Review Sheet for BIOC 460 at UA 3
Review Sheet for BIOC 460 at UA 3
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Date Created: 02/06/15
Mode 4 Both NADPH and ATP are required 3 G6P 6NADP 5 NAD 5 Pi SADP gt 5 pyruvate 3C02 6 NADPH 5 NADH 8 ATP 2H20 8H G6P primarily converted to pyruvate for ATP generation Glyco lysis Mode 4 2 NADP 2 NADPH Glucose Ribulose 6phosphate 5phosphate Pentose CO 2 Phosphme Fructose Ribose 6 phosphate quot 5phosphate Fructose 16bisphosphate DihydroxyacetoneA Glyceraldehyde phosphate 3939 3 Ph05Phate b 2mm REACTIVE OXYGEN SPECIES ROS Reactivity ROS Least singlet oxygen superoxide radical anion OZo Moderate hydrogen peroxide HOOH Most lipid peroxyl radical L000 hydroxyl radical OHo Slide courtesy of Dr Marc Tscher Glutathione 0quot yGlutamate Reduces ROS in cells GSH Reduced glutathione CO GSSG Oxidized glutathione HN Cysteine SH 0 NH Glycine lt f TO O Glutathione reduced 39yGIutamylcysteinylglycine H202 glutathione 2 H20 GSSG 2 GS glutathione gt12 NADPH NADPH H 4 pentose pathway Reactions of glutathione reduction and oxidation T ransketolase and transaldolase convert three pentoses into two hexoses and one triose for use in glycolysis Transketolase Transaldolase Transketolase Transketoase requires thiamin pyrophosphate a cofactor derived from Thiamin a watersoluble Vitamin Figure 1 Ageadjusted prevalence of overweight and obesity among US adults age 20 years and over Permquot D0verweigh1orobeseBMIgt250 l0beseBMlgt30U d so 55 lren s 1n so quot56 40 Obes1ty 2 U S Ad 1t u S 0 NHANES III NHANES 198894 199902 n16679 n8505 Tru sinnhesi 39mmg adults 1991 i1 2mm Ageadlusled byzhe dlrstl method lathe year zuuu U 3 Bureau unhe Census esllmales usmg Ihe age groups 2339 411511 and an years and aver Dietary fat makes up 40 of the American diet A major cause of disease 1995 7 1m 1991 V gt 20 1519 1015 r HeDauf l cttnnljl ErasHail 1315 Eu 117133 I39Ebct EJH 419FI33116I ENLS39ESi 3 2m Three step processing of fatty acids 1 Mobilization from triacylglycerols in adipose tissues 2 Activation and transportation into mitochondria 3 Oxidation to acetyl CoA Hormone Adenylate cyclase receptor w 9 9 9 v c o 0 o e v v 39 i a e39s LO O o LV3939 o o o t o a o n 7 Free fatty acids Hormone b1nd1ng to receptor act1vates ATP AMP C Glycerol adenylate cyclase Protein Protein G1ucagonep1nephr1ne kinase kinase adrenocorticotropin Triacylglycerol Triacylglycerol lipase lipase TOther Iipases Diacylglycerol Insulin inhibits CAMP activates Protein kinase PKA Triacylglycerol PKA activates hormone sensitive lipase by phosphorylation III Products I Glycerol water soluble absorbed by liver I Fatty acids Hydrophobic bind albumin for transport in serum Step 2A Fatty acid activation El Transported to cells bound to serum cytoplasm H20 Pmmmse albumin ATP AMP PPiL dpi Fatty acid l El Activation to Acyl CoA in cytosol by Acyl CoA Synthetase in mitochondrial membrane El Transport into mitochondria by Wageth carnitine transporter W membrane httpwwwbr00kscolecomchemistrydtemplatesstudentresourcessharedresourcesanimationscamitinecamitine1html Acyl CDA AQICDA liitf T39 synthetase lilllllw Intermitn chundrial membrane space Aw EDA t T T l 1 T 393 T J 1 Outer mito chundrial m an hrane 1 It Step 2 B Cytoplasm m 39 T 39 T 1 39 Ciarnitine T T 1 T I t I T I T 1 Outer CoA Into 1111111 111111 111 mitochondria Via the carnitine shuttle 39 1 Carnitine 1 t 1 1 H 39acyln ansferase 39 39 39 39 I I II 1 1 1 1 1 Carnitinequot l l T 1 t I I T 39 tuner acylcarnitine 39 39 39 39 l I I I mitochondrial translucasae 1 