Bc 2 Fat Digestion 1

Front 1

beta-oxidation

Back 1

Oxidation (remove 2 H by FAD) -- Hydration (to alcohol) -- Oxidation (remove 2 H by NAD) --- Cleavage (2 C)

Front 2

Step 1 - Removal of 2 hydrogens Oxidation by FAD to a alkene

Back 2

AcylCoA deH -- take H b.t al-be to put on FADH - make alkene

Front 3

Step 2 – Hydration of alkene to alcohol

Back 3

enoylCoA hydratase - add H2O to alkene (make OH)

Front 4

Step 3 - Removal of 2 hydrogens Oxidation by NAD+ to a ketone

Back 4

b-H-acylCoA deH -- take H from OH and put on NADH -- make ketone

Front 5

Step 4 – Cleavage of 2 carbons

Back 5

Thiolase - add CoA-SH - cut AcetylCoA (2C) for TCA to make NADH-FADH

Front 6

b-oxidation takes off

Back 6

2 carbons at a time

Front 7

MCAD deficiency (Medium/ Long chain acyl CoA deH def)

Back 7

Glu to Lys (unstable MCAD) -- dicarboxylic acids in urine
(adding carboxylic acids from w-oxidation FA) --> bind to Ca make kidney stone

Front 8

beta-oxidation to glycolysis

Back 8

ATP 30 to 108 need to review steps

Front 9

unsaturated lipids 1

Back 9

enoylCoA isomerase (5th enz) -- move double bond b.t al-bet from cis to trans

Front 10

odd-carbon fatty acids

Back 10

Biotin (B7) help carboxylation (add 1C to even) Coba-lamin (B12) help isomerize to straight chain to Succinyl CoA

Front 11

C12 coba-lamin deficiency

Back 11

high methyl-malo-nyl in urine (can't make into straight chain SuccinylCoA --> bind to Ca make kidney stone

Front 12

unsaturated lipids longer chain

Back 12

2-4 dienoyl-CoA reductase (6th enz) -- remove H to put on NADPH (PPP) then move double bond (enoylCoA ISOMerase)

Front 13

Methylmanyl mutate deficiency

Back 13

bind to Methyl-manyl bind to Ca to make kidney stone

Front 14

B7 Biotin deficiency

Back 14

elevation of C3 -- mild symptom -- not a lot of Odd C fat in nature

Front 15

peroxizomal reaction in high fat diet and long chain FA

Back 15

flavoprotein dehydrogenase --- electrons are passed from FADH2 (nonsoluble) to molecular oxygen making peroxide WHILE NADH can escape Mitochrondrion and passing e to O2 in mito

Front 16

Zellweger syndrome

Back 16

lack of flavoprotein dehydrogenase --- increase in peroxide and potentially hydroxyl radicals.

Front 17

Ketone Body Formation in the Liver

Back 17

1.Condensation of two acetyl-CoA’s.
2.Condonsation of third acetyl group to from HMG-CoA
3.Loss of an Acetyl-CoA to form Ketone: Acetoacetate
4.Decarboxylation to Acetone
5.Reduction to beta-hydroxybutarate (main ketone body)
9.Describe in detail the

Front 18

Ketone Body use in extrahepatic tissue

Back 18

need to explain in detail Describe in detail the synthesis and utilization of ketone bodies. BUT too tired -- will do in weekend