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29 Cards in this Set

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causes of fatty liver
EtOH
-converts to ACoA (FA synth)
-can't make VLDL (b/c nutrients needed for pcholine & aa's neded for proteins)

NASH:
insulin resistant adipose
-makes FFA's (instead of TGs)
-more FA delivered to hcyte
insulin induces lipogenic nz's
-increases production of FAs
activates pyruvate kinase & PDH (high NADH also drives)
ACoA pathways
TCA (for ATP)
Ketone bodies
FA synthesis
Cholesterol/bile salts
palmitic acid
C16:0
in every tissue except breast (decanoic for milk)
decanoic acid
C10:0
coconut milk & breast

(docosahexanoic C22:6)
oleic acid
C18:1
makes adipose
linoleic
C18:2
essential
precursor to arachadonic acid
alpha linolenic
C18:3
essential
FA at risk in hyperberic chamber
arachadonic
docosahexanoic acid

oxidize easily (ROS)
damage retina & cognition
Functions of FA
energy
hormones
increase protein hydrophobicity (myristoic a)
precursor to ketone body
overall reaction in FA synthesis
ACoA & 7 malonylCoA to palmitic acid & 7CO2, 14 NADP, 8CoAsh

(takes 7 rounds)
malonyl CoA
ONLY found in FA synth
high energy compound
donates 2 C's (made of 3)
source of CO2
lipogenic enzyme family
ACoA carboxylase (malonyl CoA)
Citrate Lyase (OAA for transH & ACoA for FA)
FAS complex
P Carboxylase (for transH,pyruvate to OAA)
Malic Enzyme (NADP+ to NADPH)
G6PD (HMP shunt, w/6PG Dh)
reason for fat storage
doesn't require water (like glycogen)
FAS
fatty acid synthase complex
ACP
pantothenic acid
7 enzymes
ACP characteristic
reactive SH group for reactions to take place
FA synth process
get ACoA out of mito
(via citrate)
convert back to OAA in cytoplasm
-goes to malate (to regenerate pyruvate & NADPH)or ACoA (for FA synth)
generate malonyl CoA (from ACoA) for FAS
FAS complex
transhydrogenation pathway
citrate shuttle
-from TCA to cyto

citrate lyase to OAA & ACoA
-OAA to malate via malate Dh (gens NAD+)
-ACoA for FA substrate (via ACoA Dh)

malic enzyme
-NADPH (using H from C lyase)
-OAA to pyruvate

Pyruvate back to mito
-carboxylase (ABC) to OAA
isocitrate dehydrogenase
in TCA
blocked by feedback (ATP)
leads to increased citrate
(OAA + ACoA)
travels out to cyto for FA synth
citrate lyase
ATP driven
gives ACoA & OAA
induced by insulin
sources of NADPH for FA synth
HMP shunt
(G6PD & 6PGDh)
transhydrogenation pathway
(malic enzyme,NADH & NADP in cyto from glycolysis)
(pyruvate carboxylase (ABC) takes it back to OAA & regens malate)
4 ABC carboxylases
Pyruvate (OAA in cyto)
ACoA (malonyl CoA in cyto)
propionyl CoA (methylmal CoA, FA & aa deg)
methylcrotonylCoA (methylmalonyl CoA to Succ CoA)
Malate dehydrogenase
convert OAA to malate in transhydrogenation pathway
(gives NAD+ - or reverse in TCA)
ACoA carboxylase
uses biotin
gives malonylCoA from ACoA
for entry into FAS complex
signalled by citrate
malonyl CoA
VERY high energy
3 ATPs
unstable
FAS complex
condensing enzyme & ACP
ACP requires pantothenic acid
holds malonyl

elongation & condensation

thioesterase clips off palmitate
thioesterase
clips off palmitate from FAS complex
Acyl Carrier Protein
holds malonyl in FAS complex
medium chain thioesterase
in mammory gland
aborts FA synth
decanoyldeacylase
cleaves C10:0 using CoAsh
makes decanoyl
"intermediate chain FA"
travels w/o chylomicrons
straight into mitos
gastric lipase can digest