TUT 7 Flashcards
(11 cards)
Which of the two nutritionally essential fatty acids gives rise to the synthesis of arachidonic acid?
- Alpha linolenic acid (omega 3)
- Linoleic acid (omega 6) –> GIVES RISE TO ARACHIDONIC ACID
Omega 3 = first double bond at 3rd carbon
Omega 6= first double bond at 6th carbon
Draw a C20:5 ω3 fatty acid. How else can you write this?
Interpretation: 20 carbons, with 5 double bonds, beginning from the 3rd carbon from the end
What are sphingolipids
Any member of a class of lipids containing the organic aliphatic amino alcohool sphingosine –> used to form ceramides
>concentrated in brain and nervous tissue
>found in membranes of both animal and plant cells
>cellular regulation, signalling and metabolism. In nerve tissue (faster action potential)
Draw structure of cholesterol
Draw and Label the general structure of a Lipoprotein:
What is the end product of beta-oxidation
Catbaolic process by which fatty acid molecules are broken down in the mitochondria to generate acetyl-CoA, which enters the citric acid cycle and NADH and FADH2, whicha are co-enzymes used in the electron transport chain
Why can ketonaemia occur in Type I Diabetes mellitus but is less likely in type II diabetes mellitus sufferers?
- No insulin, glut 4 transporters cant be used to allow uptake of glucose via adipocytes and skeletal muscles
- Body is in starved state as no glucose is entering the cells so glucose is made through the breakdown of TG
- TG breakdown into glycerol and FFA, glycerol stimulates gluconeogeneis in the liver
- FFA passes through the celll membrane, FFA is converted into acyl COA which then becomes acetlyl COA via beta oxidation
- Acetly CoA goes into the TCA cycle –> overwhelming of the TCA cycle end up with overproduction of ketone bodies
Discuss development of hyperlipidaemia in diabetic patients
Due to resistance/lack of insulin, cells produce more glucose as they cannot ‘see it’. One of these process include breaking down of fat cells
- Triglyceride to glycerol and fatty acids
- Fatty acids > Acyl-CoA > Acetyl-CoA > VLDL
How is cholesterol removed from the body and what are its breakdown products?
- Cholesterol is primarily excreted from the body in bile salt
- Unesterified cholesterol from cell membrane is drawn from the cell by an esterification reaction which is faciliated by activated LCAT
- LCAT is bound to HDL and is activated by Apo-A1, as cholesterol in HDL becomes esterified, it creates a conc gradient and draws in cholesterol from tissues and other lipoproteins, thus enabling HDL to function in reverse cholesterol transport
- NO BREAK DOWN PRODUCT –> more a precursor for vit D, hromones, bile acid
- Excess cholesterol is eliminated from the body via liver, where it will be redistributed to other tissues
- Bile acid and bile salts is thhe end products
Outline difference between the LDL receptor and the macrophage scavenger receptor
LDL receptors
- Take up LDL
- Down regulated when cell has enough cholesterol
- On tissues (liver and extrahepatic tissues)
Scavenger receptors
- Non-specific and non regulated
- Takes up oxidised LDL
- On macrophages
- Breakdown of LDL is not fast enough and can lead to accumulation of fatty acids (becomes fatty streak and form cells –> part of atherosclerosis plaque)
Outline the mechanism of action of each of the following: rosuvastatin, ezetimibe, fenofibrate, evolocumab, cholestyramine, whilst showing an understanding of lipid metabolism
Cholestyramine: Anion exchange resins, bind bile acids in intestine, decrease absorption of exogenous cholesterol and increase metabolism of endogenous
Evolocumab: Injected human monoclonal antibody, binds to PCSK9 and inhibits PSCK9 from degrading LDL receptros (increased number of LDL receptor, increased uptake of LDL, reduce LDL in blood)
Ezetimibe: potent cholesterol absorption inhibitor –> leads to increased demand for cholestrol (inhibits transport of cholesterol across intestinal wall and thereby prevents it from getting to plasma
Fenofibrate: Activates gene transcription factor PPAR-alpha (increase in lipoprotein lipase activity –> breaks down fat)
Rosuvastatin: Completely inhibits HMG CoA reductase by product inhibition (increased expression in LDL receptors) –> inhibits rate limiting step of cholesterol synthesis
