Beta Oxidation

Question 1

Steps

Answer 1

1. Fatty acids bind to albumin protein and diffuse into the cell.
2. Albumin unbinds to FA and CoA binds to FA, trapping it into the cell. This process requires the input of ATP (converted to AMP) and is catalysed by fatty acyl synthetase.
3. FA-CoA binds to FABP for transport around the cell.
4. FA-CoA complex breaks apart and FA diffuses from cytoplasm to mitochondrial matrix via carnitine. Achieved by Transferring of acyl group from CoA to carnitine, forming acylcarnitine, which can then cross the mitochondrial membrane.
5. Inside the mitochondria, the acylcarnitine is converted back to acyl-CoA, releasing carnitine via CAT-2.
6. CoA binds back to the FA.
7. Fa-CoA complex goes through multiple rounds of B oxidation where each round produces ac-CoA molecule, NADH (via cleavage reactions) and FADH2 molecules (via hydration reaction)

Question 2

Transport of FA into cytoplasm

Answer 2

FA are hydrophobic and have polar ends therefore associate with albumin protein. Once they come across a cell with low [FA], they diffuse in the cell (mostly passively, sometimes actively). FA binding protein ensures they don’t fall out of solution then Ac-CoA is bound. Trapping costs 2 ATP molecules which are hydrolysed to AMP directly and two PPi that are taken off hydrolyse again and that drives reaction to right.

Question 3

Total products

Answer 3

Breaking a CX backbone:

X/2 acetyl-CoA,

(X/2) -1 NADH

(X/2) -1 FADH2.

Question 4

lipolysis and B oxidation

Answer 4

When energy demand is low, the Krebs cycle slows down. However, β-oxidation can continue but, without an active electron transport chain until NAD⁺ and FAD runs out.This halts β-oxidation, as both cofactors are required at each step. Additionally, CoA becomes trapped in acetyl-CoA if it can’t enter the Krebs cycle, and free CoA is also needed to sustain β-oxidation. To resolve this, the liver converts excess acetyl-CoA into ketone bodies, which regenerates free CoA and allows β-oxidation to proceed.

Question 5

Fate of acetoacetate

Answer 5

Interconversion of B-hydroxybutyrate. Both taken up into tissues (incl. brain). Split in the mitochondria to acetyl-CoA. An instant source for Kreb’s. Acetyl-CoA inhibits PDH. Relieves use of glucose by brain