ehog) COA
addition o Hhofo he dousee borli.
ydrah on Aachion
hydratate
a. enyme -D'noylcoA L-p-kydory agt cok
3. lead ho Hhe frm atiou ’Lp-hydvovyayl ok
+Hho
8 hansenoylcor
oxidqhioy
3.
, hydgu alom rom B-cavleo
|· Renonal coA duhy dwguau
2 engme B-hydvoxy ayt mitchondnal
ayl oA
B-KD which js reoxiciked bu
9. leads o toom aiou NADH2
7oon
ETC ko podlue gAtP
coA
4. Thioysi 9. p-keto auyt
and' acatyl cot
aty ayACOR
cabon shote autyttranaterae
thidau / aylloA
tatalyadby engme for compluke oxidaion
2. 4-oxidaiou is veparel
&our
F. fatyJauyloA
aytcOA dehydiogenace
PADT
# FADH hans -enogleoA
Hotencylcorhydratae

dekydrgerase
NAD pbydrxyayloA
BAP CE1 NADH B-kuto aylcok sperase
tailase) cOA
yl akyl tran
auty cOA COA ( casboy shoat)
Acy

hy gyee kinane
dbwn jno FA and
bak abenu
a. Tis In adipoytesbe tuBli ad hy adioytes de bo
&- qyeol
canndt
bld andelusinel y
is hanpote thongl
ton Ta S and phos pho tipidb
tinn gyenl s onwued to gyceok 8phosphae
hy gy ceuol kinae to form guioe hy gluuonogornt
ktone bods metabo lism
ceutaly ote physiologicalical; path alogieod Jika dl'ahels
oUnol gyosnda, potongot stoavatoy gyagen,
malitus , unol
ingetine hupaiks ect p ox dation
tabohy drates ue not Buttil
whenolietouy )s quleraled in ine.
taty

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