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65 Cards in this Set
- Front
- Back
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What are the two types of carbohydrates? What do they include? |
Simple: Monosaccharides - (one carbon ring) glucose, fructose, galactose; Disaccharides - (2 carbon ring) lactose, sucrose, maltose Complex: Oligosaccharides - (3-9 carbon ring) raffinose, stachyose; Polysaccharides - (10 or more carbon rings) glycogen, fiber, starch |
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Describe starch, where is it found? |
Storage from of CHO in plants; alpha glycosidic bonds; amylose = straight chain with 1,4 bonds; amylopectin = branched chain with 1,4 and 1,6 bonds; found in potatoes, beans, breads, rice, pasta |
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Describe glycogen, where is it found? |
Storage form of glucose in humans/animals; alpha glycosidic bonds (1,4 and 1,6); liver glycogen can contribute to blood sugar (glucagon controls conversion into glucose); muscle glycogen stored for muscle use |
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How is glucose absorbed into the body after ingestion? |
Into enterocytes in the small intestine via the sodium-glucose transporter-1 (SGLT1); via symport with Na and therefore absorption is dependent on the concentration gradient across the enterocyte membrane created by the Na-K pump (ATP powered); aka secondary active transport |
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How is galactose absorbed into the body after ingestion? |
Into enterocytes in the small intestine via the sodium-glucose transporter-1 (SGLT1); via symport with Na and therefore absorption is dependent on the concentration gradient across the enterocyte membrane created by the Na-K pump (ATP powered); aka secondary active transport
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What is the GI capacity for absorbing glucose/galactose? |
5,400 g/day glucose 4,800 g/day galactose |
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How is fructose absorbed into the body after ingestion? |
Into enterocyte via facilitated diffusion through GLUT5 transporter; there is very little circulating fructose because it is immediately removed by the liver and trapped in a metabolic pathway to be altered |
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Fructose absorption problems? |
60% of adults cannot completely absorb fructose within range of 20-50 grams; GI distress after 50g of pure fructose; can occur with HFCS beverages |
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How is glucose transported across cell membranes throughout the body (not including into the enterocytes from intestine lumen)? |
Via glucose transporters (GLUT); substrate specific carrier proteins that change shape when glucose binds to move it across membranes, then resumes original shape |
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Different isoforms of glucose transporter |
The different isoforms are specialized to different parts of the body... GLUT1: CNS,erythrocytes GLUT2: highly effective/specialized; pancreatic beta cells, hepatocytes, enterocytes (out), kidney GLUT3: neurons GLUT4: requires insulin; adipose tissue, skeletal muscle, cardiac muscle cells |
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How do GLUT4 transporters respond to insulin? |
In the resting state, when insulin is not present, GLUT4 transporters reside in vesicles inside the cell and do not allow glucose entry; when insulin binds to the membrane receptor, a signal cascade occurs and GLUT4 is activated and migrates to the plasma membrane to allow glucose entry via facilitated diffusion |
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Insulin resistance and exercise effects on GLUT4 transporter: |
Insulin resistance occurs when insulin binding does not result in mobilization of the GLUT4 transporter, and therefore glucose stays in the blood and cannot enter the adipose tissue and skeletal muscle Exercise increases the translocation of GLUT4 receptors to the plasma membrane; caused by muscle contraction; therefore exercise can help decrease blood glucose |
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What is ATP used for in the body? |
Anabolic pathways; muscle contraction; nerve impulse conduction; pumping ions across membranes |
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Catabolism & Anabolism: |
Catabolism: breakdown of molecules into smaller ones; releases ATP Anabolism: buildup of molecules from smaller ones; requires ATP -glycogen>glucose -triglycerides>fatty acids -protein>amino acids |
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Oxidation-Reduction R(x)s |
Oxidized: Loses an electron, gains an oxygen, loses a hydrogen Reduced: Gains an electron, loses an oxygen, gains a hydrogen Dehydrogenase enzymes rely on B vitamins riboflavin (FAD) and niacin (NAD+) **NAD accepts two electrons plus H+ as it is reduced |
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Glycolysis; steps? enzymes? intermediates? products? |
Glucose converted into 2 pyruvates (pyruvic acid); = 2 NADh+ and 2 H+ and 2 ATP....... Glucose + ATP (->) glucose-6-phosphate via hexokinase, which is product inhibited to prevent too much glucose accumulation (in the liver via glucokinase, which is not product inhibited) (->) fructose-6-p via phosphoglucose isomerase (->) fructose 1,6 bisphosphate (rate limiting step, inhibited by ATP) via phosphofructokinase (->) (2) glyceraldehyde-3-p via aldolase (+triphosphate isomerase) (->) (2) 1,3biphosphoglycerate via glyceraldehyde-3-p dehydrogenase + NAD+ and P (->) (2) 3-phosphoglycerate + ATP (Mg2+ used) via phosphoglycerate kinase (->) (2) 2-phosphoglycerate via phosphoglyceratemutase (->) (2) phosphoenolpyruvate via enolase (->) (2) pyruvate via pyruvate kinase + ATP |