1 1 3 J 1 5 1 1 membrane Mitochondrial matrix Fatty acid oxidation B Elmoxidation Fatty acid processing Step 3 B Oxidation III B Oxidation l Occurs in mitochondrial matrix I Completely oxidizes saturated fatty acids El Even number of carbons I Two carbons cleaved from the carboxyl end El Bond broken between 0t and B carbons II Four steps Oxidation Hydration Oxidation Thiolysis I Products El Acetyl CoA gt Citric Acid Cycle El NADH FADH2 gt Electron transport chain El Acyl CoA shortened by 2 carbons I Cycle repeats II Complete oxidation of Palmitate 16C gt 106 ATP 0 H2 II R C CSC A C C H2 H2 AcleaA FAD Oxidation FADH O E R C COA C C S H 139 transA Enoy CoA H 0 Hydration HQH CJJ i C CS RC H2 CoA C H H LSHydroxyacyl 20A NAD Oxidation 3Ketnacyl CoA HS C A 0 Wmiolysis O C C A C S 0 H2 H3C s Acyl CoA Acetyl CoA shortened by two carbon atoms Ketone metabolism El Ketone bodies I Acetoacetate D3 hydroxybutyrate acetone I Formed in liver when Acetyl CoA production exceeds capacity of TCA cycle I Preferential fuels for heart muscle renal cortex not liver I Used by brain in starvation and diabetes El Ketosis gt fall in blood pH C A CoA o S H20 5 gto CoA 0 CH3 CoA CH COA S i 3 4 o D3 Hydroxy CoA butyrate S 0 HSC gto H3C o CH3 35 Acetoacetyl CoA 3Hydroxy3methyl Acetoacetate Acetone glutaryl CoA Ketogenesis EIEIEIEI Mechanism to Prevent Ketosis Free fatty W acids 1 Ketone Bodies Excess ketone bodies promote insulin release from pancreas Insulin inhibits lipolysis Fewer fatty acids reach liver less acetyl CoA for ketone synthesis Control lost in diabetics Fatty acid synthesis and B oxidation Key differences and similarities Boxidation Synthesis Cellular location Mitochondrial matrix Cytosol Acyl carriers Coenzyme A ACP amp Cysteine Electron FAD amp NAD NADPH donors acceptors 2C productdonor Acetyl CoA Malonyl CoA amp Acetyl CoA Acetyl CoA for fatty acid synthesis is transported from mitochondria to the cytosol by citrate MITOCHONDRION Fatty acid synthesis occurs in cytosol Acetyl CoA is produced from pyruvate in mitochondria Malic enzyme generates NADPH for fa synthesis Remainder from Pentose Phosphate Acetyl CoA Oxaloacetete Citrate Pyruvate CYTOSOL Malate dehydrogenase Acetyl CoA Citrate Malic enzyme Pyruvate Oxaloacetete if Malate Regulation of fatty acid metabolism by Acetyl CoA carboxylase Global ATP ADP AMPactivated Citrate protein kinase F Protein phosphatase 2A Insulin Pi H20 Glucagon epinephrine El Global l Active form of Acetyl CoA Carboxylase is dephosphorylated El AMPactivated protein kinase AlVlPK deactivates Acetyl CoA carboxylase by phosphorylation El Epinephrine glucagon indirectly inhibit the phosphatase keep carboxylase phosphorylated and inactive El Insulin promotes dephosphorylation activating the carboxylase El Local l Allosteric stimulation by citrate signals availability of substrate Acetyl CoA and ATP Fatty Acid Synthase catalyzes the synthesis of saturated longchain fatty acids El Large dimeric enzyme El Seven enzyme activities Acetyl transferase AT Malonyl transferase MT Condensing enzyme CE ms Tars39 c 9quot SH Acyl crrier protein ACP BKetoacyl reductase KR Dehydratase DH Enoyl reductase ER Palmitate Thioesterase TE Elem 553 Acetyl CoA 7 malonyl CoA 14 NADPH 14 H Palmitate 7 C02 8 CoA 14 NADP Reduction Condensation Fatty acid synthesis Occurs in cytosol Repeats gt Palmitoyl CoA 16 C I Cleaved t0 palmitate by thioesterase Stimulated by I Insulin Inhibited by I Polyunsaturated fat PUFA I Leptin El Protein honnone El Decreases food intake and increases energy expenditure