Inligting

Hoe word gliceraldehied 3-fosfaat in glukose omgeskakel?

Hoe word gliceraldehied 3-fosfaat in glukose omgeskakel?



We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

In die lig-onafhanklike reaksie van fotosintese is een van die produkte gliseraldehied 3-fosfaat, en die Wikipedia-bladsy oor die lig-onafhanklike reaksies sê dat 6 hiervan gebruik kan word om glukose te vorm. Die Wikipedia-artikel oor glukoneogenese noem dit egter nie, en die Wikibooks-artikel oor glukoneogenese noem slegs die molekule gliserinaldehied 3-fosfaat (wat ek nie seker is of dit 'n tikfout is nie, want ek kan geen inligting oor gliserinaldehied kry nie).

So hoe word G3P eintlik glukose (en is daar 'n goeie rede dat hierdie inligting nie op daardie Wikipedia-bladsye, plus die bladsy op G3P beskikbaar is nie)?


Advies aan studente in biochemie

Hierdie webwerf is gemoeid met biologie, nie met biologiese inskrywings in Wikipedia nie. Wikipedia is 'n vrywillige poging waartoe enigiemand kan bydra, en is vol foute en weglatings. Die struktuur beteken dat dit op individuele klein onderwerpe gefokus is, eerder as om 'n geïntegreerde weergawe van verskillende wetenskapgebiede voor te stel. Die student wat 'n gebalanseerde geïntegreerde weergawe van 'n onderwerp wil hê wat aan redaksionele hersiening onderwerp is, moet 'n handboek raadpleeg. Diegene wie se hulpbronne dit nie toelaat nie, moet probeer soek op NCBI Bookshelf, wat gratis aanlyn soek-alleen toegang bied tot ou uitgawes van tekste. Vir biochemie, Berg et al. word aanbeveel.

Die opwekking van glukose uit triose wat in die donker reaksie geproduseer word, word goed verstaan

Die antwoord op die vraag kan gevind word in bv. Berg et al. 20.1.3:

Die 3-fosfogliseraatproduk van rubisco word vervolgens omgeskakel in drie vorme van heksosefosfaat: glukose 1-fosfaat, glukose 6-fosfaat en fruktose 6-fosfaat ... Die stappe in hierdie omskakeling (Figuur 20.9) is soos dié van die glukoneogeniese pad ( Afdeling 16.3.1), behalwe dat gliseraldehied 3-fosfaat dehidrogenase in chloroplaste, wat gliseraldehied 3-fosfaat (GAP) genereer, spesifiek is vir NADPH eerder as NADH. Alternatiewelik kan die gliseraldehied 3-fosfaat na die sitosol vervoer word vir glukosesintese.

Berg et al. Fig. 20.9

Die Afdeling 16.3.1 waarna verwys word, is 'n algemene behandeling van glukoneogenese, wat dieselfde is in alle organismes of selle wat die ensieme besit om die unieke stappe daarvan te kataliseer. (Sommige selle het dalk nie - of hoef te hê nie - die aanvanklike stappe vanaf piruvaat. Trouens, Fig. 20.9 toon die stappe na G 6-P - die enigste stap wat ontbreek is die fosfatase-stap wat glukose genereer.) Daar is dus geen rede om 'n rekening spesifiek vir plante te verwag.


Glukose word gemaak van die trioses (3-koolstofsuikers) in plante volgens die gewone glukoneogenese-weg. Dit wil sê, gliseraldehiedfosfaat word deur triosefosfaat-isomerase en aldolase na fruktose-1,6-difosfaat omgeskakel, en dan gedefosforileer om heksosefosfate te verkry. Vrye glukose is egter nie gewoonlik die eindproduk in plante nie; in plaas daarvan word glukose aan ADP gekoppel vir gebruik in die sintese van stysel.

Ek is bevrees dat ek geen goeie open-access-verwysings oor plantglukoneogenese gevind het nie, maar dit moet in die meeste handboeke oor biochemie behandel word.


Stap 1: Hexokinase

Die eerste stap in glikolise is die omskakeling van D-glukose in glukose-6-fosfaat. Die ensiem wat hierdie reaksie kataliseer is heksokinase.

Besonderhede:

Hier word die glukosering gefosforyleer. Fosforilering is die proses om 'n fosfaatgroep by 'n molekule wat van ATP afkomstig is, te voeg. As gevolg hiervan is op hierdie punt in glikolise 1 molekule ATP verbruik.

Die reaksie vind plaas met behulp van die ensiem heksokinase, 'n ensiem wat die fosforilering van baie sesledige glukoseagtige ringstrukture kataliseer. Atoommagnesium (Mg) is ook betrokke om die negatiewe ladings van die fosfaatgroepe op die ATP-molekule te help beskerm. Die resultaat van hierdie fosforilering is 'n molekule genaamd glukose-6-fosfaat (G6P), dus genoem omdat die 6′ koolstof van die glukose die fosfaatgroep verkry.


Die 10 stappe van glikolise

Daar is 10 stappe van glikolise, wat elkeen 'n ander ensiem behels. Stap 1 – 5 maak die energie-vereiste fasevan glikolise en gebruik twee molekules ATP. Stappe 6 – 10 is die energie-vrystelling fase,wat vier molekules ATP en twee molekules NADPH produseer. Die netto produkte van glikolise is twee molekules piruvaat, twee molekules is ATP en twee molekules NADPH.


Metabolisme van koolhidrate: katabolisme en anabolisme (met diagram)

Kom ons maak 'n in-diepte studie van die metabolisme van koolhidrate. Die metabolisme van koolhidrate word deur twee prosesse gedoen: A. Kataboliese Prosesse en B. Anaboliese Prosesse. Die kataboliese prosesse van koolhidrate sluit in: 1. Glikolise 2. Sitroensuursiklus 3. Glikogenolise 4. HMP Pathway of Pentose Fosfaat Pathway en 5. Uronzuur Pad. Die anaboliese prosesse van koolhidrate sluit in: 1. Glikogenese en 2. Glukoneogenese.

