What are the 3 classes off lipids?
- Fatty acid derivatives (TRIACYLGLYCEROLS, FATTY ACIDS and phospholipids)
- Vitamins (a, d, e, k)
- Hydroxymethyl glutaric acid derivatives - HMG (KETONE BODIES, cholesterol, bile acids and salts)
What is triacylglycerol broken down into? And what happens to the products?
Fatty acids and glycerol (enzyme: lipase)
Glycerol - goes into glycolysis to produce pyruvate
Fatty acids - undergo beta-oxidation to produce Acetyl-CoA
What is the process of beta-oxidation?
Oxidation of fatty acid to smaller chain fatty acid and Acetyl-CoA (which goes into the TCA cycle) producing one FADH2 and one NADH in the process.
Beta-oxidation continues until fatty acid fully broken down (loses 2 carbons to Acetyl-CoA each time) so if C18 molecule, 8 Acetyl-CoA produced and 7 NADH and FADH2.
Fatty acid + ATP + CoA
Where does and doesn’t beta-oxidation occur?
Beta-oxidation occurs in the mitochondria.
There’s no beta-oxidation in the brain or RBC (as no mitochondria in RBC)
What can Acetyl-CoA go on to produce?
Fatty acids, products of the TCA cycle and HMG (hydroxymethyl glutaric acid)
What is Acetyl-CoA produced from?
Fatty acids (beta-oxidation)
Sugars (from pyruvate - using pyruvate dehydrogenase)
Amino acids
Alcohol
How are ketone bodies produced?
- Acetyl CoA to hydroxymethyl glutaryl CoA (HMG-CoA) using synthase
- HMG-CoA to acetoacetate using lyase
- Acetoacetate to acetone or beta-hydroxybutyrate (reduction)
All those in step 3 are ketone bodies
How are ketone bodies converted into Acetyl CoA?
The reverse of ketone body production
Where in the body are ketones produced?
The liver
Where are triacylglycerides broken down into fatty acids?
In adipose tissues
How is ketone body synthesis regulated by glucagon and insulin?
If high insulin levels, synthesis is inhibited (lyase is inhibited) but synthesis of cholesterol (different pathway from HMG-CoA) is activated (reductase is activated).
If high glucagon levels, synthesis is activated (lyase is activated) and synthesis of cholesterol is inhibited (reductase is inhibited).
Why do insulin and glucagon levels affect ketone body synthesis?
If high insulin, after eating food, so lots of glucose to use in the body so Acetyl-CoA is produced and used following glycolysis.
If high glucagon, starvation, less glucose in body so fat is mobilised to provide energy - ketone bodies are produced and transported to cells needing energy, provides Acetyl CoA when broken down for the TCA cycle.
Clinical links of ketone bodies:
Someone with lots of ketone bodies (ketoacidosis) could have type one diabetes (insulin not produced/not recognised, so no inhibition of ketone body synthesis).
Can tell if have high ketone bodies in blood by ketonuria (ketone bodies in urine) or acetone smell on breath
What transports fatty Acetyl-CoA across the mitochondrial membrane?
Carnitine shuttle transporter