Obese mice with mutant leptin gene Checkpoint I Identify Linolenic acid using its systematic nmnc H 9 H COH H 91215 octadccatricnoic acid 033 183 A 9115 Cholesterol El Obtained from diet and de novo synthesis El Important component of biological membranes St 5 w eron El Precursor of Structure l Steroid hormones Progesterone Estrogen Cortisol Aldosterone l Vitamin D I Bile acids El American Heart Association recommendatio cholesterol levels I Desirable Less than 200 mgdL I Borderline high risk 200 239 mgdL I High risk 240 mgdL and over El El El El EIIII Lipid digestion and absorption Overview Liver Iquot 39i l l Si C Stomach Mmor gallbiadder mm h I Lingualgastric lipase B m 3 5 I Churnmg coarse 432mm quot 39 Panama emuls1 catlon Small intestine contains hycirciyiic lanaimas from ma mareElsi Most digestion occurs in small intestine 90 I Enzymatic El Hydrolysis El Deesteri cation El Emulsi cation in Bile salt micelles Absorption into intestinal epithelial cell Reesteri cation Secretion Triacylglycercis transported through the binocistream via I 15 quotJeri Izw Jansi39ly TrlaiY39Q39FDUU transports3 through the Dion stream via ahylnmiernn Simage as lriaey lglycerols Adipose tissue Fatty acids assccialed with all umin mi H2O Steps of lipid digestion and absorption Step Location Enzymes 1 Minor digestion TAGS DAGs FFA 2 Major digestion all TAG MAG 2FFA PL lumen of the small CE ch01 ester CE intestine mouth and stomach lingual gastric lipase pancreatic lipase cholesterol esterase h l39 A PL FA lysoPL PLA phosp pase 2 3 Formation of mixed lumen of the small NA micelles us1ng blle salts 1ntest1ne 4 Passive absorption of into intestinal mucosa NA hpolytlc products cell 5 Assembly and export of from intestinal cells to N A chylomicrons the lymphatics Enzymatic digestion of o 0 II II dietary lipids 20 0 8 R WT 0 8 F quot 0 F50 ll HC O g Rz p HE S O C Rz o e R39 Triacylglycerols TAG H2l0 93 FbCOH DAG I Pancreatlc llpase triacylglyc erol 12di acylglycerol fatty acid Cholesterol esters Pancreatic lipase I Cholesterol esterase 39 Phospholipids 14quot H l I A II I J c o in 139 lo x a l Phospholipase A2 In Cholesterol eater Cholesterol esterase Cholesterol 0 I39D 7 ft HEEE EJ C Fl1 ll 3i 39iquot HE C Cl CE I 39 l 39 w O H O Lr I ID I T JII quotII H i HEB O T39D K Phopholipase A2 g C U T O X O O thsphalipid Lyauphosphalipid Enterohepatic circulation of bile salts El Bile l Water bile saltsphospholipid cholesterol El Bile salts l gt95 reutilized I Modi ed by intestinal bacteria I Recirculated to liver El Reconverted to bile acidssalts l Secreted into gall bladder I Released under hormonal control MAJOR LIPOPROTEINS Lipoprotein SOUI CC Major Function Apoprotein Chylomicron Intestine B48 C11 E Delivers fatty acids in triacylglycerol from dietary fat to muscle adipose delivers dietary cholesterol to liver VLDLVery Liver B100 CII Delivers fatty acids attached to triacylglycerol low density E derived from liver synthesis to nonhepatic lipoproteins tissues eg muscle adipose LDL Low Blood B100 From VLDL delivers cholesterol derived from density liver synthesis to various tissues lipoprotein HDL High Liver CII E Collects scavenges cholesterol from non density hepatic tissues and delivers to the liver lipoprotein Apoproteins recognition sites for receptors activate enzymes 5 classes A E all functions not yet known Pathways of cholesterol transport El Exogenous i r RQV39CYSL gt FIluIPsIFI 0I I From d1et 1n Imam a 7 MW r chylomicrons x H 1 3th I Thylomicrnn 39 1 llr I I ll 139 umanlz quotj remnants 39 