Iioneri werner ae iay 4) vaw the peptide bond between Ala-Clu- Cys: Wan etal Ee es Efe. f Cty, Aq old question. % gly -glu-cys 3 emer -phe -ala = Hag § , . Wis a Draw the hydroxy proline reaction .ceinss me hy Srory potne a t-coo” Wy —< -c08 2) poisonous mushrcom Amanita phalloides # ctoxic constituent of the mushroom, Ananit phalloides, inhibits “eukary rout not RA polymerase or bacterial AWA polymerase - - RMA polymerase W bwanscribes protein-encoding genes into mAWA ~- Wans-elements - €9. transcription Factors -cis-element -€9. enhancers 4) sylFonamige dvug is a treatment of bacterial ANFe ction, explain the Herined and why hones w/e ed Folate biosynthehic pacthuny 5 sulfa 3vags compete uit tre watwal subst par-aninoberonte (PABA) causing depletion of dingdxe Folate (DUF) and subsequent growth inhibition SUlFA brug inhibits dihylveplevoate synthetase. 5) Bi-Bi veaction: A reaction catulyzed by a cinfe Peinctitictne nein tal tuo products aye involved. ee | i de + glutamate Ping -Pong reactions alanin + -Xetegluierate etry» pyraicte +3} . AST, As ees i te oxaloacetate + glutamate Fru 6-9 a Ae, ey ATP increases the vote of the reaction at Jou cconcentvation. i ou A algcericaty whit ne eragme at hgh conceals bas. S ar? x myocardial infarction L9H and cK enzyme 5 gop creatine phosphate evendine + creatine z si Kinase Me LDH Jactate, ¥ pyle cae” 5 on creak bays arter epizole a ad pain EX exleletal muscle gaffer of caren monoxide onthe ongen aFFmity of henoglobin (co-Hb= carbon. monoryhernog\ovin) # 0% co-te 5 507. cow § iS pees resouthenr blott wa, IMs atechnique that can detect and D/A probes x fnal ysis af gene expression © A-dererminction of mPvilt levels Drforthern blots: sinilw +2 southern bot except Akt Ahe original sangle contain a mixtwe of «fil mndlecules that or “fransferved 40 a membyane and ye }e vadiolabeled prove. tora mutations im OWA. it combines Te Use of vEestriction eraymes, clectenoresis “Leparateh by electropho esis hen, peer: contams +ousands of immobilized DA sequences organized in 0m ova. ne aor a migos 2 Con 43 AON + FDI, + OTP + BET + COR coral shuttle 3) Daw the malate - aspartate shuttle = ap Dvaul the 3-Pp-9J tree qnivetraysferie_ capetae oie sanste 3 oF & sion a4 ee oe Wavans prcsphodiby tony mitochondrial at Ce ra “> wt aphespregyeeto\ i) Tea waite oF MO elegutente at hie 99" — ra eytosal mitechondyie. cytosol mitochondyia w) H) Wa ctose. biosynthesis ‘in seminal vesicle alse in twer J no sorWito\ OW in ens ROWE and Kidney glucose ame ‘gov dito! E puma veouctase a 5) glycogen synthesis % degradation (6 points) ep opi Rivea eT on E | > Gle-4-P sg RE a peat Jc Gle -6-P Froxpregincomatnse pyephespovy nse UOre Horses a Pi 4- ae - Syeogen agerae Sis P rapa een reapers? neay mr. We, Gle Gleb? is allestericactiater of dycogen syriiase delwanching Clea bp Is allesteric whibiter of _glycegen presage enzyme é) enzyme o€ TCA cycle that is com elitively inhibited - draw the stYincture » 7 confess succinate Sa Fumayate i Taccinete veljgemse HOG H . alone © t a “cooki F)would you expect the citric acid cycle to be more acti vatio and a high ROMIARD Vato? git he reason For Rar eeuer less when a cet has a high ATP /A0p nase and a-Xeto glurerme dehydrogenase ave inhibited by ATP RHA. x eikate aynthase , isocitrate debybrege p because these TCA exzymes ave inhibited - ys0 the TCA cycle” would be less active or Sto) cle is considered a5 @ condensation veaction(urite down the Yeaction sing cons, aha veaction in TCA cy give the name of ‘the enzyme). e cots a oxaloacetate + Acetyl -coa pe A cite ciate Sypethose DY e Ane, 3S succinyl-co © Acjl-col © ora » aie ciygen-uptle curve (fogh vereus tine) For a suspension of icltte) witochondvia when the A nee n Ahe fellas a ae weseee Hy the indicated oydey. With the adbition of each of compound, all oF the ea Fi - Succinate, ADP , oligomy cin, 2p Dinitrophenol. (3 marks) tt Pogh anceinste AOP aligomay cin, ——> inhibits ATP syrthase. at pNP __y uncoupling agent, oligo mycin sme Fine. 10) dyaw a scheme to describe (in letail) the Yole oF glucose-s-P derydrogenase (6-4-P DH) and the cons oxidant $6 averse of its Jericiency in RBCS (3 marks) bs ae 7 glucose A ae “ene e oro + auth = Ho Reaeey war oe cine eh onyger ghe-6-P c BSE specie 4b WADE ‘\ a \ 2, Lge — neo tb a L sensine aha pameonactone Wang Bycaysis: 5 % prosphogunconcli.ctone yao Gleb presthale exper as RATT a ganic ji ie) ea diol quacks saa wae Ty & fae oD Sahil by Foride (give he name of he enzyme) (smart) 1) using strictures dra Be reaction i glycolysis Tale Jno enol pyriviate aeetes ay eae phosp! Ga py oO lucride O Le dy-0l hy a using sirictw/es Yall a veaction From the pathway of gluconeogenesis catalysed by ich Vequives vietiny 6 IE pts Be guyne points)» pyriavate erate = Ga . Pangiase Bs ee tee ipochondtia) ha doo chyMidterm 2 f) draw a diagiam that shows the galactose meta bolism in Ii ae 2 Ser ee ohereppes) Heese) Fal Zo1s lactose -2-P le-teP ga Nebh gucose + QnaDt +2ADP +2pi ——>2 pyrivate + 2408 + 24° 4 2ATP +2¥g° 3) pyruvate Kinase fae aes phospho enol pyruvate Sm Leg pyruvate eg res a deficiency» hemolytic a w pyrante dehydrogenase reacti ant noth Ree Tink between geolysis and TCA oe Py Sete ae Sheetylcop , Mok deFiciency: ety- eres ety & Beet ied oon bicorder igh disens' 3) pyruvate ealeaste Yeaction: - lactic acésemia py ever heer ipkdloaceiate @ Acetyl coA i @icert cok = “g #| 7 ellg- - ae woh © coo" a Pan Wractie Aci id (cori) cycle pytone cn ams Oe glrcose glucose beam gy wi glucose glucose , p38 ee Rlactate +2 lactate } oye co ( ae live Yoos | muscle eee os BL 2 Manine 2 oe uwer anaerobic consivion liver tees muscle 6) Sov sources oF peod glucose (gluse hme r epide_—— saan ucose concent (glucose teevance 44) Vv v er / AYpalucosuria 3 Bed fw Ne 7" unantolled digbetes 2 enesis FE 3 3 ye Rov nal 2 a’ TB 2 Re 6 2 & 6 te RHO nag ela ep Hours — 2 Nee ot ae ays ied steps In glycolysisy io) regulated steps ingiuconerpans @ vedox reactions -TeA cycler ness hexokinase Disocdvate schysresenases pyriaate carboryiase eo Aeroguusente etree: Rr tokinsse LO AT? | 7) piaproenipyrate cfb ayn 5) pyrwate Kinase « ATP | 3 Frsctose-tyd-bispresPhenee b-phosphatase Jaucemate debybrogensse - vj matate velybogenace - hee yeaction-TCA Acyl li) glucose Walon veactions > Ss ree DR > ont En malic. € ‘gghuteaate OF eos se ee 2) pynwite 2 carhenyece ? etigpnal yee 3“yadenosine diphosphate (ATP): RDEONWLNEME Mono phosphate « ah Wha “9 $e co O-e°Y ot oH Ok x Fate oF pyrwnte s d) conversion to lactate by lactate Jehylregenase- reduced in cytosol - vever'sible. axacrobic conditions : uted neni ean end TAR pee mitochondria - iyveveysile- aerobic conditions sJeowersion to oialoaceiate by Pyrite earberlacee mitseketrie Welerswle: a ‘andplivokc veackon . actWated by Acelylcod - Yepleiishes intermediates oF TcA cycle ie ol jele ond jibe substrate Fe oF it uconversion to Alayine by Alanine aminotransrerase + 4 Se Sager 5) conversionto ethanol by tuo weactionsy occurs m yeast and some bacteria - TPP..dependent pathway x lethal synthesis -veaction with structwe» coal AMPsPF 0 cols Fluoroacetate Naa, Flucreacely -coA Auoectyate (Acohitase inhibitor) ce AcBhyl col gpnetese ckaF Eitvote spehase Coot me Zao otloncelate re ae a Soe yoot-cool x isocitate dehylroaencs -Yegulttion: ea on ea ise ettrate EAMES Fe eeelegtuternte A Hl gochrate 01 Bes f Be re t aw aoe ee ae miotiters oF hetose Ayansport preteins sion of TEA excl exaynes at pe eyecare? civates citrate synthase cs ines SOLTE ec rapiestee 2 rte are eryte 3 et 2) Florisine a arsenate: a-Kelogiuerede OH Sede jesayenraegier? 