813548
Description
Flashcards by Hannah Tribe, updated more than 1 year ago
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Created by Hannah Tribe
almost 10 years ago
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| Question | Answer |
| How are free fatty acids formed? | From the mobilisation of triacylglycerides in adipocytes. |
| How do free fatty acids circulate around the body? | Bound to proteins (often albumin) as a Na+ salt |
| How do fatty acids enter cells? | Simple diffusion as they are lipophilic |
| Why are intracellular concentrations of FFA kept low? | they have detergent activity |
| How are most lipids transported in the circulation? | As lipoproteins |
| Name the 5 types of lipoprotein | 1. Chylomicrons 2. VLDL 3. LDL 4. IDL 5. HDL |
| What are the constituents of a lipoprotein? (5) | 1. Apolipoprotein 2. Cholesterol 3. Phospholipids 4. Triacylglycerols 5. Cholesterol esters |
| What is the predominant component in chlyomicrons? | Triglycerides |
| Each lipoprotein has its own set of unique ______________, but some are in common with each other. | Apolipoproteins |
| Give 4 functions of apoproteins | 1. Give structure to lipoproteins 2. Solubilise lipids so they can be transported in blood 3. Can act as enzymes or enzyme cofactors 4. Target specific receptors |
| In the gut, when fats are ingested, ________ enzymes breakdown triacylglycerides to ______ ______ and _______________, so they can diffuse across the membrane into the intestinal mucosa. Here they reform into ______________ and bind with other lipids and the appropriate _____________ to form __________________. | lipase, fatty acids, monoacylglycerol, triacylglycerides, apoplipoproteins, chylomicrons |
| Chylomicrons have a very low density due to high levels of _____________ | Triglycerides |
| In which part of the cell are the apoproteins added? | SER |
| How are the chylomicrons secreted from the cell and where do they enter next? | Secreted by reverse pinocytosis into the lymphatics |
| What is the characteristic of Type 1 Hyperlipidaemia? | High plasma triglycerides |
| What causes this? | Deficiency in lipoprotein lipase or Apo C2 (binds to lipoprotein lipase) |
| What is the characteristic of Type 2 Hyperlipidaemia? | High LDL |
| What is the most common cause of this? | Genetic defect with the LDL receptor |
| What is the most common form of hyperlipidaemia, what is its characteristic and what causes it? | Type 4 - characterised by high VLDL due to obesity or alcohol abuse |
| Which fat-soluble vitamins are also present in chylomicrons? | A and E |
| Why is it useful to have vitamin E in the chylomicrons? | It is an anti-oxidant so prevents chylomicrons being oxidised, as this would make them more reactive and more likely to contribute to atherosclerosis. |
| What is the lifetime of a chylomicron and how are the remnants removed? | 1 hour, remnants removed by the liver |
| Where are VLDLs synthesised? | Liver ER and Golgi |
| VLDLs are ___________ as they circulate by the enzyme __________ ________. | metabolised, lipoprotein lipase |
| What 4 factors enhance the formation of VLDLs? | 1. Carbohydrate in the diet 2. Circulating FFA 3. Alcohol 4. Raised insulin/decreased glucagon |
| In the same way as chylomicrons, remnants of VLDLs are removed by the _________ by _____ ___ | liver, Apo E |
| After ______ enzymes have acted upon VLDLs, _____s form. These are the major carriers of __________, carrying it to the peripheries and regulating its sythesis. It is metabolised slowly in approx ___ days. | lipase, LDL, cholesterol, 3 |
| Where are HDLs made? (2) | Liver and intestine |
| What is the function of HDLs? | Remove cholesterol from the tissues and carry it back to the liver, or transfer it to VLDLs or LDLs using cholesterol ester transfer protein. |
| Where else do HDLs go? | Steroid-producing organs, such as adrenal glands, ovaries and testes. |
| Which apoprotein allows HDLs to bind to other lipoproteins and cells? | Apo E |
| Why are LDLs termed 'bad cholesterol'? | They can be deposited in vessel walls to contribute to atherosclerosis. |
| What are the 2 receptor mechanisms which mediate uptake into cells by endocytosis? | 1. High affinity LDL receptor 2. Low affinity scavenger receptor |
| What is the mechanism of action of the LDL receptor? | When the LDL binds to it, endocytosis occurs to produce a vesicle inside the cell. This fuses with a lysosome, then the LDL receptors break off in their own vesicle and return to the membrane by exocytosis. The lysosome breaks down the LDL to release amino acids, fatty acids and cholesterol esters into the cytoplasm. |
| What regulates cholesterol uptake and synthesis? | Cholesterol itself |
| High levels of cholesterol have what effect? | Inhibit the enzyme HMG-CoA reductase |
| What effect does this have? (2) | Inhibits de novo synthesis of cholesterol, and reduces expression of LDL receptors. |
| What do statins do? | Inhibit HMG-CoA reductase so prevent cholesterol synthesis. |
| What can cause loss of LDL receptor function? | Familial Hypercholesterolaemia (FH) |
| What 4 things can this cause? | 1. High serum cholesterol levels 2. Atherosclerosis 3. High risk of heart attack at young age 4. Unregulated synthesis of cholesterol (not regulated by LDLs) |
| Where are scavenger receptors located? (3) | 1. Endothelial cells 2. Macrophages 3. Vascular Smooth Muscle Cells |
| Give 2 reasons why these are different to LDL receptors. | 1. Low affinity 2. Not regulated by cholesterol |
| Name 3 things that regulate lipoproteins? | 1. Hormones (e.g. insulin, cortisol) 2. Nutrition (high fat diet, fasting) 3. LDL expression (lowered by oestrogen) |
| What are 3 causes of abnormal lipid transport? | 1. Diabetes Mellitis (increased mobilisation of FFA) 2. Genetic defects (leading to hypercholesterolaemia, atherosclerosis etc.) 3. Obesity (leading to hypertension, NIDDM, hyperlipidaemia etc.) |
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