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KIN217 exam

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University of Waterloo
KIN 217
Ken Stark

Lecture 145 questions 1. -Fats are the major source of energy in liver and muscle, not RBC or brain -TAGs are the storage form 2. In blood fats are transported by albumin -In cytosol fats are transported by fatty acid binding proteins 3. a) In the muscle, fats are metabolized by the TCA cycle and oxidative phosphorylation b) In the liver, fats are metabolized by converting into ketone bodied 4.Fat metabolism is controlled by the rate of lipolysis which is regulated by insulin, glucagon, cortisol and epinephrine 5. Short/Medium Chains- diffuse through passive diffusion Long Chains- diffuse through the carnitine shuttle Very Long Chains- diffuse through beta oxidation 6. Carnitine Shuttle: -acetyl-CoA is switched with carnitine, which diffuses across the mitochondrial membrane to the inner membrane where the carnitine is then switched back to a acetyl-CoA 7. B-Oxidation: -B carbon is oxidized to a ketone, each cycle forming NADH, FADH2, and fatty acyl-CoA -cycles continue until all C’s have been turned to acetyl-CoA -last step is performed through thiolase - alpha and beta carbons combine with a double bond, which is then broken by water and hydroxyl groups is turned into a double bonded oxygen thiolase then split it into acetyl-CoA and fatty acyl-CoA acetyl-CoA moves into the TCA Cycle and fatty acyl-CoA is regenerated 8. monounsaturated fats- isomerase shifts the double bond polyunsaturated fats- isomerase shifts the double bond while some are reduced to saturated bonds 9. excess acetyl-CoA goes through ketogenesis since oxaloacetate is in excess 10.  combines 3 acetyl-CoAs and releases 2 acetyl-CoAs  acetoacetyl-CoA forms acetoacetate which then splits into acetone and beta- hydroxybutyrate forming NAD and CO2 then transferred into the blood 11. ketogenesis is the opposite, beta-hydroxybutyrate forms acetoacetate acetoacetyl-CoA is formed from acetoacetate acetyl-CoA is then formed form acetoacetyl-CoA  acetyl-CoA then enters the TCA cycle to be used for energy 12. glucagon promotes catabolism and inhibits anabolism -insulin promotes anabolism and inhibits catabolism Lecture 15 8 questions 1. a)Preparatory Stage: - fatty acid-macoconyl-CoA a)carboxylation: biotin dependant, requires ATP b)regulation of acetyl-CoA carboxylase: -citrate polymerizes into its active form, continues until 16:0 is formed and then this is inhibited b)Fatty Acid Synthase: - elongates the fatty acid  acetyl- CoA forms a –SH residue malonyl-CoA shifts to the –SH site (pan group) acetyl-CoA is shifted to the –SH site double bond is eliminated  C is shifted to the –SH residue -each cycle adds 2 C’s, goes until 16:0 is made and released 2. NADH NAD is formed when going from oxaloacetatemalate by malate dehydrogenase NADPNADPH is formed when going from malatepyruvate by malic enzyme 3. Malate shuttle: -acetly CoA is produced in the mitochandria but fatty acid synthesis occurs in the cytosol -acetyl CoA cannot diffuse across the mitochandria membrane must be converted to citrate  oxaloacetate+ acetyl-CoAcitrate -diffuses across mitochondrial membrane to cytosol citrate oxaloacetate + acetyl-CoA -oxaloacetate is converted to malate which then diffuses back into the mitochandria or is converted to pyruvate -acetyl-CoA is converted to malonyl-CoA to start fatty acid synthesis 4. fatty acids can be elongated by malonyl-CoA as well as desaturase enzymes 5. TAGS are synthesized by glycerol (liver) and glucose (Adipose tissue)  form G-3-P G-3-P phosphatidic acid DAG TAG VLDL (secreted by liver) -uses 1ATP and 3 acetyl-CoA -occurs on the smooth ER 6.when feedings occurs insulin production is increased which stimulates glycolysis, increasing pyruvate production  pyruvate acetyl-CoA TCA Cycle Citrate -citrate is the regulator which increases fatty acid synthesis Lecture 16 7 Questions 1. lipoproteins transport TAGs and cholesterol between organs and tissues -core= TAGs -outer layer= ampiphatic phospholipids 2. -VLDL, and remnant particles are TAG rich -LDL and HDL are cholesterol rich 3.apoproteins are the protein component of lipoproteins where scaffolding happens to bind lipids 4/5.a) LDL- B100 apoprotein  high phospholipid and cholesterol content  small radius  low TAG content b) HDL- A1,AII, E,C apoproteins  high phospholipid and cholesterol content  small radius  low TAG content c)VLDL- C(exchange between different lioprotein classes), E(receptor binding for remnant particles) apoproteins  high TAG content  large radius low phospholipid