Metabolisme van koolhidrate in die sel:

Metabolisme is 'n komplekse proses van afbreek en sin­thesis van die biomolekules binne die sel. Afbreek van molekules staan ​​bekend as katabolisme en sintese word as anabolisme genoem.

Die kataboliese prosesse van koolhidrate sluit in:

(4) Heksose monofosfaat pad en

Die anaboliese prosesse van koolhidrate sluit in:

A. Kataboliese prosesse:

1. Glikolise:

Glikolise is die afbreek (lise) van glukose na pirodruivensuur onder aërobiese toestande en na melksuur onder anaërobiese toestande.

Anaërobiese glikolise word ook as Embden-Meyerhof-weg (EMP) genoem, na die wetenskaplikes wat dit voorgestel het. Glikolise vind plaas in die sitosol van die sel en word begin wanneer die ATP -vlak van die sel laag is.

Dit kan in twee fases verdeel word, naamlik:

In stadium een ​​word een molekule glukose omgeskakel in twee molekules D-gliseraldehied-3-fosfaat. Glukose word óf van die glikogeenmolekule afgesplit óf gaan individueel die sel binne en word gefosforileer na glukose-6-fosfaat deur ATP na ADP om te skakel met behulp van die ensiem heksokinase/glukokinase.

Die fosforilering van glukose dien twee doeleindes. Eerstens maak dit die glukosemolekule meer reaktief en gereed vir ander reaksies. Tweedens, omdat gefosforyleerde verbindings nie deur die selmembraan kan gaan nie, hou fosforilering die glukose binne -in die sel. Die ses koolstofstowwe in glukose-6-fosfaatstruktuur moet herrangskik word om fruktose-6-fosfaat te vorm sodat dit in twee strukture van 3 koolstofstowwe elk kan verdeel.

Die nuwe verbinding, fruktose-6-fosfaat, word weer gefosforyleer sodat elkeen van die twee, drie koolstof-eenhede 'n fosfaatgroep daaraan geheg het. Die omskakeling van fruktose-6-fosfaat na fruktose-6-disfosfaat via fosfofruktokinase is die primêre reguleringspunt van glikolise. Die laaste stap van fase een is die splitsing van fruktose-6-disfosfaat in 2 molekules gliseraldehied-3-fosfaat.

Stadium 2 van glikolise is ontwerp om anorganiese fosfaat vry te maak vir die sintese van ATP en om die gliseraldehied’'s in piruvaat om te skakel. Gliseraldehied word geoksideer, met ander woorde 'n waterstofatoom word daaruit verwyder, en gefosforileer om 1,3-difosfogliseraat te produseer.

Die NADH dra die waterstof na die elektronoordragstelsel vir die vervaardiging van 3 ATP's. In die volgende vier reaksies word vier addisionele ATP's gesintetiseer (twee elk uit beide die drie koolstofverbindings), voordat die finale produk van glikolise, dit wil sê pyruvat, gevorm word. Die driekoolstofstruktuur van piruvaat het verskeie lotgevalle, afhangende van die energietoestand van die sel.

In anaërobiese glikolise word NADH + H + nie deur die elektronvervoerketting geoksideer nie, in plaas daarvan geoksideer deur laktaatdehidrogenase, dus geen produksie van 6 ATP's nie, dit wil sê, ATP's word minder in getal geproduseer.

ATP's wat in anaërobiese glikolise geproduseer word = 4 (7de en 10de stap)

ATP's wat in anaërobiese glikolise gebruik word = 2 (1ste & 3de stap)

Daarom word slegs twee (2) ATP's geproduseer in anaërobiese glikolise van glukose.

Algehele reaksie stoigiometrie/chemiese opsomming van reaksie:

Glukose + 2ATP + 2P, + 2ADP + 2NAD + → 2Pyruvaat + 2NADH + 2H + + 4ATP + 2H2O

Glukose + 2Pi+ 2ADP + 2NAD + 2Pyruvaat + 2NADH + 2H + + 2ATP + 2H2O

Onder anaërobiese toestande:

Glukose + 2 Pi + 2ADP 2 Laktaat+ 2 ATP + 2H2O

(Regenereer NAD + sodat reaksie kan voortgaan in die afwesigheid van suurstof)

Anaërobiese glikolise wat laktaat genereer vs volledige oksidasie van glukose:

Belangrike kenmerke van glikolise:

Dit is die belangrikste roete vir glukosemetabolisme. Dit kom in al die selle van die liggaam voor. Brein en RBC is slegs afhanklik van glukose vir oksidasie en produksie van energie. In die brein vind aërobiese glikolise plaas, terwyl daar in RBC altyd anaërobiese glikolise is (as gevolg van die afwesigheid van mitochondria), wat lei tot die produksie van melksuur.

In skeletspiere vind aërobiese glikolise in normale toestande plaas, maar tydens kragtige spiersametrekking is anaërobiese glikolise die hoofweg vir energieproduksie. Alhoewel glikolise óf aërobies óf anaërobies kan plaasvind, gebruik mense vir ongeveer 90% van die tyd aërobiese glikolise. Glikolise kan geïnisieer word deur glukose wat die sel binnedring vanaf die bloed of glukose wat voortspruit uit die afbreek van glikogeen.

