energy release from fat

what are 3 biological functions of lipids

1.  components of cell membranes (phospholipids & cholesterol)

2. precursors of hormones: cholesterol → steroid hormones,   arachidonic acid → prostaglandins

3. long term fuels (triglycerides)

compare carbohydrates, fats, proteins as fuels how much energy per gram speed to mobalise

1g fat = 38kj 
1g of carbs = 17kj
1g protein = 21kj 


fat is slower to mobalise energy that carbs

structure of triglycerides and what makes it a usefull effecient fuel

 -
-  it has glycerol and a fatty acids 
- saturated: no double bonds 
- unsaturate: double bonds
- they have compact storgae as its stored as fat droplets making it an effecient fuel
e.g 

palmitic acid C 16 single bonds

stearic acid C 18 single bonds

how are triglycerides broken down

Quick summary of triglyceride breakdown and why it is called beta oxidation

1. 
   triglyceride break down into fatty acid+ glycerol 

2. fatt acid activated : fatty acid + Coenzyme A → Fatty acyl-CoA

3. Fatty acyl-CoA cant pass through mitchondrial memebrane into mitchondria where its needed so uses carnitine shuttle 

4. fatty acids break down  with beta oxidation making acetyl co a 

5. the aetyl co a can go into the TCA cycle then oxidative phosphorylation any extra can be converted to ketone bodies in the liver

the hydrogen is removed from the beta carbon of fatty acyl-coamaking acetyl co a
 

How is glycerol metabolised

• in most tissues it goes into glycolysis into pyruvate then TCA cycle to oxidise to CO2

• in liver and starvation it goes to glycolysis then glucogenesis to make glucose

How are long fatty chain fatty acids activated

Coezyem A makes high energy thioester bonds with carboxcylic acid 

What are the steps in the carnitine shuttle and why do we have it

the fatty acids change to fatty acyl-coA cant cross the mitchondrial membrane and it can only cross as Fatty acyl-carinitine 
and we need to be in the mitchondria to do the beta oxidation to break down the fatty acid

1. Fatty acyl-CoA freely diffuses across the outer mitochondrial membrane.

2. Carnitine acyltransferase I (on the outer membrane) transfers the fatty acid group to carnitine, forming fatty acyl-carnitine.

3. Fatty acyl-carnitine crosses the inner mitochondrial membrane via a translocase.

4. Carnitine acyltransferase II (on the inner membrane) switches carnitine back for CoA, regenerating fatty acyl-CoA in the matrix.

5. Carnitine is transported back into the intermembrane space for reuse.

now the fatty acyl-coA is in the mitchondria ready fro beta oxidation

Overview of beta oxidation pathway

1. removal of 2H
2. addition of water
3. removal of 2H
4. removal of 2C

What is the beta oxidation pathway

1. 

- the product is enoyl-CoA
2.

- addition of water
3.

- remove 2 hydrogen 
4.

- remove 2 carbons

How to know how many cycles of beta oxidation a fatty acid goes through

• 2 carbons removed per cycle, you need to end with a 2 carbon fragement 

• (number of carbons/2)-1

How to calculate the energy yield from fatty acid oxidation

• calculate how many ATPs made

in beta oxidation 

• NADH makes 2.5 ATP 

• FADH2 makes 1.5 ATPs

• each cycle makes one of NADH and FADH2

in TCA cycle 

• 10 ATP per acetyl CoA ( the amount of cycles of beta oxidation+ 1 is the amount of acetyl co a made.

total: TCA cycle+beta oxidation -1 ( because of the ATP used when trying to move the fat into the mitchondrial membrane)

When you metabolise odd number carbon chains in beta oxidation, what problem occurs and how is it dealt with

• normally you remove 2 carbons until end and your left with 2 carbon acetyl-CoA but now instead you are left with a 3 carbon 

• carboxylase adds another carbon with carbond dioxide so it is even

  - uses an ATP so energy release from odd number fatty acidss not as efficient

• this makes succinyl-CoA that goes into the TCA cycle

What 3 factors regulate fat metabolism

1. rate of releasing the fatty acid from adipose ( fatty) tissues is determined using the enzymes adrenaline and glucagon 

2. rate of entery into mitchondria via carnitine shuttle 

3. rate of reoxidation of cofactors NADH and FADH2 by electron transport chain ( needed from the removal of the 2H in beta oxidation)

What is ketone body formation (ketogenesis) and when does this happen

• when the liver converts excess acetyl-CoA ( from fatty acid oxidation) into ketone bodies which can be used as an energy source for other tissues e.g liver)

• acetoacetate and B hydroxybutyrate is realesed into blood stream 

• happens in: stravation, type 1 diabetes 

Why can’t red blood cells oxidise fatty acids or ketone bodies (only glucose)

dont have mitchondria

Why can’t the brain oxidise fatty acids

it doesnt have enzymes needed for beta oxidation

Why can’t the liver oxidise ketone bodies

it doesnt have enzymes needed to change ketone to acetyl-CoA for energy so dont have the enzymes to oxidise ketone bodies