and cholesterol content shifts out fat from liver d)chylomicron: -C and E apoproetins  largest radius (least dense)  increased TAG content 6. LPL digest tags in chylomicrons and VLDLs and turn them into glycerol and fatty acids to be transported to cells -HGTL work on partially digested LDLs  chylomicrons and VLDLs are synthesized –chylomicrons in the intenstine and VLDLs in the liver  fatty acids are transferred from chylomicrons and VLDLs to cells which turned chylomicrons and VLDLs to remnant particles  remnant particles are digested by LDL, which are then taken up by apo B/E receptors  reverse cholesterol transport occurs to get rid of cholesterol from cells by HDLs 7.a)chylomicrons = dietary lipids b) VLDL= dietary lipids but also used in storage and synthesis in the liver c) LDL= overflow pathway to decrease cholesterol concentration 8. reverse cholesterol transport:  cholesterol is taken up by HDLs and esterified exchange of cholesterol esters with HDLs, VLDLs and chylomicrons  cholesterol esters are there bound to scavenger receptors which are transported to the liver 9. cholesterol is a part of membranes, bile and steroid precursors 10. a) total screening formed cholesterol and a fatty acid  cholesterol is then oxidized to form H2O2  H2O2 +phenol 4-benziquinone b) TAGs form triglycerides and H2O triglycerides form glycerol and a fatty acid glycerol forms G-3-P  G-3-P forms H2O2  H2O2 4 benziquinone c) HDLs form cholesterol esters  cholesterol esters to cholesterol and H2O2  H2O2 + phenol 4-benziquinone 11. cholesterol synthesis is its own regulatory and when eaten (dietary) it is inhibited 12. abnormalities can occur : 1) fuel transport path: excess dietary uptake 2)overflow path: damages uptake of VLDLs since the Apo B/E receptor is damaged Lecture 17 7 Questions 1. used in fasting and diet, broken down for gluconeogenesis to maintain blood glucose 2. a) tyrosine NE and E b) tryptophan 5-hydroxytryptemine c)histidine histamine d) choline Ach e) glutamateGABA 3. glucogenic – glucose fat, glycogen ketogenic- acetyl coA fatty acids ammoniaurea 4. essential amino acids must be eaten non-essential amino acids can be made by carbon skeletons, cannot be eaten 5. a) transamination: -transferring an amino acid to a keto acid acceptor b) oxidative deamination: - oxidatively transferring an amino acid to make a keto acid and ammonia c) dehydratase:- removes water , intermediate that randomly hydrolyzes into a keto acid and ammonia 6. a)glutamine dehydrogenase: - transfers alpha-ketoglutarate to oxaloacetate and in the reverse as well b) glutamine synthetase: -trasnfers amino acids from one tissue to another -requires energy c) glutaminase: - hydrolyzes glutamineglutamate+ ammonia important in kidney, manages protein transport and pH control 7. urea: -neutral (non reactable), non-toxic -ammonia: -volatile, basic, small and volatile 8. Urea Cycle: ammoniumcarbomoyl phosphate (requires 1 ATP) carbomoyl phosphate citruline (releases Pi)  citruline arginonsuccinate (adds aspartate and uses ATP)  arginosuccinate arginine (releases fumurate) arginine omithing (releases urea) 9. Carbon Skeleton Metabolism: a)gluconeogenic: - increases glucose concentrations by feedings C’s into the TCA Cycle  at the level of: -alpha-ketoglutarate, succinyl-CoA, fumurate and oxaloacetate b)ketogenic: -amino acids feed C’s into the acetyl-CoA and acetoacetyl-CoA  at level of lysine and leucine c)both: -complex or aromatic structures  phenylaline, tyrosine, tryptophan, isoleucine, and threonine 10.alaninepyruvate asparate oxaloacetate glutamineglutamate Lecture 18 a) 7 questions 1. -glucose is used for continuous supply to the brain -fat is mostly used for immediate energy stores, unlimited cpacity in adipose tissue -protein is used to synthesize proteins during prolonged fasting 2. gluconeogenesis: lactate, alanineglucose -glycogenesis: G-1-P glycogen -lipogenesis: fatty acids, glycerol TAGs -fatty acid synthesis: acetyl-CoAfatty acids -protein synthesis: a.a protein 3. glycolysis: glucose pyruvate, ATP -glycogenolysis: glycogen G-1-P, glucose -lipolysis: TAGs glycerol, fatty acids -TCA Cycle: pyruvate, acetyl-CoA NADH, FADH2, CO2, H2O, ATP -fatty acid oxidation: fatty acids CO2, H2O, ATP -proteolysis: proteins keto and gluconeogenic amino acids -pentose phosphate path: G-6-P NADH, pentose, CO2 4/6. insulin stimulates anabolic paths and inhibits catabolic paths -insulin is 2 peptide chains linked by a disulfide bonds -secreted by beta pancreatic cells which increases the metabolism rate and triggers insulin secretion -insulin binds to a receptor and tyrosine kinase activity is activated