In menslike spiere word glikolise byna altyd geïnisieer deur die afbreek van glikogeen. Aangesien die menslike brein nie glikogeen stoor nie, word glikolise in hierdie weefsel vanaf bloedglukose begin. Die aanvang van glikolise word gereguleer deur die ATP-konsentrasie in die sitoplasma. Wanneer die konsentrasie ATP hoog is en ADP laag is, word glikolise geïnhibeer. Spesifiek, die ensiem fosfofruktokinase word geïnhibeer deur 'n groot ATP/ADP-verhouding. Wanneer die konsentrasie ATP laag is en ADP hoog is, word glikolise gestimuleer.

Glikolise in RBC-Die Rapaport-Lumbering-siklus:

Eritrosiete metaboliseer oormatige hoeveelhede glukose deur die glikolitiese pad. Dit genereer baie ATP wat nie nodig is nie en nie deur eritrosiete gebruik kan word nie.

As ATP -produksie deur substraatfosforylering dus voorkom word deur afleidingsweg te volg, sal dit:

(1) Verminder die produksie van ATP en

(2) Voorsien 2,3-difosfogliseraat wat benodig word vir die hemoglobienfunksie wat help om suurstof in die weefsels te ontlaai.

Daarom word 1, 3-difosfoglyceraat wat gevorm word in normale glikolise nie omgeskakel na 3-fosfoglyceraat nie, maar neem 'n omseilroete deur 2,3-difosfoglyseraat, soos hieronder-

Piruvaat is 'n belangrike regulatoriese punt vir energieproduksie. Die uiteindelike lot van pyruvat hang af van die energietoestand van die sel en die mate van oksidatiewe fosforilering. Wanneer die energietoestand van die sel laag is (hoë ADP lae ATP), gaan piruvaat die TCA-siklus binne as asetiel-CoA via die piruvaatdehidrogenase-kompleks en word heeltemal geoksideer na CO2 & H2O om energie te lewer.

Die piruvaat dehidrogenase kompleks is een van die mees komplekse proteïene in die liggaam en bestaan ​​uit meer as 60 subeenhede. Wanneer die energietoestand van die sel hoog is, is die reguleerder van glikolise die ensiem fosfo­fructokinase, en dus is daar beperkte piruvaat in die sel.

As piruvaat egter teenwoordig is gedurende die tyd van hoë-energietoestande, soos die lewermetabolisme van fruktose, word piruvaat in asetiel-CoA omskep en as lipied verpak. As suurstof na die sel beperkend is, soos tydens intensiewe oefening, gaan glikolise anaërobies voort en piruvaat word deur die laktaatdehidrogenase-ensiem na laktaat omgeskakel. Laastens kan piruvaat deur transaminering in die aminosuur alanien omgeskakel word.

Pyruvaat dehidrogenase kompleks is 'n multi-ensiem kompleks wat bestaan ​​uit 3 ensieme nl:

(2) Dihydrolipoyl Transasetilase en

(3) Dihydrolipoyl Dehidrogenase.

Hierdie reaksie vereis vyf koënsieme nl.:

(iv) Flavien adenien dinukleotied (FAD) en

(v) Nikotinamied adenien dinukleotied (NAD + ).

Asetiel-CoA wat in die bogenoemde reaksie gevorm word, kan deelneem aan die oksidasie daarvan na koolstofdioksied en water, deur TCA-siklus, of die vorming van lipiede, of sintese van cholesterol, ens., ens., wat afhang van die voedingstoestand van die liggaam en die tipe sel waar dit gevorm word.

2. Krebs’s-siklus/sitroensuursiklus/TCA-siklus:

Sitroensuursiklus ook bekend as trikarboksielsuur (TCA) siklus is vernoem na die wetenskaplike sir Hans Krebs (1900-1981) wat dit ontdek het. Hy het die sleutelelemente van hierdie pad in 1937 voorgestel en is in 1953 met die Nobelprys in Geneeskunde vir die ontdekking bekroon.

Krebs se siklus is 'n stel deurlopende reaksies (8 stappe) wat op 'n sikliese wyse plaasvind in die mitochondriale matriks in eukariote en binne die sitoplasma in prokariote. Asetiel-CoA, die brandstof van TCA-siklus, gaan die sitroensuursiklus binne die mitochondriale matriks binne en word geoksideer tot CO2 en H2O terwyl NAD terselfdertyd na NADH en FAD na FADH verminder word2. Die NADH en FADH2 kan deur die elektronvervoerketting gebruik word om ATP te skep.

In stap 1 neem die tweekoolstofverbinding, asetiel-S-CoA, deel aan 'n kondensasiereaksie met die vierkoolstofverbinding, oksaloasetaat, om sitraat te produseer, 'n seskoolstofmengsel wat deur die ensiem sitraatsintase gekataliseer word. Dit is die eerste stabiele trikarboksielsuur in die siklus en vandaar die naam TCA -siklus.

Isomerisering van sitraat:

Stap 2 behels die verskuiwing van die hidroksielgroep in die sitraatmolekule sodat dit later 'n α-keto-suur kan vorm. Hierdie proses behels 'n opeenvolgende dehidrasie- en hidrasiereaksie, om die D-isositraat-isomeer te vorm (met die hidroksielgroep nou in die verlangde α-lokasie), met cis-akonitase as die intermediêre. 'n Enkele ensiem, akonitase, voer hierdie twee-stap proses uit.

Generasie van CO2 deur 'n NAD-gekoppelde ensiem:

Oksidatiewe dekarboksilering vind in die volgende reaksie plaas. Die reaksie word deur die ensiem isositraat dehidrogenase gekataliseer. Die reaksie betrek dehidrogenering na oksalosuksinaat, 'n onstabiele tussenproduk wat spontaan dekarboksileer om α-ketoglutaraat te gee. Benewens dekarboksilering, produseer hierdie stap 'n verminderde nikotina&shimied adenien dinukleotied (NADH) kofaktor, of 'n verlaagde nikotinamied adenien dinukleotied fos&shifaat (NADPH) kofaktor.