4) malonate: grecinate OF mance» pyrantel ' i Je pata. # glucose metabolism = metabolic Fates of gucose ave glycolysis» gycogen synietfond pentose Cee) pata PPP - ovdative phase (reverse) glucose glycogen syrubests ge Roses» con 280% nave F5A0? ag ea yor yore Bg Phmachig eng 00 tno a as gun TE src HE eet on FX: rylese 6 sant re eta we 7 Sy Wibose -5-P gycoysis SPP mua A ples spice. ie col eS (omen, —Geedegyersss) if ione by enzyme thd hos biotin - ~Yeaction Kinetics en fr iavate aks py tet oxaloace: 2 a Bian is cay borlase Ta = boo @feetyl coA ie Ss coo" oe y concen Epyronie] phosphate yaw the Formation oF Fig psevemne glaconmine-6-phosphale a Fructose 6 phosphate wv See ats amino ans ferase WPS mo gy eae n degrdation (glycogenalysis)* i ee eS > gucose-t-fho rosie open 6- phosphate : BQO i Se ghacose Liver > Piveplrne | muscle => epineperine serene? segluconeogenesis - Alanine a5 & eubstvate that makes glucose » Me gece GaP oo, per =e le perck 5 Alay [ i “Seale see ag shou tre WET anor carr aerdbic glycolysis + glucose yeactions that geneme aor geen! -P DH Db-r- _guscorote. OM ae-bP 2 malic enaymes iy J pyvwrata, tg aaa eee ‘ranscriptions glacagen, epinephrine sglteocarticnids not ‘ ah insulin. (vepresion) OH # lactate os tS subcrvate (guconeogenesit)» x Manine as a substrate ( g luconeogenesi): gcse ep Suiasiescoote _ BIE ean fi 4,3 buphespheslycerste {Soe Pjptee fe me TAsT se Olycerol-3-Phagphate as a. substiate Gluconasenes glyceral glycerat phosphate, eam GAP Drea guceee: glycer Kinase year Fe Haof Wee Aenybrgenase erase ve glucose: NADPH genettion jn oxiborve pease oF PPI rere hosphote. MeO a, prosphoguconsiactone gle-b-prostote eon p= enzyme beFiciency lead 40 hemsysis: -iF Wag accumaleteee, (eine bie): ° Z woo Sanu) homoge bin | quo get og membrane tarage* fe retcn noe manesuscseninin et ete by-o8 ae 4 , eh -ot ee) eye ® = glurathion’ 165 egiiatone ecrlacetcl lucose trentseriptions mgadyerin x slucose 6. phos Sericiencys 26? SHAS 9 ye Gon GierKers isense) sy Pe ear —most common. disease , autosema| vecessive . resaili ~ manifestation > Fasting hypaglycenia ,lactic acilemia ricemiu hyper Peers shypers ne 7 PT oxy-Hb rt Rpyramte 2 WADH IF Haog accumulates hemoglobin denaturation (heinz bodies). Eman ~ membrane damage « # pyruvate Kinase JeFiciency:- phosphoenol pyruvate Re pyruate — - seeder Eee - 8-261. of normal acti oes ee pranscripbin sweatin induction) ~ kemolytic: anemia (ix common cause) - deFiciency oFATP leading to cali cuetingand ysis IMAGEN vepresion. erect, OF glycolysis intermerates and depletion of Inciate See teas = phovphe alain de phouphorsation. . 2y3-BPG concentration lepton. okine ooh-Geh inguin HK yelctosemig:. galactose alactae-t-f Fre ucese LP ieee aaa galactose accumulates andy yesuced 4o galactiid which causes cataracts. Cenbeh galactose -4-preeplate should be measured LoKnow which enzyme might be defective Le? GaltctoKinse deficiency —_seataract ost 4-phosphate uri a : Ree eae refefase JeFicieney cataract , ypoghcemia, jaundice eke ORO sH0p* | * galactose erred 9a ctitod, e e vehuetase NeWieus system lavage 2 Fructose Intolerance Fractoe CM srctae.t# a Nawe a (oar Tunes Peytic intermedi ~SeFieciency oF liver aldolase 8 (Fra 4.9 allele activity) oye wont PAE 3°13 -absence of Aldolase 8 leads 4c intracellular Wa PPiny of rut p =noke: beth Abolase Aand B cleave Fructose 446 BP Prebced during siycolysis 46 DHAP and GAP, but only aldolase 8 cleaves Symtons:-hypeglycenia—y inhibitor oF glycogen phospho lore Free! A : tose phosphate. acer, eee a eee 78° ghicose is not released From iver, (MCR canbe converted decrease in muik probucks gperuricens) excessive uric acid production destruction of INer and other. roblems- _—_——— ~depletion oF pi and ATP fe i mens £48? cell eweting mg Be F ty Cee (Ualase cv F469 mn i*TEAc cycle ~ivreversitle veactions inhibited by ATP» waow SMH > olleeseric this Yeactin + acetyl ciate *. Dagegpaceior — Ss Sars ~inhibited bye. Syvahase Loan Zeondenscany ) pot 18 Disocitnte Was eeKetogluterate, Wd Vocinbie OW 382 Linn . wage MADR ; | 3) o-Ketogluterate ame Con eee “ft, : Seecingh oA i tlpene e) Sc lg anlahre sox veal ehee + FAD [ -anon osyreses all th, cacept seeciucte DA which prodice FADN, hig OEE winter aitichy 9 isocitvate Ss onkeciy | epee inhibited by, 9) aXelogtuglaterate see ee are glaglut tt pisieaeya Succiny\ CoA \ cxgheiegiutette OH Dmalate oS 2 ocak AR inhibitors OF TEA cycle ‘i Dcitneter citrate sypuhase. oxaloacetate + Acetyl cof TE revmie [NRO a5 0 cofactor: 2) Fluoveeitwete + Qeonitase - citrate <> isocitrate Dcivate synthase 9 arsenate: «Xeloguiemte giegenace. « Hetogleeets ecco 1) Famerase: Fanerate Rp malie fa malonate: succinate Sehydvogenase . succinate Ext eed NET action: Acetyl coA-+ 3AN0* + FAD ODP + fi + Ro > 2 con + 3MOU 3Ht + FADNR+ GTP 408 cust Citrate luowectrote 2; cela ae mo" a cat con cottt a-Kekogluterate pe arsenate# Qweolysis ~veguieres steps inreversible-wuidivectional):-heroKinase 5 prosprofructo Kinase £ and pyrite Kinase « AP Ape 2) glucose am \weose -6 phosphate ingulin. - high -covbdhyeste meal (intucti leew : gtacagon. Fosting (repression) = 2) Fructose -b- phosphate GRE Fructose ty Pisphosphate OF 2687 14 MP 1 ccesteri PF © eidvate yATP 4% eg Q 4 SI prespho en prute AS Se @AMP — aoestevic: (red) nase Or-468P HADY biosyninests » glycer -aephosphate. dehydrogenase OAT Fy olanine Ia ee peng fi @iodoacerote x sierndeaier aot AR 2K L,3buphospregyeente S aysenote Grae) Goaginiter oF aletegitente 08) RAT? pao. agp reyoXinase. ond praiphaFractoknase KATP production: petegres Wirase an} pyruvate HMM - AGP AX 453 bisprasphoglycerate Sagi 3 -phosphaglyeerate - nase . # x pyrite. aX Ppate as sae pyr HK inhibibrs in. gycolyssioboacetate, arsenate gard Fluorite « Hiodoacetate and a¥senade inhibit glyceraldenyte -3- prosphate dehydrogenase. (anon biosynthesis) . a Fluorides enolase — 2x Lephesphegycerste eit prosper prute HNET reaction: glucose + 2WAT* + 2pi +2A0P —_s & pyrwyate +2AAOK 42H RATP +2Ha0 glucose be abe 5 a frit se F4,68P. 2xGAP e——> DAP Relat ae RK 443 BPglycernte. "endat ATP 2K Pyycerate 9K REgycerte ° ax PEP nop Go ath Qn pyruvatea [ Fructoses OWT5 wi } xf PONT albaase DWAP Some an | Fructose eS Fructose 4-P : -Frnctese intolerance + absence of aldolase 8 leads fo intvaccilulny trapping of Fructose +P Notes Both Albslase Aand clemle Fructose 49 BP prohce) buring glycolysis to DNABP and gyceralbehyse->fy but only aldolase B cleaves Fructove 4-P synptoms » hypoglycemia —>'nbibitor of glycogen prosphalase, so glacase is not veleased From tuer, Nactic acidoses —> when Fructose eéidiign eccter 15 400 Kigh Excessive uric acid production —> destyuction of liver and other problems Sepletion of pi and ATP call Suidting Fy . Nectoge, bieayathests “Fe glucose nee oe Fructose —__, QLUT 5 or & a . Yebuctese dehydrogenase 2 liver absorbs most of it some by akeletal m. o branBiochemistry Midterm 2 - Dec. 16, 2014 Section A, * Single-answer questions ( mark the correct answer for the following questions ) 1) 2,4dinitrophenol increases body temperature because there 2) An increase in both oxygen uptake and ATP formation. b)Adecrease in both oxygen uptake and ATP formation }__ An increase in ATP formation but no change in oxygen uptake d)_Adecrease in ATP formation but no change in oxygen uptake e) A decrease in ATP formation and an increase in oxygen uptake. A patient diagnosed with thiamine deficiency exhibited fatigue and muscle cramps. ‘the muscle cramps have been related to an accumulation of metabolic acids. which of the following metabolic acids is most likely to accumulate in a thiamine deficiency ? a) Isocitrie acid b). Pyruvic acid ©} Succinic acid i 4) Malieacid e} Ovaloacetic acid 3) Acommon intermediate in the conversi of glycerol and lactate to glucose is which of the following ? 9) Bereta First intermediate + glyeerad to glucose 1b). Cnaloscatate Mate = DRAP d) Glucose 6-phosphate €]Phosphoenolpyruvate 4) Which of the following does not contribute to the chemiosmotic force required for ATP synthesis ? a) The PH gradient across the inner mitochondrial membrane . The voltage gradient across the inner mitochondrial membrane ©) The hydrogen ion gradient across the inner mitochondrial membrane 4) The aumping of protons by the several electron transport complexes inthe inner mitochondrial membrane. ) The phosphate concentration gradient across the inner mitochondrial membrane. 5) Which of the following compounds or complexes would exist in the most oxidized state mitochondria treated with antimycin ? 2) FAD/ FADH2 nhibtors4 Function [site of action b)NAD+/NADH Siar c) Complex | ( NADH -Q reductase ) lex t Twhidited by rela, 8) Complexil (Succinate-a reductase } amytal om cemniee embeded Tw wne™% e) complex!v ( cytochrome oxidase complex ‘codingenl 7 complex Ul mitochondrial wembraxe cyanide | 7 [complex w iba 7 \eonpler agive a ‘complex VW (Ome) Ap dirikopena ncoagingagele thinsmenbrane Harrier fertachlorophod|unen raREMEMbaRe Wearrier Ggenycin [WMRIGAP LOSEP Fmctonot ATP aytheseee 6)_ Living organisms require a continual supply of energy to exist because : a) ») a 4) a ‘They are not defying the laws of thermodynarnics ‘They convert it into heat energy which powers biosynthetic re They are creating order out of disorder inside their cells They are causing entropy in the universe to increase They are closed systems isolated from the rest of the universe, actions. 