Lipid and ketone body metabolism Flashcards
(19 cards)
What are the 3 types of lipids?
- Triacylglycerols
- Fatty acids
- Ketone bodies
Fatty acid derivatives (4 things)
- Triacylglycerols (fuel storage & insulation)
- Fatty acids (fuel molecules)
- Phospholipids (membrane and lipoprotein components)
- Eicosanoids (local mediators, signalling)
Hydroxy-methyl-glutaric acid derivatives (4 things)
- Ketone bodies (water soluble fuel molecules)
- Cholesterol (membranes and steroid hormone synthesis)
- Cholesterol esters (cholesterol storage)
- Bile acids and salts (lipid digestion)
Triacylglycerol key points (5 things)
- Hydrophobic
- Stored in anhydrous form
- Stored in adipose tissue
- Utilised in prolonged exercise, starvation, pregnancy
- Storage/mobilisation under hormonal control
What is the esterification of triacylglycerols promoted by?
Insulin
What is the lipolysis of triacylglycerols promoted by (5 things)?
- Glucagon
- Adrenaline
- Cortisol
- HGH
- Thyroxine
Dietary triacylglycerol metabolism (3 things)
- Stage 1
- GI tract
- Extracellular: pancreatic lipase, bile salts and colipase
Fatty acids key points (5 things)
- Converted back to triglycerides in GI tract
- Packaged into lipoprotein particle, chylomicron
- Released into circulation via lymphatics
- Carried to adipose tissue and stored as triglycerides
- Carried to tissues as albumin-fatty acid complex when needed
Fatty acid activation (3 things)
- In cytoplasm
- Linked to CoA by action of fatty acyl CoA synthase
- Activated fatty acids don’t readily cross inner mitochondrial membrane
Carnitine shuttle (5 things)
- Transports fatty acyl CoA across mitochondrial membrane
- Carnitine converted to acyl carnitine then back again via carnitine acyl transferases (CAT1&2)
- Regulated by AMP, insulin
- Inhibited by malonyl~CoA so fatty acids not used up instantly
- Defects can occur (exercise intolerance, lipid droplets in muscle)
Beta oxidation (6 things)
- Recycled through reaction removing a C2 unit until only 2 C remain
- Ultimately generates acetyl~CoA and reducing power (NADH & FADH2)
- Occurs in most tissues and WBC
- Stops in absence of O2
- Regulated by AMP (insulin-liver)
- No direct ATP synthesis
Ketone bodies key points (5 things)
- Soluble
- Produced when acetyl CoA is in excess
- Used by peripheral tissues (muscle)
- Alternative fuel to glucose (e.g. brain)
- Acidic
Ketosis concentrations key points (4 things)
- Normal concentration is <1 mM
- Starvation is 2-10 mM (physiological ketosis)
- Untreated type 1 diabetes >10 mM (pathological ketosis)
- Sweet smell in breath due to acetone excretion from lungs
Ketone body synthesis in liver mitochondria (3 enzymes)
- Synthase
- HMG~CoA reductase
- Lyase
What is needed for ketone body synthesis (2 things)?
- Fatty acids for oxidation in LIVER following excess lipolysis in ADIPOSE
- Low plasma insulin:glucagon ratio
Control of ketone body production liver (3 things)
- NADH product inhibition
- Catalysed by:
- isocitrate dehydrogenase
- alpha-ketoglutarate dehydrogenase
Ketone body synthesis- fed state (3 things)
- Insulin:glucagon ratio high
- Lyase inhibited and reductase activated
- Cholesterol synthesis (from melavonate)
Ketone body synthesis- starvation (3 things)
- Insulin:glucagon ratio low
- Lyase activated and reductase inhibited
- Ketone body synthesis
Examples of ketone bodies in body (4 things)
- Acetoacetate
- Beta-hydroxybutyrate ( from acetoacetate)
- Melavonate (in fed state to make cholesterol)
- Acetone (excreted via lungs)