'n Tweede oksidatiewe dekarboksilasiestap:

Hierdie stap word uitgevoer deur 'n multi-ensiemkompleks, die α-ketoglutaraat dehidrogeneringskompleks. Die meerstap-reaksie wat deur die α-ketogl­utaraat-dehidrogeneringskompleks uitgevoer word, is analoog aan die piruvaatdehidrogenase-kompleks, d.w.s. 'n α-keto-suur ondergaan oksidatiewe dekarboksilering met die vorming van 'n asiel-CoA d.w.s. suksiniel-CoA.

Substraatvlak-fosforilering:

Succinyl-CoA is 'n energiemolekule met 'n hoë potensiaal. Die energie wat in hierdie molekule gestoor word, word gebruik om 'n hoë-energie fosfaatbinding in 'n guaniennukleotied difos&shifaat (BBP) molekule te vorm. Die meeste van die GTP wat gevorm word, word gebruik in die vorming van ATP, deur die werking van nukleosied di-fosfokinase.

Flavienafhanklike ontwatering:

Die suksinaat wat deur suksiniel CoA-sintetase in die vorige reaksie geproduseer word, moet omgeskakel word na oksaloasetaat om die Krebs’s-siklus te voltooi. Die eerste stap in die omskakeling is die dehidrogenering van suksinaat om fumaraat te lewer wat deur die ensiem suksinaatdehidrogenase gefasiliteer word. FAD is kovalent gebind aan die ensiem (via 'n histidienresidu) wat na FADH omgeskakel word2 wat deur die ETC geoksideer word wat 2 ATP's produseer.

Hidrasie van 'n koolstof-koolstof dubbelbinding:

Fumaraat ondergaan 'n stereo-spesifieke hidrasie van die C=C dubbelbinding, gekataliseer deur fumaraathidrase (ook bekend as fumarase), om L-malaat te produseer.

Ontwateringsreaksie wat oksaloasetaat sal regenereer:

L-malaat (malaat) word gedehidrogeneer om oksaloasetaat te produseer deur die ensiem malaat dehidrogenase waartydens een molekule van NAD + omgeskakel word na NADH 4- H +. Die vorming van oksaloasetaat voltooi die Krebs’s siklus

Die som van alle reaksies in die sitroensuursiklus is

Asetiel-CoA + 2H2O + 3NAD + + Pi + BBP + FAD à 2CO2 + 3NADH + GTP + CoASH + FADH2 + 2H+

Aantal ATP’'s wat in een TCA-siklus geproduseer word:

Die TCA-siklus produseer 3 NADH + H + en een FADH2, dit staan ​​bekend as die verminderende ekwivalente. Hierdie reducerende ekwivalente word deur die elektronvervoerketting geoksideer. Wanneer NADH deur ETC geoksideer word, produseer dit 3 ATP's en oksidasie van FADH2 deur ETC produseer 2 ATP's.

Regulering van TCA-siklus:

Die regulering van die TCA -siklus word grootliks bepaal deur die beskikbaarheid van die substraat en die inhibisie van produkte.

ek. NADH, 'n produk van dehidrogenases in die TCA-siklus, inhibeer piruvaat dehidrogenase, isosi&shitraat dehidrogenase en α-ketoglutaraat dehidrogenase en ook sitraat sintase.

ii. Succinyl-CoA inhibeer succinyl-CoA sintase en sitraat sintase. ATP inhibeer sitraat sintase en α-ketoglutaraat dehidrogenase.

iii. Kalsium word gebruik as 'n reguleerder, dit aktiveer isositraat dehidrogenase en a-ketoglutaraat dehidro en shygenase. Dit verhoog die reaksietempo van baie van die stappe in die siklus, en verhoog dus die vloei deur die hele pad.

Belangrikheid van sitroensuursiklus of amfiboliese rol van TCA-siklus:

TCA-siklus is die algemene pad vir die oksidasie van koolhidrate, vette en proteïene (kataboliese rol). Die anaboliese rol is die sintese van verskeie koolhidrate, aminosure en vette. Aangesien dit deelneem aan beide anabolisme en katabolisme, word gesê dat dit amfiboliese metabolisme is.

Dit is die aanvulling van die uitgeputte tussenprodukte van TCA-siklus. Aangesien die TCA -siklus aan die anaboliese reaksies deelneem, word die tussenprodukte van die TCA -siklus gebruik vir die sintese van verskillende verbindings. Dit lei tot die tekort aan een of meer van die TCA-siklus-tussenprodukte.

Om die TCA-siklus voort te sit, moet daardie tussenprodukte, wat tekort is, deur 'n ander proses opgevul word en hierdie proses staan ​​bekend as anaplerose. Oksaloasetaat word byvoorbeeld gebruik vir die sintese van die aminosuur asparagiensuur en oksaloasetaat word deur anaplerose vervang deur karboksilering van pyruvat tot oksaloasetaat deur die ensiem pyruvat carboxykinase.

Totale aantal ATP's wat geproduseer word wanneer glukose heeltemal geoksideer word na CO2 en H2O

(2) 2 piruvaat 2 asetiel-CoA 2 NADH → 3ࡨ = 6 ATP

(3) 2 siklusse sitroensuursiklus vir die 2 asetiel-KoA → 12ࡨ = 24 ATP

(a) Totaal 38 ATP's word gevorm wanneer een molekule glukose heeltemal geoksideer word na CO2 en H2O.

(b) Netto wins van 36 ATP word gesien wanneer NADH geproduseer in glikolise in die stap wat deur gliseraldehied-3-fosfaatdehidrogenase in die sitosol gekataliseer word, na die mitochondria vervoer word vir oksidasie in ETC, gefasiliteer deur gliserolfosfaatpendel in plaas van malaat-aspartaat .