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Metabolic pathways of CHO metabolism, what are they? (hint: all involve glycogen and glucose) |
Glycogenesis: making of glycogen Glycogenolysis: breakdown of glycogen Glycolysis: breakdown of glucose Gluconeogenesis: making of glucose from non-CHO intermediates Hexose monophosphate shunt: making of 5-carbon monosaccharides and NADPH |
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How is glucose released from liver cells? |
Glycogen can form glucose-1-p (via isomerase) which can form glucose-6-p (via isomerase) which can form glucose (+ p) via glucose-6-phosphatase, which cleaves the p frmo g-6-p via hydrolytic release; released when blood glucose is low |
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Explain role of fructose in glycolysis |
In muscles: fructose is phosphorylated by hexokinase to form fructose-6-phosphate which can enter the glycolytic pathway; In the liver it is phosphorylated by fructokinase to form fructose-1-phosphate, which aldolase and triose kinase can split to become the 3 carbon compound glyceraldehyde-3-phosphate and dihydroxyacetone phosphate which can eventually form glycogen |
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What are the products of glycolysis? Is oxygen required? |
2 pyruvate 2 NADH and H 2 ATP (net) **Oxygen is not required, occurs in the cytosol, can be reversed |
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How is phosphofructokinase regulated? What is the effect on the rate of glycolysis? |
By ATP; when ATP is plentiful there is no need to use glucose, therefore it is more efficient to store it as glycogen; this is the rate limiting step of glycolysis |
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How does the muscle trap glucose in its cells? |
By phosphorylating it, preventing exit via glucose transporters |
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Why can liver cells offer more glucose than muscle cells? |
They can store more glucose because glucokinase is not product inhibited and is responsible for conversion of glucose into glucose-6-phosphate; in muscle cells this reaction is catalyzed by hexokinase, which is product inhibited (by glucose-6-p) |
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When is glucose oxidized? |
During glycolysis; specifically when glyceraldehyde-3-phosphate becomes 1,3-biphosphoglycerate; in this process NAD is converted NADH + H, therefore g-3-p is oxidized; catalyzed by the enzyme glyceraldehyde-3-phosphate dehydrogenase |
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Compare oxidative phosphorylation and substrate level phosphorylation |
Substrate level is directly adding P to ADP to = ATP; Oxidative occurs when ATP is generated form the electron transport chain and the oxidation of NADH and FADH2 via an electrochemical gradient |
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Describe the steps of the transition reaction. What is another name for it? What are the products? |
Synthesis of Acetyl-CoA 1. Pyruvate passes into the mitochondria 2. Pyruvate dehydrogenase converts pyruvate to Acetyl-CoA ; CoA comes from pantothenic acid -Irreversible -reduced NAD to NADH -oxidizes pyruvate -occurs in the mitochondria Products: 2 CO2; 2 NADH + H; 2 Acetyl-CoA |
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Steps of the Citric Acid Cycle (Tricarboxyic acid cycle; Kreb's cycle)? What are the enzymes involved? What is used/produced in each step? |
1. Acetyl-CoA combines with oxaloacetate via citrate synthase to form citrate; CoA is removed and reused in transition r(x) 2. (->) cis-aconitate, loses an H2O 3. (->) isocitrate, loses an H2O 4. Isocitrate is oxidized to form alpha-ketoglutarate via isocitrate dehydrogenase; NADH + H is formed, Co2 is released 5. alpha-ketoglutarate undergoes oxidative decarboxylation into succinyl-CoA via alpha-ketoglutarate dehydrogenase; produces NADH + H, release Co2 6. Metabolism of succinyl-CoA into succinate via succinyl-CoA synthase; produces GTP (which can form ATP from ADP via phosphorylation) 7. Oxidation of succinate into fumarate via succinate dehydrogenase; produces FADH2 8. (->) malate; loses H2O 9. Oxidation of malate into oxaloacetate via malate dehydrogenase; produced NADH + H and the cycle starts over |
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What steps of the TCA produce NADH? FADH2? GTP? CO2? |
NADH: 4. isocitrate -> a-ketoglutarate 5. a-ketoglutarate -> succinyl CoA 9. malate -> oxaloacetate FADH2: 7. succinate -> fumarate GTP: 6. succinyl-CoA -> succinate CO2: 4. isocitrate -> a-ketoglutarate 5. a-ketoglutarate -> succinyl-CoA
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What are the products of the TCA? From one pyruvate? From one glucose? |
From one pyruvate: 2CO2; 3 NADH + H; 1 FADH2; 1 ATP (via GTP)... So, for one glucose: 4 CO2; 6 NADH + H; 2 FADH2; 2 ATP |
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What step of TCA involves substrate level phosphorylation? |
Step 6. Succinyl-CoA -> succinate via succinyl-CoA synthase; involves direct transfer of phosphoryl group (PO3); GTP can donate P to ADP to = ATP |