7). Glucagon has which one of the following effects on glycogen metabolism in the liver 2 a » a 4 a The net synthesis of glycogen is increased Glycogen phosphorylase is activated , whereas glycogen synt eikos Both glycogen phosphorylase and glycogen synthase are activated 8) Hyaluronic acid is a: a) ») a a) a 9} UDP glucose is : a) ») a ¢) a 10) The rate-controlling reaction for glycolysis is a ») a d) e) Glycoprotein High molecular weight, positively charged polysaccharide Polymer which contains sulfate Glycogen phosphorylase is inactivated , whereas glycogen synthase is activated . Phosphoglucomutase is phosphorylated alycesslaninaggenns ochonivoin strate my guawona _ Bernaaton sulfate ~Keratan sulfate, Repeating disaccharide of glucuronic acid and N-acetyl glucosamine. Ghepartn Upoprotein. ‘Armajor intermeciate in the pentose phosphate pathway Directly required for the production of lactose Required for the biosynthesis of glycerol Oxidized by NAD to produce UDP-glucuronate The direct precursor to the amino sugars Glucokinase. Inhibited by AMP. ‘Activated by citrate a = Phosphofructokinase, @ F 2,69 » Ant fructoki ee 4 3 ee Ac * F580 FP Sma glucose 3 prdteog\year ghe-b SYeesen ycoprotein n CZ aiielgit gle-4-P —y WOP-gncose } mae SES» \uctose WOP-gainctose. guese VoP-giucwonate oF vor+ Multiple-answer questions Mark the correct answers {more than one) for the following questions : 1) Mark the enzymes that catalyzé thé anaplerotic reactions : veplenish intermedinzes of TeAeyde eres AS they axe YEmoved For the cynineds oF glace, ae. MD ree deserter Seg hrerpas ks ener la ee ©) Succinate dehydrogenase. 1) pyavate —> oAA - pyrwiate carboxylase 6) Fumarate hydratase. D) glutamate —yatetoguierie glutamate dehydrogenase ¢) Pyruvate carboxvlase, Sete ce ae = Matiyinalongl-Cof mactase aminoaciss —» Fumerate ceninatransreraces 12) -Amyloseist) S)pyructe Sy malate. = Malic enzyme 2) Abranched homopolysaccharide b) Alinear homopolysaccharide. (yplpranehed) 6) Alineacheteropolysacharide ~anylese (15-20% oF sareh a oy t ~dmylopectin( go - 85% of starch) ©) Can be detected with Benedict's reagent. Section 8 1) Using structures write the reaction of oxidative decarboxylation of a-ketoglutarate, give the name of the; ind cofactors \geded (3 points } ex-Keteglurerate dehy bregenase & Ketogluterate 3 succiny\-CoA 2) TeAcycle:(6 points) TPF slipoate FAD a). Several enzyme reactions inthe TCA cycle are practically reversible, Why 76° values (igen) lve the name of the enzymes that catalyze these reactions. ciwate synttase pgneiite DK )_ Using names write the reaction that s inhibited by citrate, “2 &-Ketegters’e give the name of the enzyme ? We ae i aceryl-CoA + ottloace tale > citrate 3) Draw a diagram that shows gluconeogenesis with lactate as a substrate. (4 points ) give the name of the enzymes that are involved in gluconeogenesis but not in glycolysis . ard jruvate carbowlase y enopopynulate carboryKinase » Fricke 496 and glue 4) OnE ot ete Engi rcasunesee” | ERT anemia, give at least two enzymes connected with the metabolism of glucose 6- phosphate in the erythrocyte. ( 3 points ) e gieose--phosphade dehydrogenase , glutathione Yeductase and gluathione peroxidase 5) Calculate the yield of ATP when 2 moles of glucose are completely oxidized to CO2 and otic meatal ree penis Sara ‘tee = gyestyssn Aimee oF glucose to moles of psrante is eitelGer 6 mess ct TT “Cheseler complete ofdstion oF The X males oF pyre tveugh the TCA cyst on 30 moles of ATP. i i 3bor jotal yield there fore being either fe ee mole e. glucose to cog and 2° Thus 2 mles of gues 36 moles oF ATP From the complete oxidation > FA or Fo moles oF ATPArgenote \s an inhibitor of EB aleteguterle ON (TEA cycle) GAP DW (glycolysis)Liens:BIOCHEMISTRY :POLISE 7-11.2014/ TEST 2 — CARBOHYDRATE ... BTW PD HAVE 5 TESTS WITHIN THE COURSE 1): Corrected and translated : HERE YOU GO |LETSIDE_ONE ANSWERS CORRECT: HII ‘ 3 where elucokinase (GIs im acive form, {*: means connection in the coral ( 8. GKRP*Fru-6-P+GK : bknesrs-Pack cen? rr 36-P°6K doef PrckRe RP" oe slycogen degradation a, UDP-glucose b. glucose-1-phosphate ° py fi @AMP see gucose tp 3 e. water molecule3-Gluconeogensis appears only in liver and kidenys because in another organs and tissues there is a lack of. a pyruvate carboxylase b.phosphoenolpyruvate carboxylase ¢. fructose-t, 6-bisphosphatase diglucose-6:phosphotase ——iwusscle \aeXs thisenzyme e-Lactate dehydrogenase 4. Glycogenosis type Il ( Pompe's disease) is caused because of lack of: a. glucose-6-phosphatase bb. acid maltase ( lysosomal a-glucosidase c.amyl-, 6-glucosidase d, branching enzyme fe. muscle phosphorylase 5. Activator of salivary amylase is: 2. inorganic phosphate b.Ke Pal d. jodoacetate e.Mn 6. Fluoride stops activity of: a. glucokinase . dehydrogenase of aldehyde 3-phosphoglycerine c. phosphofructokinase d, e. transketolaseMORE THAN ONE ANSWER MIGHT BE CORRECT: RIGHT SIDE ling is made from: 4, lactate dehydrogenase and dehydrogenase glucose-6-phosphate b. dehydrogenase of aldehyde 3-phosphogliceryne and 6-phosphogluconate lactate dehydrogenase and malate dehydrogenase of mitochondriom . dehydrogenase of aldehyde 3-phosohogliceryne and lactate dehydrogenase e. lactate dehydrogenase and malate cytosolic dehydrogenase.esorption transport of glucose to enterocyte cell by apical membrane appears with share of: aGLUTL b.GluT2. .GLUTS d.GLUTa. e.SGLT1. (MP is a positive allosteric effector of: a. pyruvate kinase b. phosphofructokinase 2 c.muscle glycogen phosphorylase d. glycogen synthase e. dehydrogenase glucose-6-phosphate |. Products of the reaction ci a complex of B-glucosidase present i der of. enterocytes are: _:000000 a. fructose b.galactose glucose d. maltose i e. isomaltose 5. UDP-galactose: substrate oF avecction catalyzed bg the synthesis oF lactose a, ipa substratum of eetelysed+eaction bylactove-synthase pits the prodact of the reaction eatalgsed by herose-+f wridyiy trans ease cis a substrataim in process of glycosylation of proteins 4d. is a main substratum of aldose reductase e. arises directly from UDP-glucuronide6. Choose correct sentence about phosphofructokinase 2: a. PFK.2 isa bifunctional enzyme a me 6 9P39FK PFK.2 in heart causes increase in Kinase activity of that enzyme pFX 2eactive)—» © F 46 aI vr F 6 meets 4. in liver xylulose 5-phosphate causes increase activity of fructose-2, 6-bisphosphatase . allosteric activator of PFK2 is a protein GKRP 5) OPEN QUESTIONS : Gh-o gycevatdehyde Fructose 4-P ayo ap Age notes pyvavate SLA, oxalcelote — Sqrepuation of city ee callesteric + acetyl CoA (activation) Gin yatvix of titochordvid) transcription» glucagon, aliencine, Sucocorticotdxjabcia) i MatY IX of Ansulin (vepresion) -pytuvate carveniase s Hit veplenihes intermediates of the TCA cycle. ng ey K provides substraies For gluconergentsis. See acon iyveversible yeaction. grequives biotin, feor by biochemi 1s: reaction from gl is 2) Writs ume of this enz Age ATP neta i ‘e yuvete — epyraiele Knase deficiency: phospheencpyvivate rane? % chemelytic anemia-plericiency oF AT lead to (pep) Kinase Cell suiting and lysis @rthoP ~Accumulation oF glycolysis ilermeliates ATP, alanine, and Sepledion. nee ae of laciate and pyruvete. 