(c) Netto wins van 39 ATP vind wel plaas wanneer glukose teenwoordig in die glikogeen direk geoksideer word.

Daar is 'n paar reaksies wat plaasvind in die sitosol wat NADH produseer. Hierdie NADH moet geoksideer word deur die elektrontransportketting wat in die binneste mitochon en shidriale membraan geleë is. NADH is nie deurlaatbaar vir die mitochondriale membraan nie, daarom werk pendelstelsels vir die vervoer daarvan.

Daar is drie pendelmeganismes:

(1) Gliserofosfaat-pendeltuig

(2) Malate- Aspartaat-pendeltuig en

Glikogeen is 'n polisakkaried wat uit glukose bestaan. Dit is die bergingsvorm van glukose in die liggaam. Glukose benodig meer water vir berging, maar glikogeen kan met baie minder water gestoor word, dus word glukose as glikogeen in die sel gestoor.

Die grootste hoeveelheid glikogeen word in die lewer en spiere gestoor. Lewerglikogeen verskaf glukose aan ander selle en handhaaf die bloedglukosevlak in normale hoeveelhede. Spierglikogeen dien as geredelik beskikbare bron van glukose tydens strawwe oefening, vir glikolise in die spier self. Glikogeenmetab&shiolisme sluit glikogenese en glikogenolise in.

3. Glikogenolise:

Die afbreek van glikogeen na glukose staan ​​bekend as glikogeenolise.

Glikogeenfosforilase is die sleutelensiem van glikogenolise. Dit werk slegs op α-1 → 4 glikosidiese bindings en stel dus glukose-eenhede een vir een uit die lineêre ketting vry, totdat twee of drie of vier glukose-eenhede naby die vertakkingspunt oorbly.

Die oorblywende drie glukose-eenhede wat deur α-1 → 4-bindings gekoppel is, word deur die ensiem glukaantransferase na 'n ander lineêre ketting oorgedra, en laat dus een glukoseresidu gekoppel aan α-1 → 6 glikosidiese koppeling, waarop die vertakkingsensiem inwerk ( amylo-l,6-glikosidase) en sodoende vrye glukose vrystel. Indien glikogeen alleen aan die werking van fosforilase onderwerp word, sal dit lei tot die vorming van 'n glikogeenmolekule met elke tak wat slegs 4 glukose-eenhede het wat die ‘limiet dekstrien’ genoem word.

Regulering van glikogeenmetabolisme:

Glikogeenmetabolisme word wederkerig gereguleer, hoofsaaklik deur die werking van hormone. Ten tye van skok en opgewondenheid stimuleer epinefrien glikogenolise, beide in spiere en lewer, terwyl glukagon glikogenolise slegs in die lewer stimuleer onder hipoglisemiese toestande. Insulien inhibeer glikogenolise en bevorder glikogenese.

Glikogeenbergingsiektes:

Glikogeenbergingsiektes is 'n groep oorerflike afwykings wat gekenmerk word deur gebrekkige mobilisering van glikogeen en afsetting van abnormale vorme van glikogeen.

4. HMP Pathway of Pentose Fosfaat Pathway:

Heksose monofosfaat shunt pad of die HMP pad is 'n alternatiewe pad vir glukose oksidasie. Dit gebruik nóg produseer ATP.

Die hoofdoel of betekenis van hierdie pad is:

I. Dit produseer die reducerende ekwivalente NADPH + H + , vir die sintese van lipiede (vetsure en steroïede) en hou glutathion in verminderde toestand in RBC.

II. Dit genereer ribosesuiker (pentosefosfaat) vir die vorming van nukleïensure.

Die organe waarin HMP-weg voorkom, is dié wat aktief met lipiedsintese gemoeid is, soos die vetweefsel, nier, lakterende melkklier, lewer, RBC, skildklier en gonades. Dit vind in die sitosol plaas.

Die stappe wat by hierdie pad betrokke is, is:

Transketolasie reaksie:

Oordrag van 2-koolstofdeel d.w.s. aktiewe gliselaldehied staan ​​bekend as transketolering. Dit word deur die ensiem transketolase gekataliseer en die koënsiem is Thaimine-pirofosfaat (TPP). By tiamientekort (ook in pernisieuse anemie) word transketolase-aktiwiteit in bloed verminder.

Transaldolasie reaksie:

Oordrag van 3-koolstof-eenheid, dit wil sê aktiewe dihidroasetoon staan ​​bekend as transaldoladon. Dit word deur die ensiem transaldolase gekataliseer.

5. Uronzuur Pad:

Dit is 'n sintetiese pad vir die verskillende uronsure.

1. Dit produseer glukuronsuur wat deelneem aan die ontgifting van galpigmente, fenole, aromatiese sure en steroïdehormone.

2. Dit verskaf glukuronzuur en galakturonzuur vir die vorming van glikoproteïene.

3. By laer diere lei hierdie pad tot sintese van askorbiensuur (vitamien C).

Metabolisme van fruktose:

In die dieet word fruktose verkry uit vrugte, heuning en tafelsuiker (sukrose). In die menslike liggaam is dit die suiker van die semen en vrugwater.

Essensiële fruktosurie:

Dit is 'n genetiese defek waarin daar uitskeiding van fruktose in die urine is as gevolg van die gebrek aan die ensiem fruktokinase.

'n Persoon toon 'n afkeer teenoor vrugte- en fruktoseryke diëte as gevolg van die tekort aan die ensiem aldolase-B.

Metabolisme van galaktose en sintese van laktose:

In die dieet word galaktose hoofsaaklik afkomstig van die melksuiker laktose. In die liggaam word dit omgeskakel na glikogeen of kan deelneem aan die sintese van die melksuiker laktose in die lakterende melkklier.