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Describe mitochondria structure, how does it allow for ATP synthesis? |
Has Inner membrane and Outer membrane formed into cristae and matrix; this structure allows a separate compartment to create high concentration gradient of H (between inner and outer membrane); H gradient allows ATP to be produced via ATP synthase |
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Describe the steps of the electron transport chain (occurs in mitochondria) |
1. NADH or FADH2 transfer their electrons to the electron transport chain 2. As electrons move through the ETC, some of their energy is used to pump H into the inter-membrane space, resulting in a steep concentration gradient between the inter-membrane space and the matrix 3. H diffuse back into the matrix via ATP synthase, which is coupled with the production of ATP; the H then combines with O2 to form H2O 4. ATP is transported out by a carrier protein that exchanged ATP for ADP (antiporter) |
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How much ATP/ energy molecules are produced in every step of glucose metabolism? How much total? |
**NADH = 3 ATP; FADH2 = 2 ATP Glycolysis: 2 ATP & 2 NADH + H (6 ATP total) Transition: 2 NADH + (6 ATP total) TCA cycle/ETC (per pyruvate): 3 NADH + H; 1 ATP; 2 FADH2 (12 ATP per one pyruvate) (per every glucose) = (24 ATP total)
Grand total = 36 ATP from complete oxidation
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Why is oxygen important in the electron transport chain? What happens without it (in electron transport chain only)? How many ATP are produced in anaerobic respiration? |
Without oxygen H cannot be converted into H2O in the mitochondria matrix; therefore the H gradient is not possible; the electron transport chain cannot accept H (protons and electrons); NADH and FADH2 are unable to be oxidized and much less ATP is made (2 ATP in anaerobic respiration) |
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What stimulates glycogenesis in the liver? What inhibits it? What happens when blood glucose is high? |
Glycogenesis: stimulated via insulin; inhibited by growth hormone; = creation of glycogen from glucose; when blood glucose is high insulin is secreted from the pancreas, glucose enters cell and is phosphorylated into glucose-6-phophate, which can enter glycolysis or be used for glycogenesis |
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What stimulates glycogenolysis in the liver? What happens when blood glucose is low? |
Glycogenolysis: via glucagonor epinephrine; = breakdown of glycogen into glucose; when blood glucose is low, glucose-6-phosphate can be produced from glycogenolysis or gluconeogenesis (formation of glucose from amino acids, glycerol); glucose-6-phosphate can enter glycolysis if needed; in liver, phosphate can be removed and glucose can be released into blood |
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What affect does thermogenin have on metabolism? What is another name for it? Where is it located? What does it do? |
Thermogenin (aka uncoupling protein) is released by the thyroid hormone and causes an increase in metabolism (associated with heat generation); It is located in the brown fat in the inner mitochondria membrane; allows H to leak back into the matrix, disrupting the proton gradient and making ATP synthesis less efficient |
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What happens to pyruvate in the absence of oxygen? |
1. Pyruvate does not enter the mitochondria for the transition reaction, is oxidized to form lactate instead via lactate dehydrogenase; in this r(x) NADH + H is converted into NAD (NAD can be used in glycolysis) 2. Lactate leaves the cell and is picked up by the liver (Cori Cycle) 3. Liver cells can convert lactate into pyruvate 4. Pyruvate can eventually then be used to make glucose and glucose can be sent to muscles via the blood |
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Describe the Cori Cycle |
Lactic acid is formed in the muscles from glucose in the absence of oxygen (lactic fermentation); which then travel through the blood to the liver, where it is converted into glucose (gluconeogenesis); it can then travel back to the muscle cells (and on and on) |
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Describe the steps of glycogenesis (synthesis of glycogen) |
1. Glucose enters cell 2. It is phosphorylated by hexokinase in muscles (glucokinase in the liver) into glucose-6-phosphate; ATP is used; Gluconeogenic precursors can also form glucose-6-phosphate! 3. (->) Glucose-1-phosphate via phosphoglucomutase 4. (->) Active UDP-glucose via uridine triphosphate (UTP) 5. Then glycogenin primer changes it into unbranched glycogen which can form branched glycogen |
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Describe the steps of glycogenolysis (breakdown of glycogen) |
1. Glycogen phosphorylase releases glucose-1-phosphate from the non-reducing end of the glycogen chain 2. It is phosphorylated into glucose-6-phosphate 3. In liver only glucose-6-phosphate is converted to glucose -elsewhere in body glucose-6-p enters glycolysis |
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What are the blood sugar levels in a normal person, a pre-diabetic person, and a diabetic person (after fasting 8 hours)? |
Normal: 70-99 mg/dL Pre-D: 100-125 mg/dL Diabetic: 126 + mg/dL |
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What are the blood sugar levels in a normal person, a pre-diabetic person, and a diabetic person (2 hrs after eating)?