1,3- BPO concent ation elevation ‘soncentration of fructose-6-phosphate for phosphofructolkinase|:_ake Yale-contalivg reuction For shedy \ce of positive allosteric effect notes ee ; i Fra -46-OF tive ic eff prucsese ub phos phot TIL tors. @¢-4,68P ame iS oration) Scitrate yA ATP is both am iwhibitor and a sabstrite. how? -A4 low cone. ATP enters only the catayticcenter | because oF highaFFinity = stimuledion ce cone. is hgh par? ill also enters the lstere center = inhiWnton. phosphorylase, giweagon rote. glyeageiedegradoatan ae glucagon in glycegen metabaisn 4 a glycogen. } we SG gycegen phasphoiyast PKA ole “eo Geet ae ae) So 1 \ geetbesheomas ahs Krose Y SUSIE protein. phosphatases syegen phosphorglase Bleep 6.Drawa scheme in form of sequence ofconsecutive metabolites) transformation of gevatleysayaldelyde2-phosphostyeerine (GAP) in ctonlazi whi uses b ‘from position a : wl PEPCK= phesphoenolopyruete carbory Kinase 3 2 transcription:.glucagen yadvenatin(epinephin) y glucccorticotd(ieheti 3 ~ insulin (repression) Ros ie z 3 : & a7 iad fy 2 pH Yo Aig di ke | 88 FCP CH Bim’ 2 25, oe © SEs sae cee st | 2845 9 gots; — ded, 5 RY Se F FS SH 8 Aawi fd 2 Ff q atMid-tevmd 2015 A)using structures urite Hee regulatory step in bile acid sytthesic(name of enzyme and coftciey) Fe eget age Ft east - j lesterol tes ot hy dro) lesterol oh Ce Noam >’ oer (eipra: cote! @ cholfe acid O Cy, & yo oH ate 2s Dthe question whether Fatty acids can be converted into glucose in humans has along standing ¢yadition in biochemistry ,and the expected ansuer is "Wo", houever there is pathway dn which gluconeogenesis From Fatty Acids is Feasible Inhumans .Using names write the pathway From Fatty acid metabolism uhich provides precursors of oxaloacetate . give the name oF enzyme and mark cofactors (3 points). ae A0PsPi optonyl col D-methyl malonyl-Cof g——___-» methyl malonyl.cof epics ee PIP Iony| cod cafbenfose Salas Sete ae Yacemase Succinyl co 3)explain how insulin controls the ee medlnsionf CoA mitase lipolysis in adipose tissne, vequiated by insulin im adipose Hesue . adenul Give the name of the enzyme that Grae enyly! cyclase © 5 phosphediestevase @ ans the hhsrmge Leah yen the veactions ehgcatapolon oF Ketone bodies in peripheral issues. name of enzymes. Oia we ay hate 4 i Stes icetylcoa Bhy droxyburyrare -, Acetoace See's Acetoacetyl CoA ng ty Cito phorase) Sliver lacks this enzyme 5) compare the process of oxilatim of very long chain Fatty acids w cand ith B-oxidution. (3 points -the process differs From B oxidation in that molecular og is used in i rain s the First oxidation step, which Forms hydragen perorile (yo, ,uithout the generation of FADH -/VADN is generated in the second shin step of peroxisomal Fatty acid oxjjation. - shorter chain Fatty acid travel 40 mitochondria jwhere P- oxidation occurs generating ATP. jé)How ynany moles of ATP will be produced as tne yesult of the oxidation oF 2cebyl - CoA (acetyl coA wits enter the TEA exele) Hat is Formed From complete Jegrabation of 2 moles oF lauric acid (explain vesuld) (t point) Laurie aci) Re G heelyl CoA = bX = PA moles (72-2) = FOXR moles =|4O a ae eg. myvisticacid Mc —y¥ Acetyl cof = FX = BU mdes (B4.2) = B2X A mdes aLEIE a a cod =BXIR=% mdes (96-9) = UXR moles = 188 eames at oe ee, =P KIR=108 MACS —(Jo6-2) =1o4x2 mols = 212 leg. stearic acid 18 ¢ —>}r Fiorn Final 2018 + {)urite down a Yeaetion that produce an inhibitor For the carnitine shuttle (amavis) {iN covwitine shuttle is eee db - . der S "y Malonyl CoA which inhibits the outer mitochondrial membran ond ri e enzyme eptt Aue ADPepi Acelyl CoA ee Malonyl coA erohe limiting, and regulated sepin FA ayetnes: cof carbonjiase ° ct-€ -Scon Qyraaie “ove ~ciy-C-SCOA ; SoS. epinephri state (end prodned © Siucagon , epinephrine hi AMP and palmi 2) patkuay ¢ ror probuction oF gly cerel relpkste in iver" and abipese:tesue Fal 205 gue adipose tissue $ giyeolyes glucose lysis ie fa ond? glycolysis wal gece’ oy arp mo 508 ycer-p OF SR gle glycerol phosphate % me a od! sere! phosphate hr 3) major condve point For cholesterol bosyninesig vate limiting enzyme) Fusl 2015 3-hy Svony s-metiylalttagl -cof nenlenate HMG-CoA veductase CHG cof) Qhsulm stating eg! Siva statne plot: OM? QB —- SPhleacd pchdtesterah BAT Spon eatin on 9 corto 1) enzymes of Puoridstionn® Fatty acy cobs Epon) Aral 2015 A)Acy) CoA derybragenase. engl con hydratase. 2) PAyNOLY Acyl cof Jehylregenase- 4) p-Velo thiolase St (oxidation) (hydration) @rilarion) ‘ (cleavage) Words or biochemical symbols WYite doun the Yeaction oF phosphatidyl choline Diogpthess ie te vom he enzyme « Explah uihy the ynetkioning metabolism is sbengly associated with this Yeaction (enzymes and col (u mark) Final 2015 AK SAM prosphatidyetnclamine 3G 3S, phosphatidyl methyl vans! Fense _prosphatidyl choline. is generated by the methylation of _ SAM derates the methyl group and methionine is veede) For the biogynbresis oF SAM. [ aidern 4 + methionne wottay Et _ S-Alenosylmetrionine (6) 4 ee Sotae choline prosphactiby etmanolainine ie presence of SAM: 5 of Ariancyiglycere'* From glucose = (4 mark) Final ROWS A lipogenesis the gyrcthesi ele malonyl CoA hee concarrotsioseMidterm 3+ x biosynthesis oF mcainle qaeornean® HOP casi 2 Acetyl coA eggehey Hctoncey cok soe HMG-CoA yaaa A Ww gorbat Sol “ove ety Feet oh ene ly wf WIG -COR Yeductase activity w cholesterd biosynthesis: ble acl y chlesterot Hig Day aiget (4 a) © Meval ovate HAG.coA reductase activity € — % oaytime® a x desaturation of Fatty Meld » msl connm, peemeiee er ae eee rea bens bare vente ot oe saturates Fatty acyl cof a = Marosntarated Fay acy! cot $8 Fotmine wa a ratty ef CoA desaturase mafece sat i jis eemecon jeic acid. eg. stenrayl-Coh a fe soma oles =) se oessenennrzimnar seg aces proce bceicoh (ey -ScaN ny gpleent (cach eae ~ enh gaduct of obb-cuin FR AF Ber B- ovation + propionyl-CoA ce speete a j ry ay ae Gore acer, seeppercx cuysors oF ona) E> ona _propionyl-coA canbe converted 40 glucose { provile pve; ) ee eas ropiony|-coA —vistit-», methyl malonyl CoA EM giccmicaie TEA eyete a pony een reget en ee Sao ee) oh secon ay # Fatty acid q fatty acid +14 MAUP* + Beon4 Zeog +6HR0 production oF cytosolic Acetyl - con, cite seu hs Sinja Lage 4e oxaloacetate + Acetyl con nee © cit7o! See ‘ofa ahcety| CoA “rinsultn mitochonsrion, cytoso\ we the serine residue in aceiyl CoA ae ete is - Aauget oF ag Steps and enzymes of B- oxidation » D oxidation > Acyticotmbehysrogenase Fu AMP dependens proteln Kinase is wuatated to Alan a) dybration enol cof hydratase whot is a NKely conseduence de tris case ite Y ‘con dehybrngenase jonne ota aie Jatt are Palate re enanesis oa? pont RE yeool-3-P pyruvate “2 goin cnaaceste A RS a PEPCK - ayer < coo”, igor MSP ctyok pyravate f Perbenlase 50° ‘ cy -€ -COO™ @ Acetyl con = 0703 aes 7 i = " eeteee ees cyloset the een Sesct plots A)araw a diagram oF level of Ketone b dies inthe blood during Fasti i i 101 01 an) explain why B-hy2r Dutyrate isa better energy souree than acetoacetate eer ee Y cnyhrergnnyrate peryivoss ~Aceloacelate can sponlaneously breakdown to acetone which, cammtt be used by the body for Fi = Porydroybatyrate sch ait 90 Wis a higher energy molecule. 1 aysMor Fasting e-b-pDM , bp -guconate OF and malic enzyme s) una ave the NADPH Sources Batty acid synthesis wn Qle-b-f ON 6: gconee PPP glucose eat moe ps?” eos | De alate, Se AAMZS pypunte on cot Set oot wok gee FLEP ae Sag eae RAP co cn MOM NR ate fealty acid synthase hunt ec eagme OR nalony cA oft Efacey coh earboryase ne a aceyi oF citvos ae Ace cof} etek iavete citrate mitochondria YW) Fo hyeronese Feaction and its Yegulation --Yeguiaters step in bile acid sgntnesis® cholesterol Sass” P acrywary chotester\ Fat hyronsluse taped) \ eee ag vegulation oF ccyp at gene promoter by pile acids and oxysterels- al iteaeid : 1 rAcbieacisare “S°° “le nie bad to te FR BRIG recentorsy hich ahaactivete the » Aho? she, hp promotor SKP promoter turns onthe HP gene GAR gene fr the HP gene blocks the expresion of the cyptad promotor” hich Woks the gene and hence no cyptat is produced hividing, bile acid synthesis - unset 08 Os ad yeu pnt aierois y except te) multe the cexpresion asame sory For omy For cypFad yhence mncreasiy bile acid. syninesis-Mid tern 3 wveguaarion oF choleserel Ddioeynthesis 2) Sterol -dependenr reguintion oF Jere ext expression of UNG CoA SRE of Reductase gene- 2) ster -Indepentent prosphori WNG.coA vebuclase activity Is controlled aster |dephospharginon pression: vejuciase gene is controled Wy phouphatyated Form —invcrive s ef) covalently through the actions oF Ampactivates ft ane Wanserption Factor, SREB? that binds OHR at cis-actey rosphory Inked Form. active. roketn Kinase (AMPX)y ond a phospho protein. prosphatase (insulin , @glucagen) ster\ accelerie enzyme degradations proietn of EA membrane Yeduciase WsaF is an nreyl Havin lation» ©! in, @ gacager » a te ee juhibitors oF HAG CoA Yebuctase - stadia tvigs » compe g)iniibred by dss © KVeguiarion oF Aeelyl-cot cardoryiOs® (ace) carborglic acid (24- civvate) long chain acyl coAs and phos A) short-term regulation oF ACC pydveny yi 2 lovg-serm Peguation of Wis carbonyl Aion 1s bots tae. vate