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Catabolism vs Anabolism

Breaking down vs Building up


Oxidation vs Reduction

Oxidation - loss of e-, loss of H+, gain of O
Reduction - gain of e-, gain of H+, gain of O


Process, Location & O2 requirement

Glycolysis, cytosol, no O2

PDC/ Krebs Cycle, mitochondrial matrix, needs O2

ETC/Oxidative Phosphorylation, inner mitochondrial matrix, needs O2


Goal of ETC

1. oxidize (empty) e- carriers
2. make usable energy (ATP)


Process of ETC

- Taking e- through its carriers to the last e- carrier which is O2 and it will then be reduced to H2O
- The more NADH that is put into the system, the more e-, therefore the more H+ protons being pumped against the gradient through ATP synthase to allow ADP to phosphorylate to ATP


How much energy is 1 NADH and 1 FADH2?

2.5 and 1.5 respectively


What if there is no O2 in ETC?

E- will not go through carriers so you will accumulate NADH and have a decrease in NAD+ and FAD


How do you allow glycolysis to happen without O2?

For 1 pyruvate (glycolysis makes 2):
- reduce it to ethanol (yeast) & lactic acid (muscles) by oxidizing NADH produced back to NAD+


Problems with proceeding with glycolysis with no O2?

- end products are toxic
- only make 2 ATP per glucose vs 30 (not enough to survive)


Reciprocal Regulation

Same molecule regulates 2 enzymes in opposite ways
Eg. Citrate inhbits PFK -> inhibits glycolysis BUT activates Fruc 1,6 bis Pase -> activates gluconeogenesis


Role of Fruc-2,6-bisP

Signals abundance of glucose, therefore:
- high glucose -> activates insulin -> activates fruc-2,6-bisP -> activate glycolysis to break down glucose molecules to ATP

- low glucose -> activates glucagon -> inhibits fruc-2,6-bisP -> activates gluconeogenesis to make glucose


Glycogenesis vs Glycogenolysis

- synthesize glycogen because high blood sugar
- Hormone produced: insulin
- Glucose is converted to glycogen and is stored in liver and to a lesser extent in skeletal muscle

- breakdown glycogen to glucose because low blood sugar
- Hormones produced: glucagon & adrenaline


Why do you tap into liver and not skeletal muscle for glucose?

Need glucose 6-P to make glucose and phosphate is negatively charged & cannot cross the skeletal muscle membrane


What does the Pentose Phosphate pathway achieve?

Produces 2 NADPH & ribose 5-phosphate



- reducing power for anabolic rxs
- eliminates free radicals, protects cell from DNA, membrane & other damage
- is an e- carrier


Ribose 5-phoshpate

- nucleotide synthesis (if a cell is dividing, it needs this ribose 5-phosphate)


FA Metabolism

Release of FA
- triglyceride (1 glycerol + 3 FAs) + lipase will break it down to individual components

Conversion to acyl Co-A
- FA in presence of ATP will react with CoA and make 6 carbon aceylCoA in the cytosol
- will travel to matrix and enter b-oxidation where it will go through 2 rounds (first releasing 1 acetylCoA, then 2, total of 3)
- then will enter Kreb's Cycle


FA Oxidation (FA breakdown)

Saturated Fat
- 6C acyl CoA which will be oxidized to introduce double bond by converting FAD to FADH2
- further oxidize to intro carbonyl so will convert NAD+ to NADH
- break it into a 2C acetylCoA through B-oxidation, and 4C (Which will subsequently break into 2 acetylCoA by feeding back into B-oxidation)

Unsaturated Fat
- 6C acyl CoA (where double bond may be in wrong place so may have to rearrange
- oxidize to intro carbonyl so will convert NAD+ to NADH
- break it into a 2C acetylCoA through B-oxidation, and 4C (Which will subsequently break into 2 acetylCoA by feeding back into B-oxidation)


How to make malonyl Co-A?

Acetyl CoA (2C) + bicarb (HCO3-) in presence of ATP will make Malonyl CoA (3C)


FA Synthesis - Activation & Elongation


Acetyl CoA + acyl carrier protein (ACP) -> Acetyl-ACP + CoA -> Acetyl Fatty acide synthase (Acetyl FAS)

Malonyl CoA + ACP -> Malonyl-ACP + CoaA

At the end stages of both, it'll be active & react with each other

- Both react (5C) but lose 1 C through CO2
- Forms 4C-ACP
- Then have NADPH from PPP which is reduced to NADP+
- Still have 4C-ACP
- Then further reduce another NADPH from PPP to NADP+
- Form 4C-FAS which goes back to the cycle
- 4C-ACP goes from ACP binding site 1 to binding site 2 FAS
- 4C FAS is now active but ACP binding site is empty so malonyl-CoA (3C) will bind at ACP
- the 2 react and you lose 1 C and end up with 6 C which will enter the cycle again etc



Where acetyl Co-A react together to form ketone bodies

- During long term starvation, blood glucose levels fall
- To meet energy demand, FAs are oxidized to form acetyl CoA
- Levels of acetyl-CoA increase; some feed into Krebs Cycle while some react togehter to enter brain
- Ketone bodies can pass through blood-brain barrier and be reconverted to acetyl CoA during starvation


Ketone Body Formation

acetyl CoA + acetyl CoA = acetoacetate --> hydroxybutyrate + acetone (all 3 are ketone bodies)


How can having too many ketone bodies result in suffering from ketoacidosis?

Ketone bodies have H+ attached to it so it makes it acidic thus blood pH is low. Too many will make it too acidic


Protein Catabolism

Proteins from body break down into individual A.A.
- A.A. can be used to make other proteins needed by body OR
- forms amino (which in turn becomes urea which is eliminated via urine or other nitrogenous compounds eg DNA bases)
- forms carbon skeleton (which in turn pyruvate can form glucogenic a.a. or vice versa / acetyl Co-A can form ketogenic a.a. or vice versa