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Normal: <140 mg/dL Pre-D: 140-199 mg/dL Diabetic: 200 + mg/dL |
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Describe the steps of gluconeogenesis from pyruvate (backward glycolysis) |
1. 2 pyruvate (->) 2 oxaloacetate via pyruvate carboxylase; 2 ATP are needed 2. 2 oxaloacetate (->) PEP via PEP carboxykinase ; 2 GTP needed 3. 2 PEP (->) 2 3-phosphoglycerate 4. 2 3-phopshoglycerate (->) 2 1,3-biphosphoglycerate via phosphoglycerate kinase; 2 ATP needed 5. 2 3-phosphoglycerate (->) fructose-1,6-bisphosphate; NADH needed 6. (->) fructose-6-phosphate via fructose-1,6-biphosphatase 7. (->) glucose-6-phosphate 8. Which can then become glucose when the phosphate is removed |
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What can be turned into glucose via gluconeogenesis? |
Pyruvate, lactate, glycerol, oxaloacetate, glucogenic amino acids |
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What is the structure of a triglyceride? |
A glycerol connected to 3 fatty acid chains |
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How are dietary fats incorporated into chylomicrons? |
1. Bile salts emulsify fatty acids and monoglycerides, forming a micelle 2. Micelles can contact epithelial membrane of enterocyte and diffuse into them 3. Formed into triglyceride in the enterocyte 4. Triglyceride and cholesterol are surrounded in phospholipids and a protein coat, forming the chylomicron (a lipoprotein) 5. The chylomicron leaves the enterocyte via exocytosis, enters the lacteal (lymphatic system) and can deliver the triglyceride to adipose tissue for storage |
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How is fat mobilized from adipose tissue cells? |
Hormones, like adrenaline, can stimulate the breakdown of triglycerides by activating: -hormone sensitive lipase (in adipose tissue), which breaks down triglycerides into fatty acids and glycerol which can enter the bloodstream -fatty acids are shuttled into mitochondria by carnitine, where they are catabolized by beta oxidation -beta oxidation = Acetyl-CoA, NADH and FADH2 |
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Describe the process of beta oxidation, in general |
Fatty acids are broken down into 2 acetyl-CoA; each time an acetyl-CoA is broken off, 1 NADH and 2 FADH2 are produced; occurs in mitochondria |
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How does lipid catabolism fit into metabolism? |
Beta oxidation of a triglyceride can result in two acetyl-CoA which can enter the TCA and the ETC; aerobic respiration of one 18-C fatty acid yields 147 ATP (!) |
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Why are carbohydrates necessary for lipid catabolism into energy? |
Because oxaloacetate is necessary for the citric acid cycle to run, and the primary source of oxaloacetate is pyruvate (from glucose); there must be enough oxaloacetate to bind with every acetyl-CoA -excess acetyl-CoA can be used to make ketones or fatty acids -this means carbohydrates are needed to burn fat |
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Describe the process of ketone body formation |
1. Acetyl-CoA combines with acetyl-CoA to produce acetoacetyl-CoA 2. The CoA is removed, giving acetoacetate, which can become acetone or beta-hydroxybutyrate |
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Why are ketones produced? |
Some formation is normal in a healthy body; They are dervied from excess acetyl-CoA that cannot enter the citric acid cycle due to a.) low CHO (glucose) intake or b.) CHO uptake impairment (diabetes) -Ketogenesis serves as an overflow pathway to use acetyl-CoA when there is not enough oxaloacetate; they are sent to tissues via blood where they can become acetyl-CoA again and be catabolized for energy as oxaloacetate becomes available |
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What is ketosis? Ketoacidosis? |
The excess formation of ketones; it disturbs the body's Ph balance -Ketoacidosis: high amounts of ketones leading to low Ph which can cause coma and death |
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What are liporoteins made of? |
lipids and proteins |
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What are the major lipoproteins? & Where are they synthesized |
Chylomicrons: formed in intestine, enters lymph, and carries dietary fat VLDL: formed in liver, enters blood LDL: formed in blood from VLDL, transports cholesterol to cells HDL: formed in intestine and liver, transports excess cholesterol from cells to liver |
