After the fat is absorbed, the chylomicrons enter the liver and tissues, where they are utilized. Fat circulates in the blood and enters the liver and cells.
Table of contents
- Fate of fat in circulation
- Fate of fat in the tissues
- Fate of fat in the liver
- Role of the liver during carbohydrate deficiency
- β-oxidation of fatty acids.
Fate of fat in circulation
Lipoprotein lipase acts on the circulating chylomicrons, VLDL, and triglycerides to make free fatty acids and glycerol. This lipolysis reaction remarkably increases adipose cells’ free fatty acid and glycerol content.
Feeding increases Lipoprotein lipase activity. Therefore, more free fatty acids and glycerol enter the fat cells after feeding.
Fasting and stress decrease Lipoprotein lipase activity, so little free fatty acids and glycerol are available for the fat cells.
Fate of fat in the tissues
Hormone-sensitive lipase catalyzes stored triglycerides into free fatty acids and glycerol. As its name suggests, it is hormone-dependent.
Growth hormone, glucagon, cortisol, epinephrine, and norepinephrine increase activity.
Insulin, prostaglandin E, and feeding decrease its activity.
In this way, we observe that feeding favors fat accumulation in the adipose cells.
Fate of fat in the liver
As chylomicrons enter the liver, ‘liver lipase’ breaks it into free fatty acids and glycerol. This is a very quick reaction.
Phase I metabolism of fat
Triglycerides————–free fatty acids + glycerol.
The glycerol is utilized in the carbohydrate pathway. Glycerol in the carbohydrate metabolism may combine to form fats.
Phase II metabolism of fat.
The fatty acids are oxidized to ‘acetyl-co A’ by β-oxidation of fatty acids.
Phase III metabolism of fat.
‘Acetyl-CoA’ is usually wholly oxidized to form CO2, H2O, and energy.
‘Acetyl-CoA’ may form pyruvic acid and may form carbohydrates.
Excess ‘Acetyl-CoA’ recombines to form ketones.
Role of the liver during carbohydrate deficiency
When carbohydrate concentration decreases, the liver can increase fat metabolism to produce more acetyl-CoA and aceto-acetic acid for energy.
When carbohydrate concentration increases, the liver converts it into fats and stores it.
β-oxidation of fatty acids.
When chylomicrons enter the liver, ‘liver lipase’ breaks them quickly into free fatty acids and glycerol.
Triglycerides————–>free fatty acids + glycerol.
Fatty acids are long-chain, mainly with 16 to 18 carbon atoms, like palmitic acid, stearic acid, and oleic acid.
In the liver mitochondria, these long-chain fatty acids are broken into two carbon molecules: acetyl-CoA. A chain of 16 carbon atoms produces eight acetyl-CoA.
This is an oxidative reaction in which two carbon acetyl-CoA are serially split off from the long-chain fatty acids.
An 18-carbon fatty chain acid will form 9 acetyl-CoA.
Acetyl-CoA is an active acetate which may be used in three ways:
1. to produce energy.
2. to form ketone bodies
3. to form glucose.
4. to form fatty acids.
5. may cause acetylation reaction.
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