Laktose-intoleransie tipe II:

Dit is as gevolg van die tekort aan die ensiem galaktose-1-fosfaat uridieltransferase, wat lei tot die ophoping van galaktose in die bloed, dws galaktosemie en uitskeiding in die urine, dws galaktosurie. Sulke babas is onverdraagsaam teenoor laktose en dus vir melk. Hulle toon simptome soos diarree en braking wanneer hulle melk gee. Laktosevrye melk is die enigste middel.

B. Anaboliese prosesse:

Die anaboliese prosesse van koolhidrate word hieronder gegee:

1. Glikogenese:

Sintese van glikogeen uit glukose staan ​​bekend as glikogenese. Glukose wat as glukose-fosfaat in die sel vasgevang is, word gemuteer na glukose-1-fosfaat deur die ensiem fosfoglukomutase, wat op sy beurt na UTP geskakel word deur die ensiem glukose-1-fosfaat uridieltransferase (pirofosforilase) wat UDP-glukose vorm.

Glikogensintase voeg glukose (die geaktiveerde UDP-glukose) by die glikogeen-primer (voorafgevormde gli&sikogen met 'n paar glukose-eenhede) deur α-1 → 4 glikosidiese bindings te maak en vorm dus 'n lineêre ketting van 10 tot 12 glukosereste, almal gekoppel deur α -1 → 4 glikosidiese binding.

Op hierdie tydstip verwyder 'n ander ensiem, dws vertakkende ensiem (glikosiel-(4 → 6) transferase) 6 tot 7 glukose-eenhede uit die lineêre ketting en dra dit oor na die ander ketting en heg aan deur α-1 → 6-koppeling, wat dus 'n vertakkingspunt skep . Die proses van byvoeging van glukose deur glikogeen sintase tot die lineêre ketting en vertakkende ensiem wat die vertakkingspunte skep, word herhaal en sodoende word glikogenese voltooi.

2. Glukoneogenese:

Glukoneogenese is die vorming van glukose uit nie-koolhidraatbronne. Glukoneogenese help om die glukosevlak in die bloed te handhaaf, sodat die brein, RBC en spiere glukose daaruit kan onttrek om aan hul metaboliese behoeftes te voldoen wanneer dieetglukose laag is. Hierdie proses is baie nodig in die liggaam omdat die brein en RBC slegs glukose as energiebrandstof gebruik.

Die belangrikste nie-koolhidraatvoorlopers van glukose is laktaat, glukogene aminosure (almal behalwe leucine) en gliserol. Laktaat word deur RBC in glikolise gevorm omdat mitochondria afwesig is. Laktaat word ook gevorm deur aktiewe skeletspier wanneer die tempo van glikolise die tempo van TCA-siklus oorskry, word die piruvaat wat gevorm word omgeskakel na laktaat.

Aminosure word afgelei van proteïene in die dieet en tydens hongersnood, van die afbreek van proteïene in skeletspier.

Glycerol is afgelei van die hidrolise van triasielglycerol (TAG).

Glukoneogenese vind hoofsaaklik in lewer en niere plaas. Dit kom ook in 'n mate in brein en spiere voor.

Glukoneogenese vind plaas tydens:

(2) Om laktaat wat in RBC en spiere gevorm word skoon te maak,

(3) As die koolhidrate in die dieet laag is,

Glukoneogenese is amper die omkeer van glikolise, behalwe by drie stappe wat onomkeerbaar is in glikolise. Hierdie stappe word omgekeer deur ensieme wat bekend staan ​​as die sleutelensieme van glukoneogenese, dit wil sê daardie ensieme wat slegs vir glukoneogenese spesifiek is, maar nie vir enige ander pad nie.

Die sleutelensieme van gluko en shineogenese is:

1. Piruvaatkarboksilase (of karboksykinase)

2. Fosfoenol piruvaat karboksykinase

Die proses van glukoneogenese is soos volg:

Rol van 2,6-Bio-fosfaat in glukoneogenese:

Fruktose 2, 6-bisfosfaat (of fruktose 2, 6-difosfaat), is 'n metaboliet wat allosteries die aktiwiteit van die ensieme fosfofruktokinase 1 (PFK-1) en fruktose 1, 6-bisfosfatase (FBPase-1) beïnvloed om glikolise te reguleer en te reguleer glukoneogenese. Fruktose 2, 6-bisfosfaat word gesintetiseer en afgebreek deur die bi-funksionele ensiem, fosfofruktokinase 2/fruktose 2, 6-bisfosfatase (PFK-2/FBPase-2).

Die sintese van fruktose 2, 6-bisfosfaat word uitgevoer deur die fosforilering van fruktose 6-fosfaat met behulp van ATP deur die PFK-2 gedeelte van die ensiem. Die afbreek van Fruktose 2, 6-bisfosfaat word veroorsaak deur defosforilering, gekataliseer deur FBPase-2 om Fruktose 6-fosfaat en P te produseeri. Fruktose 2, 6-bisfosfaat stimuleer glukose-afbraak verder deur vermindering van glukoneogenese deur allosteriese inhibisie van fruktose 1, 6-bisfosfatase.

Hormone wat glukoneogenese reguleer:

Glukoneogenese word gestimuleer deur:

4. Epinefrien stimuleer ook maar in 'n mindere mate

Glukoneogenese word geïnhibeer deur:

Omskakeling van spierglikogeen na lewerglikogeen deur bloedlaktaat en terug na spierglikogeen deur bloedglukose staan ​​bekend as Cori’s siklus.