um El Endogenous l Synthesis in liver and transport in VLDL LDL II Reverse cholesterol transport HDL precursors I39rum liver mu intestine I I Delivery of cholesterlt arty acids MH111uer1IlusclE adipose tissue a glycoproteins LDL g LDL receptors plasma membrane wk 939quot DefectShere evTeeeL akin hypercholestero K E N39D39III CH TVEI i315 RETURN OF L39DL clathrin we RECEPTORS TD meted e I PLASMA quot Q 7 EHIZIDSIZIWIE MEMBRANE vesicle I B UD DI39NE DF39F g f m TRANSPDRT VESIIZLES 11H FUS39IEIN WITH 39 ENDUSUME Ra g f H a 7 Apo TRANSFER TU B100 processing LveeeeME Neiman Pick defect free cholesterol Primary function deliver cholesterol to tissues Oxidized LDL and Atherosclerosis El LDL l ROS gt Oxidized LDL l Uptake by quotscavenger receptorsquot on macrophages that invade artery walls become foam cells I Elicits CE deposition in artery walls I AtherosclerosisCAD can develop Stages of Atherosclerosis 3D EDiagram Inside of arteryblood stream j Endothelium Normal Artery Wall Outside of artery Free radicals Injury In ammatory cells Calcium Lipid core amp Plaque Clot Plaque Rupture 7 with Clot ACEI VICOA r l HMGanA IllHydrant ll mdl G39 l A netmanmyIEQA mmwlglumw l op Mevalonlr acid 1 L l I Acemacelate Sn ualene AEE39IDEIEE IH39IE u 1 I I r a Shula5mm Cholesterol lowering drugs F413 I m a HUGE quot CH2 CH2 39 EH2 DH quot5quot Equalsme r E I Enaneynl HQ DH Movalonie acid Cholesteml GETHWD El Inhibitors of HMG CoA Reductase rate limiting step I Statins L t t H IATf II Lovastatin Mevacor was 1 m L0 El Pravastatin Pravocol L F H I Atorvastatin Lipitor acr 9 O 0 CH3 El Nlacm I Inhibits lipolysis in adipose source of liver TAGS HJCquot El Lowers VLDL synthesis Aminotransferases A Concentrate nitrogen from free amino acids in a few compounds B In cytosol of most tissues A Liver Kidney Muscle C Major aminotransferases by activity 1 Aspartate Aminotransferase 2 Alanine Aminotransferase 3 Glutamate Aminotransferase D Require pyridoxal phosphate 1 From Pyridoxine Vitamin B6 E 0c Ketoglutarate OLKG is most common acceptor glutamate is most common product A Glutamate is oxidatively deaminated to NH4 and CL KG OH H l N CH3 Pyridoxine Vitamin BS 0 H 2 O OH 07 0 0 N CH Pyridoxal phosphate PLP Aspartate aminotransferase Aminotransferases are used in clinical diagnosis Aspartate Amino Transferase SGOT AST GOT 39 El Normally intracellular Elevated in serum due to tissue El lg ALT G PT 39 Alanine Amino Transferase SGPT damage I ClIThOSlS Toxic or isch emic H Eij injury I Drugs or toxms Acme vim hepatitis 393 l Congestive heart Alcoholic hepatitis failure Chrnnic hepatitis Hepatitis Cirrhusis Heart disease Narmal MUSCIC Injury in an 1m 3m mm 30130 mm Uperli Glutamate dehydrogenase I First committed step for amino acid OXIdatIVC degradation d o f I Liver Mitochondrial matrix eamlna Ion O l Uses either NAD or NADP glutamate I Liberates amino group as NH4 I Accounts for most of nitrogen from dietary protein 0 D II ll C U EH33 Glutamate 60 Hi HH dehydrogenase 33H H HAW Ho NH NADH L1 or HAD PH 2 4 13H or NADPH H I a 0 0quot 6 0 H II 0 CI Glutamate m Ketoglutarate I O O 2 ADP 2 ATP H l I M l l HjN C O P J NI I 13 Step 4 Thu carbon nitrugcn band uf CM 39 39 arginine is l1ch mlyred in a reactinn I 2 0 catalymd by mmmzse tu give the cycle a 39 afar T Carbamayl pl39lnt upl39lflth39 transit Prndud urea hlus nrnithine ready m 112 La39banioyl P hmphaw it HlNc0 13mm 10 UI39J39lithi E J rupLal tup l nnn prntein amino acid In give 9 H L NH3 citrullinu in a rmcliun catalygLd by I unu n n m nnwmr mrruyiusez CQCY q I