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Major components of chylomicrons v. VLDL, LDL, and HDL? |
Chylomicron = 90% triglyceride VLDL = 60% triglyceride LDL = 45% cholesterol HDL = 45% protein |
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What are apoproteins? & their functions? |
Associated with lipoproteins, easily transferred among lipoproteins in the blood -f(x)s structurally; binding site for receptors; activators/co-enzymes involved with lipid metabolism |
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What are the major apoproteins and f(x)? |
Apo-A-1: Major HDL protein; activates lecithin cholesterol acyltransferase; also on chylomicrons Apo-B-48: exclusive to chylomicrons Apo-B-100: exclusive to LDL/VLDL; binds LDL receptor Apo-C-II: activates lipoprotein lipase in VLDL, IDL, HDL, and chylomicrons Apo-C-III: inhibits lipoprotein lipase inVLDL, IDL, HDL, and chylomicrons Apo-D: in HDL; cholesterol ester transfer Apo-E: binds LDL receptor in VLDL, IDL, HDL, and chylomicron remnants Apo(a): in LDL only, bonded to B-100; forms lipoprotein(a); delivers cholesterol to sites of vascular injury |
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What is lipoprotein lipase? Where is it found mostly? What does it do? How does insulin effect its activation? |
A triglyceride hydroxylase attached to the luminal surface of endothelial cells in capillaries -has a high affinity for lipoproteins via Apo-C-II esp. triglyceride rich (chylomicrons) -mostly in fat, skeletal muscle, and heart tissue -lipoproteins bind to LPL, allowing for the breakdown (hydrolyzing) of triglycerides into FA and glycerol -many LPL can act on lipoprotein at once -various versions/isozymes in different tissues -LPL in adipocytes is activated by insulin; after several days of high carb diet, more LPL is activated (may pre-dispose for fat gain) |
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What happens to the chylomicron once it enters circulation? |
1. Recieves Apo-E and Apo-C-II from HDL 2. Interacts with LPL, giving FA and glycerol to surrounding tissues 3. Chylomicron (CMR) remnant is formed; Apo-C-II is returned to HDL; CMR is picked up in the liver (which recognizes Apo-B-48 and Apo-E) via receptor mediated endocytosis 4. Dietary cholesterol delivered to the liver in CMR can be repackaged into VLDL and sent to circulation for distribution or conversion into bile salts **dietary cholesterol inhibits cholesterol synthesis by the liver |
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How does a chylomicron eventually become LDL? What happens to the intermediates (how are they taken out of circulation)? |
1. Chylomicron broken down by LPL, remnants picked up in liver; cholesterol remnants become VLDL in liver 2. VLDL (containing triglycerides, Apo-B100 early on, Apo-CII from HDL, and Apo-E from HDL) transports triglycerides from liver to fat and muscles; once TG used it is converted to IDL 3. IDL from VLDL in blood can be converted to LDL or removed from circulation by LDL receptor 4. LDL (containing cholesterol and Apo-B100) can carry cholesterol to extra hepatic tissues such as adrenals and adipose tissue and be taken up by receptors |
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What happens to LDL ? |
It can enter cells in liver, adrenals, or adipose via LDL-receptor mediated endocytosis; LDL rceptor bind to Apo-B100 -cells that need cholesterol can take up LDL or make cholesterol -once taken up, cholesterol can be incorporated into cell membranes or stored as cholesterol ester |
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What is the role of LDL in atherosclerosis? |
LDLs can penetrate vascular wall endothelium, become deposited, and get damaged by oxidation -attract macrophages who ingest the LDL -macrophages become "foam cells" which can undergo apoptosis and release pools of lipids into the vessel wall (plaque) -cytokines and growth factors cause smooth muscle cells to form a collagenous cap -cap grown and can constrict the vessel (angina) -cap can eventually rupture and = exposure of collagen and lipids which can = heart attack or stroke |
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What is the f(x) of HDL? |
Retrieve cholesterol from tissues and return it to the liver; comes from liver and small intestine; contains protein, Apo-A1, Apo-CII, Apo-CIII, Apo-D, and Apo-E |