linn and the phar eset € Aces Enzyme systhesis/ degradation regulated step in Folly acid synthesis qinsalln “allestertc regulation 7 @ che , es @ long chain Fatty agycot (end prodick of pasenny) aden by ANP -acttanted proven Rivest Trenckivates fhe ergs omens _ phosphorylation! deghoaprargstors fl _ Enzyme ayranesis / 309 fon rerazyree PRA : aden 1 oar Teach vy ve-Secdng uf Diets: a overvVieu oF lipolysis and oxitebion of Fatty acids> gecrened vy diabetes of Wy Fasting ed hohe a ecceal oil FFA royce! Vyase A | abipote cel mentane = Arn iti 40 Blood stream cava OE eee T eet Fatly wel? cytosol cof Fatty agl C8 fatten synthase Fatty agleon aaloyt co 9 F cpt ANecvondvial Fay 21 carve OTE membrane cavnitie cpt at cra COR , Fatty 00) ae, jg oF Kelene BOBS Trento te enon i oe ce ¢ RAcetylcoA yee?” peescacey CoA - @.cok me 00 ie obit Beet ee 3 xbiosyntnesis of mevalonate cytosol oy appa coh oF ac cot RE *7°2, mevalonate SN Acero. Ryicon Metet Be NG-6o8 Lo a ARcely COR Spar AEMANC a a_i * aaacet woyninesis of rosin gondin » oe Zi con OF Dietavy linoleic @cid Avachidonic acid & ap 0G eae pth organ 90: Spee orygense pevonivase ee Sesneaation eel enspinn wot preegluinzenex Apolipoproteins: CA ecilor —_.agec-t» CET? innibiior + LEAT activator” apon-t fr mt Tapoeay Vet acter TapoB-¥B: simctwal protem er -OP ? EcMts LPL ite elylemicrn, x symthesis oF cholesteryl esters > renee de inpie acs mest _faiyoctct $°°_, cho ae esters 203 eI BS cholesterol S42 > cho ee (ol eislecoel Fe "A Sieehaom p Fachybvory daietet Fat hy bronylase (ey Pe (eutic acid) ex) Reyicon -cnasten! acyl noms Femse (act) oft we : e aca Scholicacid Coot WD) Ao R “oH Lecitit ce achteaste eclerol esters | Yegulation of cyprat gene promoter by bite acl and ops | cholesteo! HEE \eethin ao ee @ApoA-\ papoe-+ apo xTAG glucose concn < concent om re Ta Bish yevvauthe vea ction that js, inhibited by nicotinic acid ywhich decreases secretion oF VLDL by #he liver Tiacylgyce! ~Lier he blood VLDL {p-Diacylalyceror ——o— a SADE | cone ( a tye nsrerc | (Tas) Adipose tissue Reto i 0 . : is moogMid-term 4 -2015 4 Using structures write dovin the Venn of Get Methionine synthesis ”.name oF enzyme 3points. Lagi 7 s-Adenossl-t-mednionne (sha) T-meonine adensest Hewsferee wee Me ui od oY fy onsen ie oy arp tay-g on oH L-methionine CW A) vsing names write. Soun Ame Yeaction inhi ion Inuibited by i and cofactors if needed) - (3 points) i Myce fherelic aci Ue espa heer tho Mat NADA IMP S77. Xontosine ynonophosphate VAP derysrogenase Omgcoghenslic acid (rus) 3 SEMP Cond product) Which evgan ! Hiss © has a central Function j ae ction i i fhe origin °F nirogen For glutamine. sgnthens ait Sutomite spree. Draw a Saghyamthat shou ey organ) tissue. (3 points). CEES pose cc Keto glutarate 500" Ot at coor # Yeaction of glutamate Jehydragensse. pe heath : cso occurs primarily in liver and Kidney « x Yeaction oF glutamine synthase oecw’s i Primoyily inthe muscle and liver Hs ca gis ’ cha Gy coo" cof] a fon i ' / : Final ; Reaction catalyzed by an enzyme the deficiency of which results in phenylXetonenria. (PKU), ols a fo ase crea and cofactors ig weede)) (3 marks > z 205 seembghibianleran eo. Oi eee i L-phenylalanine SS aBEe atyacil- €00% ctin-gh-coo” Os fler H) DYaw a general diagrewn of iron absorbtion and Hansportation across the basolateral membrane to cireulati 2 delivery to diverse tissue .. i enzymes Fee Geerattars ‘Ce peas re tissue Mark the most important transl caters, proteins or brian, Lilian ee No alimentary tact tumen or organs dug Fasting sale. 5) Draw a diagtre that shows jelervelationships oF 9) ; ligt the enzymes required by glucagon in gluconeogenesis kat do you tank about the levels of wren excretion inthis state (6 points): -€FFect on pathuay a senate Be ic xy Kinase Fikctose- 156 - bisphespratase. and glucase.b- phosphalase:Mid-term Ut yobs bicycles common steps between the TCA ant wea eyecle wea Wc 4 ° malate ~ ey Nes (esu,) As hima isan oe, ArAcycle 2% ornitine Aspartate ciivulling cytosol ccna oftthine carbamoyl phosf) Ke mate ca Se ae S eunarate = ae PE Sls matte err #Vitortin Bip veactons ig Me homo cysteine aire methionine Cz ayrshase. «+ Lmethyl malonyl CoA _ Beraigpneaul_» succiny cof i a meAiyl malony| cof en s ee # pothuiey ofc cholamine> (nese net fh uur © \2-—-» Cpe ie oe as ‘opt > soprnwe es aOR aan Ayyostne Reh alnse pebyarenslase Mme SphvansFerase Yay bergase Jiminary'step In Je mavoparvnay oF purine biogyie 4 5-prospheribesyl-4-pyrophgd hate 9p) symresiss 7 ‘ ‘ "ae 33 ajaribasl pyre heehee eo-vibose 5-PreHOte —PaBFatan f ae qa opi Qarne nucleotide posphoryvosylamine si Senge commitigd ihe Weve patton) ve purine binepabeste phosphoribeesl pyrepres ete S jhaghe-p-0-rwosiianin (PREP) PRPP gical amisotvans Fevase Si ao IMP ea : OP, oe aeserine biogntbesis, 4 tele! Bs "aot pte te 3 phosphosering cerake a phospharyary pyre SZ zs an ne eae pore M nae eee fee 5 gee ae rd Sot x00 2695 x serine hydro} roms Ferase Yeacton 54, we reversivle cleavage oF glycine by the mt 7 Fe Hg mae Leg WEA ely THE) er eemace ne Gane ow gen ace Serine varerymeniy ans Fete pee glycine z wane an Laces ARO sant” sn pcs: cae ASPRIOGNOSE ees Aspartorelaghs asparagine (asn) reponse Soca OD gspartthe ax gruhesis of ustamine "Eyulaes Intestinal peristalsis ae Wistidine pee Ristomine potent vasodilator fiopa tcarbeglses oo Gog cemlonin ae Weave yrs peal melitor oF ategic reactions MCI Se vepanne ety Mai aN aq degradation oF Histidine » race oa LW sAilnemia Yesults From beFiciency oF rey Siege Wistii anmonia-lyase - Formiminaghutamic acid cece a sharpie yrasose Yeactons ibentvis Jeciciency oF vik 80 Fol vo ™y thes Ry = lyreclne Wire eee veoction » sane eaatteahe> vote | Mee Serpe? Mle a ia Tyrosine Iydronyok MF eae oe wrt oH gow ie ay, dy gia wyrtcn 0 4 9 din ‘ 4 He SyNInesls OF ine 4yroshe i ith Eg porate a “Calvi, vorepvephrine FH piney wien coo” co payaeoee + cl weea weve ecw Wet Watch 4 ors ‘tee 3 ch, oe a import yo) PACNON yo ea is “4 Wo a oH of x specific Yeactions that vequire SAMs nethion: eee ip eee ae Abenos _ Norepinephrine 4 mame beet qe) ne seamatirinarense ; Midterm 2015 Acetyl serotonin melatonin. a “SAR -guamboacetate ae creatine Fina 2015 Gn ter) T prosphatidy eanctamive “seston > phosphatidyl choline leotides _Mucleotises A RS nethy tated nelMidterm Aust : using structwes diautne Yeaction that con be. inhibited by 5 FAUMP ONE the name oF enzyme) © man’) 56 (ela) une sv) WW Mernlene TAF bY, one wa te AR Tymidytate sprthase a ‘6 7) =. uw e fl why i a write eee ion hat convert s mu a fi Awrite doup she Yeaction jhat converts nucleotide to the deay Fort a oti rm: name 0: inhibitor. ae es ay Form: name oF enzyme and @ igre (3) tired NOP Wop Vibonucleotive veductuse Drive. oxide Fey nth» aye A Jerk Ma0P Woo Lat ae iii aa gee f eavtaine vginine Hvala i onnthine "Sate? Bi Taira ovite aprtae Wo + citvallin | Argmine — ese rane (Fecheme, FAD; FYU, BHu) x creatine biogyminess aa ar i ‘yginine, ‘ouawiboaceb’e See" Trniinetransrese me ‘in Kidney, in wer my W) glucose tolerance test = ck 4o normal level within 2h. DP rinayvaalipeale, Ovaeeere sheuN ee ba dw + diabetic cin Habetic people glucose Level uill not go back to normal inh. 35 norma! i oo ser in Fed state with reactions hat generate aD N+ enzymes 7 gueste LW ore gucotoey oP ort 08 b.prosregucen )osphagtucoralactene ————7 aiyoaet aces bps Sete i a ae a pate | ver eee 3 é € ee FF Se ca qceyicoh ee metiy ; AA. Sig A TAG Se8) Samminolevulinic acid ALA) bio synthesis committed and yate-contreling step im hepatic porphyrin ven on Suceinyl CoA + glycine __ PLP AAS §-aminolevuls y os ALA synthase Sr ati om) ae heme fend product) F) heme deqradadion: con yleeigiesy Tnuhich carbon monoxide is genemrted ME sy vgofast ADF BuDPCA 3y0P heme biliverdin NA Tene ongewe”? tavetnenace Peabin 80% bilivibin Jighcamnit ER So 1 cytosol blood aM ila monoghacwronit ® synthesis of & yrethionine and szadenoeyinetionne (aciie methionine): Kio methionine MY sremensginetionin® aes? 5 Nenosylhomocysteine ad (sam) 6A) | ae secn = ws. 2 iat Feeme Brena c sitet og, ihe Sonthase homocysteine a WAS r+ z 9) Glutamate i soit reagan Jo) olwlanate eee e Uslusens a Luctoanarte, ome Keloginiarate utomate Ae MY MA > gutamine 3 Gueaave coor 9 Gudanne” 7 coor coor DH cos “Synthase witew ez0 an wit en cH, om? ay ae Was e eta, a a gta i Tudarninase eta oo" door sy, ee