liver: -stimulates glycogenesis and suppresses lipolysis -stimulates lipogenesis adipose tissue: -stimulates lipogensis and inhibits lipolysis muscle: stimulates protein synthesis, glycogenesis 5/7. glucagon stimulates catabolism and inhibits anabolism -single chain molecules liver: -stimulates glycogenolysis, gluconeogensis, oxidation of fatty acids -inhibits glycolysis, glycogenesis, and lipogenesis adipose tissue: -activates hormone sensitive lipase releasing glycerol and fatty acids into blood muscle: -no glucagon receptors -epinephrine stimulates glycogenolysis -glucagon binds to cell membrane receptors -makes cAMP which phosphorylates PFK-2 -PFK-2 degrades Fruc-2,6-BTPase which disinhibits Fru-2,6 BTPase-1 -this then stimulates gluconeogenesis and inhibits glycolysis 8. a) RBC: anaerobic, use only glucose b) Brain: -continuous supply of glucose -when starved, uses ketone bodies c) Adipose: -stores energy as TAGs -hormone sensitive lipase releases fuels d) Skeletal Muscle: -least discriminate e) Liver: -maintains blood glucose postprandial: glycogenesis, and lipogenesis Fasting/Exercise: glycogenolysis, lipogenolysis  Starvation: glycogenolysis, and lipogenolysis 9.a) Postprandial: -increased insulin release and decreased glucagon release -glucose is made into fatty acids and cholesterol -fatty acids and made into TAGs and used in storage -amino acids are taken up by tissues as well as turned into proteins -extras are deaminated to glucose b) Fasting: -insulin secretion is damaged and glucagon secretion is increased -muscle makes lactate which is used in gluconeogenesis when oxidized to pyruvate -hydrolysis of TAGs occurs by hormone sensitive lipase -fatty acid oxidation and protein breakdown is stimulated c)Starvation: - chronic low insulin and high glucagon -decreases metabolic rate and the thyroid hormone -TCA cycle is slowed down causing a accumulation of acetyl-CoA `10. Stress: -increased sympathetic nervous system -anabolic pathways are inhibited and catabolic paths are stimulated -increases metabolic rate and fatty acids become a major source of energy -releases fatty acids and glucose Lecture 18 b) 3 Questions -Types 1: destruction of pancreatic B-cells -no insulin, cannot take up glucose into tissues -high blood glucose levels -liver metabolizes fatty acids into ketone bodies (causes acidosis or fruity breath) -Type II: insulin resistance occurs (cells do not respond to insulin) so insulin secretion is impaired -inhibits hormone sensitive lipase Lecture 19 8 Questions -1. a) carbohydrates: -liver causes glucose metabolism and stores glycogen b) protein: -synthesizes albumin, as well as plasma alpha and beta globulins 2. a) C-reactive proteins: bind damaged products and infective agents b)Complement Factors: -stimulate phagocytosis of foreign particles c)Protease inhibitors: -promotes protein synthesis for repair 3.Bilirubin: catabolic pathway of heme -must be metabolized further since its water soluable -bilirubin binds to albumin and carboxylic acid side chains are esterified to increase hydrophobicity bilirubin is then catabolized to form stercobilinogen 4. Bile Acid: -emulsifies at for digestion -cholesterol excretion -hydroxylates cholesterol to synthesize bile which is then reabsorbed into the intestine 5. Drug Metabolism: a) add a polar group:- oxidation or hydroxylation by a family of P-450 b) conjugation: -methylation or acetylation or glucuronidation or sulfation 6. P-450: heme containing proteins that metabolize 7. Pharmacogenetics: -an individuals response to drugs -pharmaceuticals are metabolized by CYP2D6 -variability can occur due to different gene expressions being duplicated or SNPs or an altered gene or enzyme 8. Cycooxygenase: -arachadonic acid goes into COX 1 or COX2  COX1 (death) prostaglandins appropriate defense response -COX2(damage) prostaglandins inflammation and pain 9. Hepatotoxicity: -toxic effect drugs produce through metabolites on the liver a)acetaminophen: -causes cellular peroxidation b)caffeine: offsets CNS c) Mathocarbamol: -relaxes muscles d) Colace:- shuts down the GI tract and causes constipation Lecture 20 a) 3 Questions 1.Purine Synthesis: a) De novo synthesis- ribose -5-phosphate IMP -done by adding 2 formyl groups from folate, amine from glutamine, and CO2 from amine, glycine and amine from aspartate b) Nucleotides are formed from IMP: - IMPadenylosuccinate and XMP -adenylosuccinate AMP (done by adding aspartate-amine) -XMP GMP( add amine group from glutamine) -fumurate is released -GDP, AMP, and NADH are made 3. Pyrimidine Synthesis: a) De novo synthe
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