B-Oxidation

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1. Release of Fatty Acids

- Fasting or Starvation: Glucagon activates HSL which releases FA's from triglycerides in adipose tissue in order to conserve carbohydrate reserves.

- During prolonged activity: Adrenaline activates HSL which releases FA's from triglyceride stores in adipose tissue in oder to provide extra fuel for muscles.

Fatty acids are released into the plasma.

2. Fatty acids are transported to muscle cells.

- Fatty acids are insoluble in water, need to be carried via protein albumin. (albumin has hydrophilic surface and hydrophobic interior).

- FA rapidly diffuse across muscle cell plasma membrane (lipophilic).

3. Fatty acids combine with Coa in order for oxidation.

- In the cytosol FA's are converted to FA-Coa via energy. Fa + COASH + ATP -> FA-Coa + AMP + pyrophosphate

4. Fatty acids are transported across mitochondrial membrane to mito matrix.

- Short chain FA's (<C12) can diffuse across membrane.

- Long chain FA's need carnatine + CPT I and II (carnatine palmitoyl transferase) to transfer across membrane into mito matrix. (see pic)

5. B-oxidation occurs in mitochondrial matrix.

- Each cycle of B-oxidation acts on two carbons on FA chain and produces FADH2, NADH and 1 Acetyl CoA.

- 1. Oxidation (FADH2), Hydration, Oxidation (NADH), Thiolysis (Acetyl Coa).

- If unsaturated FA, extra hydration step.

If uneven carbon no. final cycle give proposal 3C- CoA. An extra carbon is added to form methylmalonyl CoA (4-C). This is isomerism to TCA-intermediate Succinyl-CoA.

7. Regulation of B-oxidation.

- Coenzymes: Riboflavin(FADH2) and Niacin (NADH)

- Oxygen needed to support ETC and recycle oxidised forms of coenzymes (FAD and NAD+)

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