co-wta 1) Alonine See Gut) fn \a)heporrte minors Ferase (AST) Sy z axaloacen® coe ruvake, aspartate te ge alanine 9y) cls \elene e pe wee cqhetjotenie gutomote Bs orten acketegt ee “ coo" Jransinitter that gels regraded box! st agnthess Yeaclion of an inhibitory neure y3)Glulamate secarboxylages % es ear dele eke sxitoacih p ( EAE, jutonle AEF y.anhobstyrte Cons eres a efimincoabyle glutarcte wen s KG x ates wrarboniase iho donsamiase Th hugo er ge < en ie e 1 [007 es abolism oe oka oom pete ap i ee 5 Aeeyl con Oe je Acetate Reaut con ethanol Sse acetaldehyd eae ae cany edisulfivam) Ene ele) ip) creatine, nets Yeaction& the spontaneous production oF eveaitaine From creatin phosphader gor Reanie Ee entine Aes creatine phospht© rcscent gematim OO ic (wnengynatic) cx) - brain. ‘ mea fat aS [exe 7 muscle and Brain Rens = Megane tae Exe 5 aMidterm Ue > “npzinosine al ae (BAS biogymthests: cay Lean SHEE \ x purine nucleotite cycle 0 HVE Hg THF | AS sya, AS ascedengosuceite oN ig | spare re No ‘adie adenine mono Phefh THE Nest we” a a gua | AMP UK, Rap beanies = B nove pashan oF purine Hogttnesty 2 : Vibose-5-P. a iN ror ibosil_ pyrophosphak fi 4 " 0 es prof! a) pyrophosphate ees =e “> phosproriboss amine, Opi °. aynidotransferase S purrwe nuclectile Oe gu GPR ao ca pre ep ah ° hy , ae reaction iwibited by nydopherlic acid? eee Ime 107 1 A nodne nae, Noe Kanes ronophosp hate oe Yeaction marbled by gh conversion of wacleoth to the Jeary Form: woP awe? ban ONPe ebietong red 09-0 Prue Lo) Vivonscleotbe 1 on ok Mecis une onyirag wen secorbamey\ phosphate synthase (cps-D ye CpSalle te Hilla, coger RATP 4H —> ear vanag pone 180047 ghanne + cope 2P—> carbancy shoot @ieteesigutanse part ow? x veoction inhibited by puorowncil te miiyinte ayrcthesis WarPeMee OH une ara? 3 Ea gmt OFOUMP - " re Dieser cena Wes sa sage We sonny _geestin cf eee oe A Raber weiss reaction: Yan Gea s godionificntn pruseT reactions ~eactir catalysed by monoatygenese eOPhatt + Eee oes zOetoxiFicatan phase ir reactins -g\wesRiOne Rx asst ei aut ued substance cee ee - ‘acid Aransport - copper vinding ie ler ae uiashione Functions Detoxification - 721 ag commutes sep ™ hepa per pyre beagn Ee 5-omnolevalinste (ag) sikeci : cing \ CoA + SYNE Fig a cook ee geal rns ceo SeoA esis w Ala. synthasesFee Su Bee Tae ae = balubi, MesA OTIS ver gu0Pah 300? 80%, pillrubydighucurene Teme onygense bilivubin. ER VEE gory bilyubin monegncrene @ ‘(havnt ethanol eae BS ee Liver / ~ethanot Se AB, aceta Welyle anes ‘AON ae ite es ter zi © disu\fvom 1A PRERE AAO _ ethanol SR MEA 5 Acetaldchyde MEOS ER vitamin D3 aot F-Dehybro cholesterol __L > previtamtn 03 ____sviteumnin 93 ——> 26 hybrory cholecotciFerol (25609) kin. liver a5 bgieyese Kiduy Lachyarwoiase Gey) 1,25 DikySeoty chaecalelferol Cealcitvio))geinbegtation oF — oyan Metabolism s Very Import For midterm wb Fina, fA pre seee M foe oss 4y tecapest ith 5K Reais Je“Vitamins & Biotms hy = pyraiate carly fgrucont? {ges pyridol hash (PLY) : ‘Alani cto tanstense (ALY) \ = Aspartsle pa ee o ie ; Lp vate | otthoncetate Phosphatidylcholine +3 SAH Phospatidylethanolamine +3 SAM~ Reaction with diacylglycerol and CDP-choline is also correct and points were given for it. IIL. Write down the overall reaction of primary fuel oxidation in the brain in the fed state. List 4 major processes or pathways that are connected with this oxidation. (5 marks) CH;,05+ 60. ——» 6CO,+6H,0 + Energy Glycolysis TCA Pyruvate dehydrogenase Oxidative phosphorylation ‘Minor reactions - Substrate level phosphorylation wi term2 IV. Draw a plot (graph) that shows the effect of F-2,6 —BP and citrate on phosphotructokinase 1 activity at constant ATP. (3 marks) ATP constant} + citrate PFK | activity [F-6P]V, Draw a diagram that shows the galactose metabolism in the liver (give the names of enzymes). (4 marks) Midterm & aniacrose eu |e oS eaunctose+P uop-wvcose RN ocseee ce a ee ke ewcosee suycosen Syummests unosesphoephatave cides exyCouvsrs wid teMM Uy, Suggest a mode of action for fluorouracil in cancer chemotherapy. (2 marks) Fluorouracil first is metabolized to $.fluoro-2'-deoxyuridine 5'-monophosphate (FAUMP) and FAUMP is a potent and specific inhibitor of thymidylate synthase what results in inhibition of mucleie acids biosynthesis. st the major functions of glutathione, What are the amino acid components of aterm Ev uf glutathione (2 marks) MVS tevin. tk A tripeptide consisting of glutamic acid, eysteine, and glycine + An important antioxidant - Itplays a role in the transport of amino acids = Detoxification w0t27 vu, Explain why the sober (abstaining) aleoholic is not very responsive to barbiturates. Write the reaction. (4 marks) The alcohol-induced cytochrome P-450 enzymes metabolize barbiturates and many other drugs in addition to alcohol. Therefore the sober alcoholic is not very responsive to this drugs. wome,ynidtermMt vi. Are purines and pyrimidines major sources of energy in eukaryotic cells’? Explain (1 mark) In eukaryotes, purines and pyrimidines are not significant sources of energy. Whereas the carbon atoms in fatty acids and carbohydrates can be oxidized to yield ATP, there are no comparable energy-vielding pathways for nitrogen-containing purines and pyrimidines. No ATP is produced by substrate-level phosphorylation during purine degradation to uric acid or ammonia nor during pyrimidine degradation. mite 2% vu. What is the effect of increasing concentration of each of the following on the rate of glycogen degradation in the liver? (a) cytosolic Ca", (b) plasma glucagon, (c) blood glucose. (6 marks) (@ Increasing the concentration of cytosolic Ca, increases glycogen degradation. Ca”, partially activates phosphorylase kinase by binding to the calmodulin subunit of the enzyme. Phosphorylase kinase in turn catalyzes the phosphorylation and thus the conversion of inactive glycogen phosphorylase b to active glycogen phosphorvlase a, the enzyme responsible for breaking down glycogen. (b) Increasing the concentration of plasma glucagon stimulates glycogen degradation in the liver When glucagon binds to specific receptors in the plasma membrane of liver cells, these receptors siimulate the activity of adenylate cyclase, which catalyzes the production of cAMP. cAMP in turn activates protein kinase A, which activates phosphorylase kinase and inactivates glycogen synthase. [c) Increasing the concentration of glucose in the blood decreases glycogen degradation and increases glycogen synthesis. As a result, protein phosphatase-1 activates glycogen synthase via dephosphorylation and glycogen synthesis increases.Essential Study Tips for Final exam 4. Purpose of a pathvray—what’s the overall function? 2. Names of molecules going into and coming out of the pathway 3. How the pathway fits in with other pathways 4, General metabolic conditions under which the pathway is stimulated or inhibited 5. Identity of control points—which steps of the pathway are regulated? 6. Identity of general regulatory molecules and the direction in which they push the metabolic pathway 7. Names of reactants and products for each regulated enzyme and each enzyme making or using ATP equivalents 8. Names of molecules in the pathway and how they're connected 9, Genetic diseases and/or specific drugs that affect the pathway 10. Essential vitamins and cofactors involved in the pathway 111, Specific molecules that inhibit or activate specific enzymes 412, Names of individual reactants and products for nonregulated steps 13. Chemical structures Example of Objectives for Integration of Carbohydrate and Objective 1. Describe the pathway for the storage of glucose in the liver in the fed state? How is this pathway regulated? 2. What pathway provides for the production of pyruvate to be used for fatty acid synthesis in the fed state? How is this pathway regulated? 3. During the conversion of glucose to fatty acid, how is pyruvate, produced from glycolysis, Converted to citrate in the cytosol? In which compartment does each reaction take place? 4, What are the sources of the reducing agent used for the reductive biosynthesis of fatty acids? '5, Which enzyme controls the pathway for the synthesis of fatty acids from acetyl CoA in the cytosol? How is this pathway regulated? 6. What keeps newly formed free fatty acid from entering the mitochondria in the fed state? 