Glukose word eers omgeskakel na glukose-6-fosfaat deur heksokinase of glukokinase, met behulp van ATP, met die byvoeging van 'n fosfaatgroep. Glukokinase is 'n subtipe heksokinase wat in mense voorkom. Glukokinase het 'n verminderde affiniteit vir glukose en word slegs in die pankreas en lewer aangetref, terwyl heksokinase in alle selle teenwoordig is. Glukose 6-fosfaat word dan omgeskakel na fruktose-6-fosfaat, 'n isomeer, deur fosfoglukose-isomerase. Fosfofruktose-kinase produseer dan fruktose-1,6-bisfosfaat, met behulp van 'n ander ATP-molekule. Dihidroksiesetoonfosfaat (DHAP) en gliseraldehied 3-fosfaat word dan uit fruktose-1,6-bisfosfaat deur fruktosebisfosfaataldolase geskep. DHAP sal omgeskakel word na gliseraldehied-3-fosfaat deur triosefosfaat-isomerase, waar nou die twee gliseraldehied-3-fosfaatmolekules op dieselfde pad sal voortgaan. Gliseraldehied-3-fosfaat sal in 'n eksergoniese reaksie geoksideer word na 1,3-bisfosfogliseraat, met die reduksie van 'n NAD+ molekule na NADH en H+. 1,3-bisfosfogliseraat sal dan met behulp van fosfogliseraatkinase in 3-fosfogliseraat verander, tesame met die vervaardiging van die eerste ATP-molekule uit glikolise. 3-fosfogliseraat sal dan met behulp van fosfogliseraatmutase in 2-fosfogliseraat omskakel. Enolase, met die vrystelling van een molekule H2O, sal fosfoenolpiruvaat (PEP) van 2-fosfogliseraat maak. As gevolg van die onstabiele toestand van PEP, sal piruvaatkinase die verlies van 'n fosfaatgroep fasiliteer om die tweede ATP in glikolise te skep. Dus, PEP sal dan omskakeling na piruvaat ondergaan.[6][7][8]

Glikolise vind plaas in die sitosol van die sel. Dit is 'n metaboliese pad wat ATP skep sonder die gebruik van suurstof, maar kan ook voorkom in die teenwoordigheid van suurstof . In selle wat aërobiese respirasie as die primêre bron van energie gebruik, kan die piruvaat wat uit die pad gevorm word, in die sitroensuursiklus gebruik word en deur oksidatiewe fosforilering gaan om oksidasie in koolstofdioksied en water te ondergaan. Selfs al gebruik selle hoofsaaklik oksidatiewe fosforilering, kan glikolise dien as 'n noodrugsteun vir energie of dien as die voorbereidingstap voor oksidatiewe fosforilering. In hoogs oksidatiewe weefsel, soos die hart, is die produksie van piruvaat noodsaaklik vir asetiel-CoA sintese en L-malaat sintese. Dit dien as 'n voorloper vir baie molekules, soos laktaat, alanien en oksaloasetaat.[8]

Glikolise gaan melksuurfermentasie vooraf, die piruvaat wat in eersgenoemde proses gemaak word, dien as die voorvereiste vir die laktaat wat in laasgenoemde proses gemaak word. Melksuurfermentasie is die primêre bron van ATP in diereweefsels met lae metaboliese vereistes en min tot geen mitochondria nie. In eritrosiete is melksuurfermentasie die enigste bron van ATP, aangesien hulle nie mitochondria het nie en volwasse rooibloedselle het min aanvraag vir ATP. Nog 'n deel van die liggaam wat geheel en al of feitlik geheel en al op anaërobiese glikolise staatmaak, is die lens van die oog, wat sonder mitochondria is, aangesien hul teenwoordigheid tot ligverstrooiing sou lei.[8]

Alhoewel skeletspiere verkies om glukose in koolstofdioksied en water te kataliseer tydens swaar oefening, waar die hoeveelheid suurstof onvoldoende is, ondergaan die spiere gelyktydig anaërobiese glikolise saam met oksidatiewe fosforilering. [8]

Die hoeveelheid glukose wat vir die proses beskikbaar is, reguleer glikolise, wat hoofsaaklik op twee maniere beskikbaar word: regulering van glukose heropname of regulering van die afbreek van glikogeen. Glucose transporters (GLUT) transport glucose from the outside of the cell to the inside. Cells that contain GLUT can increase the number of GLUT in the plasma membrane of the cell from the intracellular matrix, therefore increasing the uptake of glucose and the supply of glucose available for glycolysis. There are five types of GLUTs. GLUT1 is present in RBCs, blood-brain barrier,ਊnd blood-placental barrier. GLUT2 is in the liver, beta-cells of the pancreas, kidney, and gastrointestinal (GI) tract. GLUT3 is present in neurons. GLUT4 is in adipocytes, heart, and skeletal muscle. GLUT5 specifically transports fructose into cells. Another form of regulation is the breakdown of glycogen. Cells can store extra glucose in the form of glycogen when glucose levels are high in the cell plasma. Conversely, when levels are low, glycogen can be converted back into glucose. Two enzymes control the breakdown of glycogen: glycogen phosphorylase and glycogen synthase. The enzymes can be regulated through feedback loops of glucose or glucose 1-phosphate, or via allosteric regulation by metabolites, or from phosphorylation/dephosphorylation control.[8]

Allosteric Regulators and Oxygen

As described before, many enzymes are involved in the glycolytic pathway by converting one intermediate to another. Control of these enzymes, such as hexokinase, phosphofructokinase, glyceraldehyde-3-phosphate dehydrogenase, and pyruvate kinase, can regulate glycolysis. The amount of oxygen available can also regulate glycolysis. The “Pasteur effect” describes how the availability of oxygen diminishes the effect of glycolysis, and decreased availability leads to an acceleration of glycolysis, at least initially. The mechanisms responsible for this effect include the involvement of allosteric regulators of glycolysis (enzymes such as hexokinase). The “Pasteur effect” appears to mostly occur in tissue with high mitochondrial capacities, such as myocytes or hepatocytes, but this effect is not universal in oxidative tissue, such as pancreatic cells.[8]

