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29 Cards in this Set
- Front
- Back
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causes of fatty liver
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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) |
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ACoA pathways
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TCA (for ATP)
Ketone bodies FA synthesis Cholesterol/bile salts |
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palmitic acid
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C16:0
in every tissue except breast (decanoic for milk) |
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decanoic acid
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C10:0
coconut milk & breast (docosahexanoic C22:6) |
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oleic acid
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C18:1
makes adipose |
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linoleic
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C18:2
essential precursor to arachadonic acid |
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alpha linolenic
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C18:3
essential |
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FA at risk in hyperberic chamber
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arachadonic
docosahexanoic acid oxidize easily (ROS) damage retina & cognition |
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Functions of FA
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energy
hormones increase protein hydrophobicity (myristoic a) precursor to ketone body |
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overall reaction in FA synthesis
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ACoA & 7 malonylCoA to palmitic acid & 7CO2, 14 NADP, 8CoAsh
(takes 7 rounds) |
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malonyl CoA
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ONLY found in FA synth
high energy compound donates 2 C's (made of 3) source of CO2 |
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lipogenic enzyme family
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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) |
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reason for fat storage
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doesn't require water (like glycogen)
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FAS
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fatty acid synthase complex
ACP pantothenic acid 7 enzymes |
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ACP characteristic
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reactive SH group for reactions to take place
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FA synth process
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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 |
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transhydrogenation pathway
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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 |
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isocitrate dehydrogenase
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in TCA
blocked by feedback (ATP) leads to increased citrate (OAA + ACoA) travels out to cyto for FA synth |
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citrate lyase
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ATP driven
gives ACoA & OAA induced by insulin |
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sources of NADPH for FA synth
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HMP shunt
(G6PD & 6PGDh) transhydrogenation pathway (malic enzyme,NADH & NADP in cyto from glycolysis) (pyruvate carboxylase (ABC) takes it back to OAA & regens malate) |
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4 ABC carboxylases
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Pyruvate (OAA in cyto)
ACoA (malonyl CoA in cyto) propionyl CoA (methylmal CoA, FA & aa deg) methylcrotonylCoA (methylmalonyl CoA to Succ CoA) |
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Malate dehydrogenase
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convert OAA to malate in transhydrogenation pathway
(gives NAD+ - or reverse in TCA) |
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ACoA carboxylase
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uses biotin
gives malonylCoA from ACoA for entry into FAS complex signalled by citrate |
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malonyl CoA
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VERY high energy
3 ATPs unstable |
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FAS complex
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condensing enzyme & ACP
ACP requires pantothenic acid holds malonyl elongation & condensation thioesterase clips off palmitate |
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thioesterase
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clips off palmitate from FAS complex
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Acyl Carrier Protein
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holds malonyl in FAS complex
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medium chain thioesterase
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in mammory gland
aborts FA synth |
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decanoyldeacylase
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cleaves C10:0 using CoAsh
makes decanoyl "intermediate chain FA" travels w/o chylomicrons straight into mitos gastric lipase can digest |