7. How does insulin affect the delivery and storage of free fatty acid into adipose cells in the fed state? 8. What are the pathways for the synthesis of triacylglycerol in adipose from glucose and free fatty acids? How is the production of glycerol phosphate regulated? 9. What happens to the glycerol released in the lipoprotein lipase reaction in the fed state? 10. What pathways provide blood glucose during fasting? Why are these pathways active? 411. Glycogen is not made in the liver during fasting. Why not? 12. Giycolysis does not function when gluconeogenesis is functioning. What factors turn on Waceygiutamate +co8 catalyzed by M-aedbigiianate eynirase- U4) nitrin oxide biosywthesis PoHk MOP" 6 Arginine * NO + citrulline nitvi: oxide sprit (Fe-heme » FAD, FMA BK) aver oa cotate gute akeoseaente alanine « a Xelogiuterde ———> Pyrwiate + gutante ALT on iy glutamate + acetyl cod dy acetyiguranate __ *F ee —~s 2ADP efi carbamoyl Phespl synthase (eps) Carbamoy\ phosphate 5) pathuays For pra duction oF glycerol phosphate inliver and adipose tissue» Liver” glucose Y gycotsss Dinyivorpacetone phospale (onar) wane glycent-P dehyhagenase AOS neo" ; ly cero gyyentl phosphate dyes pe gueose glycolysis pilydronjaceione phosphate (onaP) re) glycol -P Deby bragenase glycera phosphatenee of B onllation of Fatty acyl col (2 points) Lacy) CoA dehydrogenase. A) enayl col hysractese. Dp hySrouy aegl cof Sehybyogentse 4) B-Keto thiolase « ie te Kinase by glucagen.. A veguiation oF Pyvava’ cates ae es Ss | leads to inactiation oF pyruvate Kinsse in tiver-, are Spee Can «PP; when bleed glucose levels are lowly elevated glucagon increases the intyaceltular level of CAMP, which causes fetive prten Kinase PEP the phosphorylation and inactiation oF Pyrivate Kinase . ah. therefor, PEP is unable to eontinue In glycolysis, but inetead Le enters the gluconeogenesis Pathasay- pytente RIF pyyniate Mose Kase, 2 Cnactve) AYP Gctive) Pyrwvore S)Aspicin inhivts prostaglandin (enzyme ,mechaniem an} lype oF inkivition) =. ake synthesis of Prostaglandins canbe inhibi For example, Aspirin (nonstevoidal axti-inFlemmat event the synthesis oF the parent prostagl @ 2) pe Prostag| ted by @ number oF unvelated compounds. of) agents [rsA105}) Inhibits both Cont and COKR and thus, landin POU, 9) hepato cetular Joundace py incrensed Unconjugated bilivubin levels inthe blood : Wneveased Wobllinogen inthe urine. prevalecyie, bamaye con cluss Uwconjugated bilivubin levels Inthe bleed te Yesult of decvensed Conjugation. urobilinogen ig Meveased in the uvine because he, decreases the enterohepatic clvculation oF this compound increase as « Patic damage pallowing more to enter the Hood, From HS Altered ints ane uvine « 10) Fetal ond adult hemoglobin. soe il) enzyme deficiency lead to hemolysis -has the highest hich, prevalence inthe midlle east, tropical affiea andAsia, and i > parts of tre mmaltervancan Geen *, 6 -phosphogluconolactont { Ye gucese phosphate MRO AEN,» “ he § o* ae dehydrogenase ih a cu oll ch-ok a ; 5 Bk m partial pressure (PO, mug) Ho-cll Wo - cll ony gen pay got ci et) chee ot ' = 12) Widney inlongcterm. Fasting (3 pei) ety~ ° o cHy-? 7392Final brochem 29 reset 2015 ishg structures draw the venction catalyzed by an Enzipne jnvdlved in nilvogen metabolism that ts epee t) especialy actwe Mt Ki ms ce Mame of enzyme term ot 7] a not t) especialy ney dat, not m sKele tal s le. write oF enzyme (3 points) Mid-temt ath glutarnine BRE. glutamate giwrayninas € coo aa 1 coe Ns WtcN We cua hy ly es Hy eae om 2) structure @F cholesterol « wR gee a yo BD list oF vedon yeaction in TCA cycle = @ pointy) Jise citrate dehydrogenase * g)acxeteglaternie derylragenase 3 sieciwite dehydvogenos€ 1) malate dehydrogenase . ion DP +pi +Rtyo ——> 2cog 3A tem W Krebs cycle _NET react Acetyl CoA + BHAT + FAD + 4) penal ingavchion. - cK and LDH in one graph: Die FADHRAOTP 4 HT Lo extent oF enzyne incre pays “artery episode1D) phenyl butyrate + vep plop bt ee cycle enzymes aie vine ge utyrate is a prod that is yapldly converted to phenylacetate ywhich combines with glutamine to Form phenylacetgl glutamine - The phenylacetylglutanine , containing Ratoms of nitrogen, is excreted inthe uring ,thus assisting in clearance of nitrogenous waste. A) bisphosphoglycevate jnFluence on the oay hempbobin curve Jrenpentee the importance of 3 BPO as an allosteric ‘ i Yequltor of hemoglobin’ O aFFinity § a 3 iti Pon D glycogen synthesis menzymes ond reginton (fee Fh Clare Generac NOs glycogen poe One genes siete felines top le Branching enzyme Hblood le \evel 5% insulin, 5 glycogen synthesis b bleed Gle \evel ——>* glucagon > glycoge geqosation « giejancl consumption may cause hypoglycemia in a Fastig jnaivival (2 points) -exgain- the # high aon [WAD™ varior. inhibition oF gluconeogenesis : - carbonation of pyruvate to ovsloacetate y pyruvete carborylase This reaction ig important because Crepirskes he TCA cycle intermediates, on) proties eubstiole Fo gluconeogenesis CT a Jovlveaction wit vitamin By — enzyme and co Factors (ecto) vat THF homo cysteine 8 merhjonine mresthionine syndase |))-9ap dw the replication Forke Mlipogenessopen questions aditional Exam Ao» Dusing structure write down the Yeaction which leads to the Formoction shay carnitine shuttle (write the name oF enzyme). Fan inhibitor of the Abp epi Acetyl con oe Botin 5 alonl oA Acetyl coh catbonge © 2 3 Chg - -scoa tock -cty-t -ScoA veaetion inhibt aes pe" ee Mevalonote HMG-CoA veductase (HME - CoA) Ostatin e.g. simuastatin Sbile acid , cholesterol OMevalonate 3) cori cycle + glucose glucose > glucose 1) vegulated enzgnes oF geonengenesis: int eae 4) pyruvele carborylase alactate Q lactetec} Alactote 2) phosphoencipyrwinle corboryKinase liver bleed — | muscle 3) Fructose-t,6 diephespte wer anaerobic condition 4) glucose _b- phosphatase 5) Now many ATP molecules (NET) will be generated daving the conversion oF glucese to lactate, Explain» -glucose ——> glucose-6 _ phosphate on ee = Fructose -é-phosphate ———> Fructose tyb-Biephesthote iene) ar? 3-Bisproophogce™ ie ae are _2 3 phosphoglyc evalthyde 4 t, ail cuete _2 443 Bispresprageerate eth gle vat tap pyruvate —oapyrnwate ea > ies NADH sumaery 2 ATP Mar yotic maa G)dvau the structure of ew 57 unvansiated YES'O" gus. eb vegion 0, aa yegion e082 : (AMAR) > poly tai Psources crs nccee eon, 5 yeoreP — hoursP) reaction Inhibited b aan oealh * acetaldehyde He Geelalbengie OF "acct © onns-bigul van (fniabasy geperal)- used For the jreatment oF alecholism. 10) puri. BE eae structure + 2 glycine copa 2 Wh 1, 1 ie met eny tetrahyhre Felete Le a (ear) ett ie ©) amilentrage oF glutamine I) tegration oF ovgan metabolism in Fed state ge fee fan y a pom > ances ia i. pep ren ge acely\ CoA PPP egle-&P \ Q guece!3P & ‘acely! coh ——» FF Auipose pee Te 19" blochemishy aasitional EXO 2015 3+ (name of enzyme). 4) using, structure, ig peal Which leads to Formation of an inhibiter oF carnitme shuttle « aces con NC pen iB zralaylco® Reagent or mate ScoA ie eign - SER Alusiny structwe , ABA eee Yea ction (enzymes and pofactors) * ghatomnmte pI {Amino butyrate » (GABA) oo | eee . co Wats n all" eta aed Ry ; i et ‘ coo" coo iain. Byy - Enzyme and cofactor > he deel of homocysteine with vita Dreaction which deca homocysteine methionine caine antec ion of glucest to lactate. Elaine Wiorw may ATP molecules (VET) wil BE generated = she cones 2-6. phosp are tT = gucose ———> ues 1a bvuckese £p—— > ee 246°! en om ts ie "i at -2 apne ghoopheslyceraldeyle —> ee 4,3-' ee hy ey a? sae j a? ame 4 4,3-bepr gy cele 9 ae QA 4 prospho json 2 2 a 9, pyraate g lactate Hyfructose indolerance, wis in hypoglycemia e os > 4,688 eMainy ruciese Se, “3 fructase 44. Tres Fenzy —p fructose 2° qlycalstic glyceralhy 26 ——> Be mesiates _deficieney of liver are “a (fiutep aldolase activity) : yeleased From liver ween ae OF glycogen phosphorylase ee on? and pi hyper wiceni i Auhy ethanol Consumption may canse dypolglycemia. mo Fasting “Nigh 108 /1100% tion _rnibilion oF gluconeogenesis: eas oF pyywate +0 dale ac fefleriches the TCA cycle intermediates rate fhe een juhen is it given and how does VF work * aelabolicm of nityoyen ina posient uth a def enram: hate egriheo “phenylbutyrate converts nitrogenous waste Ose ae ae oll prodrug tat is rapidly converted te phenylacelate which combines wih glutamine te From psogucese is not individual » ehate by