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Indicate the importance of triglyceride fat for long term fuel storage

The amount of glucose in the blood has to be kept at a limit, and constant, this is because glucose is reactive and so we wouldn’t want too much of it in the blood. Therefore, after a meal, when we have a lot of glucose in the blood, insulin will be produced in the B cells of the pancreas, and will stimulate both the liver and muscle to form glycogen out of the extra glucose. If glucose still remains after the stores of glycogen are replenished, the excess will then be converted into fat for long term storage. Fat is formed in the liver.

We know the structure of triglycerides is an esterified glycerol backbone, with three fatty acids attached to it. There are many different types of fatty acids: they can have different lengths, different amounts of double bonds-desaturation. The liver is capable of converting acetyl CoA from the link reaction into different types of fatty acids, which can then be added to glycerol. However, we do not have enzymes that are capable of desaturating the fatty acid chains, but because some of these fatty acids are essential to the body; they become ESSENTIAL fatty acids.

Examples of this are Oleic acids (from olive oil) which is C18 unsaturated and Elaiolic acid C18 unsaturated, trans acid.

Linoleic acid is C18:2

Linolenic acid C18:3

Fat storages are important because even though it does take energy to perform lipogenesis, the benefit of not having excess glucose in the blood and having energy storages when needed outweighs this cost. Fat yields about twice as much energy as glucose.

It is important to note that free fatty acids cannot remain truly “free” in the blood – they are attached to albumin.

It is also important to note that fatty acids from fat can act as fuels for muscles, the liver and especially the heart which uses exclusively fatty acids for energy.


Describe the role of adipose tissue lipase in the breakdown of triglyceride into fatty acids and glycerol

Because fat is stored in adipose tissue, its breakdown starts in adipose tissue. This process is activated by ADRENALINE and GLUCAGON (both fasting hormones).

  1. TRIACYLGLYCEROL LIPASE converts triacylglycerol into diacylglycerol and a fatty acid (the fatty acid can travel in the plasma bound to albumin)

  2. DAG LIPASE then converts diacylglycerol into monoacylglycerol and a fatty acid

  3. MAG LIPASE then converts monoacylglycerol into glycerol and a fatty acid.

We saw that the fatty acids all travelled in the blood bound to albumin. But what happens to the glycerol?

Glycerol is water soluble so can be taken up by all tissues, where it can

  1. enter the glycolysis pathway for conversion into pyruvate (and then possibly the TCA cycle)

  2. enter the glycolysis pathway in the liver and be converted into glucose by gluconeogenesis (in cases of fasting or starvation)

NOTE: glycerol is the only part of the triglyceride which can be converted back into glucose. You CANNOT CONVERT FATTY ACIDS INTO PYRUVATE


Describe how fatty acids are activated to their CoA esters, and how they are transported into mitochondria via the carnitine shuttle system


What is needed for fatty acid synthesis:

1. For it to be able to enter into the mitochondrionwhich is not permeable to fatty acids. For this to happen CARNITINE is used: carnitine can be recognised by a carnitine palmitoyl transferase which can allow it and its attached fatty acid to enter the cell.


Coenzyme A forms THIOESTER bonds with carboxylic acids. What this means is that a CoASH (coenzyme A) binds with the fatty acid via an ACTIVATING ENZYME (ATP is used)

  1. This fatty acyl CoA needs to move into the mitochondrion so it is conjugated to CARNITINE by CARNITINE ACYLTRANSFERSE I

  2. Acyl carnitine is shuttled inside via CARNITINE PALMITOYL-TRANSFERSE I


Acyl carnitine is converted back into acyl CoA by CARNITINE ACYLTRANSFERSE II located on the inner mitochondrial membrane

  1. The liberated carnitine can move back out into the cytosol

2. The actual processing of this fatty acid. Its oxidation (B-oxidation) happens in the mitochondrion in the following steps:

  1. Activation by ATP

  2. Oxidation of two H+ atoms given to FAD

  3. Hydration

  4. Oxidation of two H+ atoms given to NAD+

  5. Thiolysis: removal of a 2C unit = acetyl CoA which can enter the TCA cycle and be fully oxidised

All these steps are repeated again and again, as two C atoms are removed each time. So for example, a fatty acid with 16C atoms will produce 8 acetyl CoA molecules, with an ATP yield of 8*10(per TCA cycle) = 80 ATP.

Add to that the 7 repeats of B-oxidation producing 7NADH+H+ and 7FADH2, with 2.5ATP and 1.5ATP respectively, about 106ATP molecules are formed from a 16C fatty acid.

If a fatty acid has an odd number of Carbon atoms, a HCO3- molecule is added to make it four membered. An enzyme requiring COBALAMIN (B12) is required for this. (Cobalamin is called that because it has a Co, cobalt group in it).


Describe the enzyme reactions of the beta-oxidation pathway that yield acetyl CoA, NADH+H+ and FADH2

Removal of 2H atoms from the fatty acyl CoA by acylCoA dehydrogenase leads to FADH2 production.

Removal of 2H atoms from 3-L-Hydroxyacyl CoA by 3-L-hydroxyacyl CoA dehydrogenase produces NADH+H+ (in this step, there are now two keto groups on the B-ketoacyl CoA molecule, which makes it unstable and likely to be cleaved.

Indicate how the process yields ATP when linked to oxidative phosphorylation


Summarise the factors regulating fatty acid oxidation

  1. ADRENALINE and GLUCAGON activate the lipase enzyme (that starts cleaving the triglyceride)

  2. The rate of entry into mitochondrion via the CARNITINE SHUTTLE is a rate limiting factor

  3. The rate of reoxidation of the cofactors NADH+H+ and FADH2 by cytochrome/respiratory chain

There are about 135,000 kcal of triacylglycerols in our adipose tissue.


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