lgN C N1 1 Ornithine q H DPOIAL Urea 2 H N C NH1 H20 I Rxns 1 2 1n 5 Lle mltochondrla HN C11 35 in c tosol I HI39 C I39I i2 CM CH2 H C NH L quot LH COOquot EH 3 Cilrullima I 3 4 1 EW L UD H C NH I 3 H N C N CH WI 39 00 Ccm H 207 Arginim H3 H I39H3 R l N Ll39 ll C I 1 COO r t H Sft39p J Argininntiuccinahe is Split into I 0L L RE I 1 argininu a pmbuin aminu 39 id and C LI 1 Coov l39uma rate a cycle hy pn39nd LIclL I I143 I M pnzyme i rirgmiuosuniiml C H C I d 11 Farm f I 39 SIB 2 Citrullinu cumbims with 009 H COO aspal tatt a protein amino acid Tn give Fumamte Argininosuccimm a rgin inusuccinatu Thu I3sz me is nrllginn mmrt n mh39 sypuhrmt Fumarate and aspartate link the urea cycle to other metabolic pathways a w OLKeto acid Carbamoyl Citrulline Aspartate Phosphate aCld Ornithine Arg39n39no39 Oxaloacetate succinate I A Malate r r 1 Arginine Fumarate El Fates of oxaloacetate l Aspartate Transamination I Glucose Gluconeogenesis l Citrate TCA I Pyruvate Mitochondrial shuttle Hyperammonemia El Ammonia intoxication I Levels gt 1000 umoll El n15 to 50 mmolL I Toxic to CNS El Tremors blurring of Vision coma death El Hyperammonemia I Acquired El Liver disease I Genetic El Any of enzymes of urea cycle El Omithine transcarbamolyse most common El All result in mental retardation The rates of the citric acid cycle and oxidative phosphorylation are driven by cellular need for ATP overriding control I Oxidative phosphorylation is regulated by ADP levels I Electrons transferred to 02 only if ATP is produced El Oxidized electron donors return to TCA NAD FAD regenerate FADHZ NADH AeetleoA 1 czHgoscwx 0 QHz rad amp CW0 Ubiqui GE 6 m none reduo chrome Q use c oxidase ox GI Succinate Fumarate sass ysdftxe l ADP added nearly exhausted 02 consumed Time The pentose phosphate pathway is linked to glycolysis gluconeogenesis oxidative El El Uses G6P produces GAP Fructose 6P for glycolysis Regulated by availability of NADP Oxidative phase I NADPH El biosynthesis of fatty acids other biomolecules I G6P from gluconeogenesis El reduction of glutathione I Ribose El Nucleotide synthesis Nonoxidative l 5C sugars to 3 6 carbon units for glycolysis nonoxidative Glucose 6phosphate 2 NADP F9 2 NADPH Ribulose 5phosphate l Xylulose 5 phosphate C5 5phosphate C5 Sedoheptulose 7phosphate C7 E hose Xylulose 4phosphate C4 5phosphate C5 Rate of fatty acid synthesis is regulated by availability of acetyl CoA and ATP El Acetyl groups carried to cytosol as O k COA eltrate H3C 5 Acer A Regulatory enzyme l Citratemalate shuttle HCO W Acer A El Citrate stimulates regulatory enzyme 3 a39bm y39a e of fatty a01d synthes1s Activated by citrate ATP Ii Inhibited by palmitoyl CoA MlTOCHONDRION CYTOSOL 0 Acetyl CoA Acetyl CoA 39OOC COA Citrate Citrate C 5 H2 39 M I ICOA Oxaloacetete a any mm Oxaloacetete Coordlnates fatty ac1d Malate oxidation with energy need Pymvate LC NADPH Pyruvate Fatty acid oxidation is regulated O by ATP compartmentation ll R7CH27CH 27CH zicisco FAD R7 HzicH CH 7375C 01 H O Dehydrogenati on El H y drati on CIDH R CHz IZ CH 2 SCOA H NPD 9 R CHzicrcH ESQ 0A SC 9 R CH 2 c SCOA CH 2 C scoA Fatty acid oxidation requires ATP be synthesized l requires NAD FAD from electron transport l simulated by ADP Malonyl coA inhibits acylcarnitine formation I Formation of Malonyl coA inhibited by ADP I Prevents transfer of fa into mitochondria for oxidation l fas incorporated into VLDL sent to adipose for storage Oxidation Thiolysis 39 l C arnitine x v v v mm a r l 11 x 1 l l 1
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