Created by Evian Chai
over 4 years ago
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Question | Answer |
What are the three steps of fatty acid synthesis? | 1. Acetyl CoA from the cytosol is transported into the mitchondria membrane 2. Malonyl CoA synthesis from acetyl CoA 3. Fatty acid chain Synthesis |
How is acetyl CoA transported into the mitochondrial membrane? | It combines with oxoloacetate to form citrate, which enters the membrane It then breaks down into Acetyl CoA+oxoloacetate again |
How is acetyl CoA converted to Malonyl CoA? What enzyme catalyses this? What is this rxn stimulated by? | 1. Acetyl CoA+HCO3- --> Malonyl CoA (ATP-->ADP+Pi) 2. Acetyl CoA carboxylase 3. Stimulated by insulin |
What is the rate limiting step of Fatty Acid Synthesis? | The conversion of acetyl CoA to malonyl CoA |
What are the two purposes of Malonyl CoA? | 1. Precursor to fatty acid chain 2. Inhibits cartinine transferase, which is important for fatty acid oxidaton (so lowered oxi. of fats) |
How is malonyl CoA converted to a fatty acid chain? What type of reaction is this? What enzyme is required? | 1. Malonyl CoA+Acetyl CoA-->Fatty acid chain 2. Reduction reaction (requires NADPH) 3. Fatty Acid Synthase |
Triacylglycerol (TAGs) are made of what? | A glycerol (G3P) + 3 fatty acids |
What are the four sources of G3P for TAG synthesis? | 1. Glycerol from glycerol kinase 2. Oxoloacete-->DHAP-->G3P via TCA cycle 3. Amino acids (fumarate/pyruvate) via TCA 4. Reducing NADH via G3P Dehydrogenase |
Where in a lipoprotein are TAGs, cholesterol and esters located? | Inner layer of lipoprotein |
Where in a lipoprotein are apoproteins and cholesterol located? What else is in the layer? | Out layer Phospholipid Bilayer |
Which of the TAGs are the largest, have the lowest density, and mainly come from dietary sources? | Chylomicrons |
Where are chylomicrons formed? What are packaged together to form one? | In the SER of epithelial cells in the small intestine - TAGs, cholesterol, cholesterol esters, B48 |
What is the role of Apoprotein B48? | Transports Chylomicron to lymphatic system |
What does a chylomicron pick up in the circulation? | ApoE ApoC2 Both picked up from HDL |
When a chylomicron breaks down in the capillaries, what are the three components and where do they go? | 1. ApoC2 returns to HDL 2. B48/ApoE is reuptaken by ApoE receptors on liver 3. TAG is broken down by lipoprotein lipase into glycerol+fatty acid |
What happens to glycerol after it is seperated from TAGs? | Goes to liver for gluconeogenesis |
What happens to the fatty acids from TAGs? | Fatty acids enter adipocytes (tissue) for esterification into TAGs |
What activates the lipolysis of TAGs? What enzyme is used? | 1. Insulin/ApoC2 2. lipoprotein lipase |
Which lipoprotein mainly carries endogenous TAG from the liver? | VLDL |
Where is VLDL from and what are packaged together to form it? | From liver to tissue TAGs, cholesterol, cholesterol esters and B100 packaged together |
What does VLDL pick up in the systemic circulation? | ApoC2 ApoE Both from HDL |
What does VLDL break down to in the capillaries? | 1. TAGs 2. Intermediate Density Lipoprotein (IDL) |
What happens to IDL? | Doesn't live very long Returns ApoE/ApoC2 to HDL |
What is LDL made of and what happens to it? | 1. Made of TAGs+B100 2. 50% goes to liver, 50% goes to peripheral tissue via B100 receptor |
How does LDL deliver cholesterol to peripheral tissues via the B100 receptor? | 1. Enters via endocytosis 2. Lysosome breaks down LDL, leaving cholesterol 3. Cholesterol enters nucleus |
What does cholesterol normally do in the nuclues? What can obstruct this process? | 1. It inhibits the synthesis of enzymes that produce cholesterol, thus lowering cholesterol production 2. A deficiency in B100 receptors can lead to high LDL levels/arteriosclerosis |
Which Chylomicron is a shuttle for apoproteins and delivers cholesterol from tissue to liver? | HDL |
What converts Nascent HDL to HDL? What is required for this reaction? | LCAT ApoA1 |
How does HDL transport cholesterol from tissue to liver? | 1. HDL uptakes cholesterol from peripheral tissue 2. Cholesterol combines with fatty acids to become cholesterol esters 3. Delivered to liver for elimination |
What are 3 genetic causes for elevated lipid levels (hypercholesterolaemia/hypertriglyceridaemia)? | 1. Defective LDL (B100) receptor increases LDL in blood 2. Lipoprotein lipase deficiency increases chylomicrons/VLDL in blood 3. ApoC2 deficiency so lipoprotein lipase cannot be activated |
What are three secondary causes of elevated lipid levels? | 1. Obesity 2. Diabetes II 3. Dietary fatty acid |
What is lipoprotein A? What does it do? It's levels are increased by what? | 1. It is LDL+ApoA 2. Slows breakdown of blood clots by competing with plasminogen/fibrin, increases CHD risk 3. Increased by transfat/cholesterol |
To prevent the synthesis of cholesterol, which enzyme must be inhibited? What inhibits it? | 1. HMG-CoA reductase, because it catalyses the rate limiting step in the conversion of acetyl CoA to cholesterol 2. STATINS can inhibit it |
What do the following do? ApoB48 ApoC2 ApoE ApoB100 ApoA1 | 1. Apo48 Transports chylomicrons into the lymphatic system 2. ApoC2 Initiates the hydrolysis of TAGs for absorption 3. ApoE Enables reuptake of remenants 4. ApoB100 binds to LDL receptors allowing for uptake in tissue 5. ApoA1 activates LCAT to convert nascent HDL to HDL |
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