pyruvate carboryfase SThis veaction ig importaws because’ and provikesaubshiset For guconeaseresis \butyrate {5 a acelylgluanine - Lane phenyl eens containing 2 atoms of mikregen is excrete Im the urine y thus neleale He eal =e ang) y ne assisting in cleavonce of pre)g)Methods For veguleting Acelyl-CoA carboxylase activity » allosteric regulation eer © (Hybrorytricarboylic acid) long-chain Fatty acyl CoA © (end product of the pathnay), phorylation. [dephosphorylation = phosphorylation by AMP-activated protein Kinase or protein Kinase A inactivates enayne grelein amounts decreased by Jnbeles ory Fasting OE and increased by Ye-fecding lon-Fak diets . pls Enzyme syndhesis degradation” 10) overall reaction of Monoorygensses - enzymes OF cytPUSO group WAOPH+HY 4 On 4 RH ——>y ARDPY 4 Ho + Roll erchiotic (pharmacentical ethanol toric substance) I)How to dlagnase Helicobacter pylori infectionsreaction x Uvease fest nae 3 econ teas fi 5 oie wvease Ea . Ms wea) 12) what ove the Vochenical consequences of elevated purines level in : Ufesence of HPRTase ‘ L oacltgiadis -clinicol symptoms Mental vetardation » self-mutilation, increased uric acid ynewologieal deFects and eer behavior. i) what role does RHA play other shan tramsmigion oF genetic massage > RNA has 5 basic roles inthe cell: 4) serves as the indermedtate inthe Flo 2) Auld molecules (tPA) Serve as ajaptors that brings specifi 3)RIYA molecules ave important Functional components of the molecular mackinery called ribosomes » 1) small nuclear RAACar RU) ond microRNA miRUA) are vowed in RAIR splicing and gonesregeletion. describe or dyaw the glucose Stimulated, insult secretion + 0b puherestic athe B cells ave the most important glucose -sensing cells it the body Lile the liver; B cells contain, GLUT-2 Jrans porters and have gluceXinae activity, and thas ean phospho glucese in amounts proper tion! 4o is actual concentration in the blood. eIngestion. of glucose of a carbehyraie-rich. neal Jeads 4o a vise in Hood glucose, which is a signal For increased insulin secretion. as welas decrensed gucagon synihest and release) a glucose is fe mast important siimulus For insulin. secretion, 1) of information From pif to proteln. ‘camino acid to vibosome:mRuh comples. 1B) draw a Hagia of HDL melabelém=Fina, 2013: 4) using structure draw the last reaction of gluconeogenesis. give the Mame oF Enzyme. * yoow eB Ps fe" ol iQ Zoe se oh glucose -b-phosphate ir p.peaphaiaet vo\e_fh we Yeguittion of activity transcription ~ elucsgen, adventline » glucocorticoids (induction) - insulin (vepression) wlver and Kiley ave Ree only organs Aut veleuse Ree gicose From gu? ~this prO cess vequives 2 proteins .glu-b-p Hanslocase (Wansports glu-b-p across EA mem - ERenzyme , 9\u-b phosphatase (found only in quconengentc cell) x deFiclency oF gu-b.phowphatwe leads to von GierKers disease xmuscle glycogen cannot be used to maintain blood glucose level because muscle lacks glu.6-preephaiase- Dusing struchwes wire ey Lager In case of enzyme deFiciency (ame oor, acted 0) byane) Q2015, -ch-coo™ al se et i (84) Coe ia elghobnpers siya hopin 5" Neeaiane L tyrosine prenylalayine ry drorylase “pu, idk PKU, caused by a deficiency of phenylalanine hybroryluse ~ chatacievized by accumulation oF Prensiatonine, Pe ce (and a deficiency oF tyrosine) es amperes enc 4o arinmals Using names write down the reactions with the name oF enzymes Ge paint Mb accumulates in Wook. -brain damage , coma, deatrrlack of ATP n newel defect: inthe Win. omnia i wale ue gutamate unin piles the Wein of COMA levels to Fail and the TCA cycle 4o stop Yesulting in permanens cel damage - aceteguutarele causing glwtanate. a> x. Ketoghurerete det Se Gallosterie erghogem o eincreaseh gamut eat te ghanne Fratin shen leplles gutanate toes needed to mae, O48 (0 ree My ATPAR gutamate Famer g\wraynine — @ 2015 lig eg goctins oF guanine: 3 points A tripeptide consisting oF gulamic acid gcysteine and glycine ome acid transport : 5 ie -An important antioxitant a) DetexiFication « ~ Detoxification 3) Reduction agent ~ plays a vole in the dansport oF amino acis. 1 steroid hormone metabolism: B)Xenobictic, metabolismFinal 2013 = 8) how many ATP molecules (ne) wil be generned turing the conversion oF glucose to lactate - Eiglain your ealetakion. 3 pony _ glucose > gliucose-6- phosphate tarp -4ATP a Fructose -& phaphele —>> Fuclose 4,6 Bisghosphate -1MP = -4.anP es 1g, aphospejyccllehyhe —y 2 1,3-Biphosphesyerst= Rawk — on bat? © 2 ty3 Bsplorpaglycernte a2. 3phaspheayeerte a aarp RAP / 2. phosphoenopstavate —> 2 purwinte ome aah 6-6-(¢) oR pyvuvate lactate = RNAON (GyB Ar? ~ ghucose PI sasnnary bar arP—gcese> Jackate draw a di 4 fies {) das a diagram of the cori cycle under whodfeonditins vould ou expect the evi efele tobe actives 3 porns? oo Acid Cori) cycle is a metabolic pathway in which lactate produced by anaerobic gly eclysis inthe cles. a Vive blood | muscle glucose gucose> gircose gluconeogenesis is Gare ayesuibps 2a0P Qlactate gladete el -2 lactate *P)dra he enygen binding curves oF hemaglcbin wher the lok) oF 2,3 B/G GHB is the Fotlasing> F mmol and © mma! L Gltue curves should be on one plot) 3 points. 5 s aS visphosphoglycerote is an allosteric vequistr of Hb'S Ox aFF ity. i fe # “e = 2,3 BPG binds svenghy to tee Beony Form of He but only weakly tothe ory Form. 3 epinaghrine : is Brean OWA (exa pode’) gran mo 7 ubew civote 2015 Abe > aise the a ways Hat acetyl-CoA carboiylase canbe regulated e 4) short-term regulstion of ACCE Wybrorytricarborylic acid (eg. cite) Jlohg-chain acyl CoAs and phosphorylation /dephosph 2) long-term veguinion of Acc Enayme syniness/begvaatin, afl Anis courboryetion is bot #he Yoleiing ant the vealed Hep in Fath acid anthesis ~ allosteric vegulation > citrate © oe long-day Fatty acyl coh (end prOduck oF the pathos) au insulin _ phosphorilatin] dephesphory lation phospherslation by AMP-activated protein Kinase e¥ protein Kinase A inactivates ene he "he _Enzyne bguhessJegadations Enagrc gtohin amounts creased ly Habel 0” by Fasting amd increased by ¥e-Fthn let bit Q)Draw the structuye of exkayetic mfuh(3 part). 5? untranslated Yeon 49 “by mFoppP a »)"Final 2013 Q2015 2 points) 10) Explain a mote oF action Fer Flusrowacil iN cancer chemotherapy (3 poinis) AUK metabolites: 5-Fluorowacil (5-FU) 5 -Aurcewiine 5 Hiphoctate a -onalog of uncil nop Face 8-deorjuithe 5t-monophosp) - Converted tothe active metabolite FUTP and FDUMP ~ FUTP mig esFiciently incorporated indo Rl —>inhibits its maturation _FDUMP=15 0 potent and specific ievercible inhibitor of thymidylate synthase , resulting in the inhibition of DTAP synthesis and leads +o ““Ahymineless leah Fr eels Final ZoUrs- 4) Write doum a reaction thet produce an mhibiter for the camitine Shuttle coynitine shuttle is Whibites by Aalonyl CoA, which inhibits #ihe cuter mftechon ° a So Bleu. aseon an ett Vimiti uledled step in Faity ati eae Toe-limiting. and vega etep Fat Acetyl Co carborlare Irial en menbrane enzyme cpTt ° i Clg C~SCOR ap i Acetyl coA A) write down aveaction regulated by glucose-b-phosphates ' _hexokinose (ail dgsues) ig tnibited by its product ubile guucokinnse (liver and gancrease) is not 4063 ene (ineversivid steps in. she herokinase> al sleric- gle-bp inhibition ae y glace Kinase > insulin, Jponcton we oY mp | AP as Nigh carbonate meat G glucose NA 5, qucose-6. phosphate ensen : hexokinase a at in ‘repression 3) write down the reaction thot converts nucleotive to the deory Form: n ~De nove synthesis oF Reowyribonuctectives fom vibomclecthes name Me inhibitor. Toonucleoti bee wee secs QeGo, Pee = vegulation: * y 4 arden, toetang Keil ©) actus stes: gape - MTP © “Wo? "wor irre ge hia Fibonucleotibe vebucinse rymidine diphosphate (TYP). Uma) ighigen HTS Yauue “MONO Ua earncta “Mle vebuctese ribonucleotide reductase i ible For maintai praecblalee ase is vesponsible for maintaing « balances supply of the deonyribonudectiles reid jor control point For ma 4) cholesterol biosynthesis t gueortet® mvt, cof-f% Yegulation oF cholesteral synthesis: WG -caA (G-Eoh ve aes 4) stera-bependent vegulation af gene expression, F : $5 2@ ‘slevol-acceevatel enzyme bere es @stoting eg, sinvosta Jster-inegenent Pe rating pile acid » cholestere! i ma a “a a i 1) hormonal Yegulttions “oheagen a0 she satin dvugs ae ‘i 5) inhibition by drags = Yate-limniking enzyme - ——__—_—_— —_