Another mechanism for controlling glycolytic rates is transcriptional control of glycolytic enzymes. Altering the concentration of key enzymes allows the cell to change and adapt to alterations in hormonal status. For example, increasing glucose and insulin levels can increase the activity of hexokinase and pyruvate kinase, therefore increasing the production of pyruvate.[8]

Fructose 2,6-bisphosphate is an allosteric regulator of PFK-1. High levels of fructose 2,6-bisphosphate increase the activity of PFK-1. Its production occurs through the action of phosphofructokinase-2 (PFK-2). PFK-2 has both kinase and phosphorylase activity and can transform fructose 6 phosphates to fructose 2,6-bisphosphate and vice versa. Insulin dephosphorylates PFK-2, and this activates its kinase activity, which increases levels of fructose 2,6-bisphosphate, which subsequently goes on to activate PFK-1. Glucagon can also phosphorylate PFK-2, and this activates phosphatase, which transforms fructose 2,6-bisphosphate back to fructose 6-phosphate. This reaction decreases fructose 2,6-bisphosphate levels and decreases PFK-1 activity.[8]


10 Steps of Glycolysis, Enzymes involved and Regulatory Enzymes of Glycolysis

Glycolysis (Glyco=Glucose lysis= splitting) is the oxidation of glucose (C 6) to 2 pyruvate (3 C) with the formation of ATP and NADH.

  • It is also called as the Embden-Meyerhof Pathway
  • Glycolysis is a universal pathway present in all organisms:
  • from yeast to mammals.
  • It is a universal anaerobic process where oxygen is not required
  • First phase of cellular reparation in aerobic organisms
  • It occurs in the cytosol of cell cytoplasm in both eukaryotes and prokaryotes

In the presence of O2, pyruvate is further oxidized to CO2.
In the absence of O2, pyruvate can be fermented to lactate or ethanol.
Net Reaction:

Glucose + 2NAD+ + 2 Pi + 2 ADP = 2 pyruvate + 2 ATP + 2NADH + 2 H2O

Here is the video that explains 10 Steps of Glycolysis

2 stages of Glycolysis

First phase: Preparatory Phase or investment phase Phosphorylation of Glucose and its conversion to Glyceraldehyde 3-phosphate. 2 ATP used in this pahse

Second phase: Payoff phase

Oxidative conversion of Glyceraldehyde 3-phosphate to pyruvic acid

(4 ATP and 2 NADH produced)

This reaction requires energy and so it is coupled to the hydrolysis of ATP to ADP and Pi.

Enzyme: hexokinase (regulatory step). It has a low Km for glucose hexokinase phosphorylates glucose that enters the cell

Irreversible step. So the phosphorylated glucose gets trapped inside thecell. Glucose transporters transport only free glucose

Reaction 2 : Isomerization of glucose-6-phosphate to fructose 6-phosphate. The aldose sugar is converted into the keto isoform.

This is a reversible reaction. The fructose-6-phosphate is quickly consumed and the forward reaction is favored.

Reaction 3 : is another kinase reaction. Phosphorylation of the hydroxyl group on C1 forming fructose-1,6- bisphosphate.
Enzyme: phosphofructokinase. This allosteric enzyme regulates the pace of glycolysis (rate limiting step).
ATP is used
Second irreversible reaction of the glycolytic pathway.


Reaction 4: fructose-1,6-bisphosphate splits into 2 3-carbon molecules, one aldehyde and one ketone: dihyroxyacetone phosphate (DHAP) and glyceraldehyde 3-phosphate (GAP).
The enzyme is aldolase.

Up to this step 2 ATP is used
Second phase: Payoff phase
2 GAP molecules generated from each glucose, therefore each of the remaining reactions occur twice for each glucose molecule being oxidized.


Reaction 6: GAP is dehydrogenated by the enzyme glyceraldehyde 3-phosphate dehydrogenase (GAPDH). In the process, NAD+ is reduced to NADH + H+ from NAD. Oxidation is coupled to the phosphorylation of the C1
carbon.

1,3-bisphosphoglycerate is formed

Reaction 7 : This high energy bond of BPG at C-1 is hydrolyzed to a carboxylic acid and the energy released is used to generate ATP from ADP.

Reaction 8 : The phosphate group shifts from C3 to C2 to form 2-phosphoglycerate.


Reaction 9: Dehydration reaction catalyzed by enolase (a lyase). A water molecule is removed to form phosphoenolpyruvate which has a double bond between C2 and C3.


Reaction 10: Enolphosphate is a high energy bond. It is hydrolyzed to form the enolic form of pyruvate with the synthesis of ATP. Irreversible step


The route of ethanol formation in Zymomonas mobilis

1. Enzymic evidence supporting the operation of the Entner-Doudoroff pathway in the anaerobic conversion of glucose into ethanol and carbon dioxide by Zymomonas mobilis is presented. 2. Cell extracts catalysed the formation of equimolar amounts of pyruvate and glyceraldehyde 3-phosphate from 6-phosphogluconate. Evidence that 3-deoxy-2-oxo-6-phosphogluconate is an intermediate in this conversion was obtained. 3. Cell extracts of the organism contained the following enzymes: glucose 6-phosphate dehydrogenase (active with NAD and NADP), ethanol dehydrogenase (active with NAD), glyceraldehyde 3-phosphate dehydrogenase (active with NAD), hexokinase, gluconokinase, glucose dehydrogenase and pyruvate decarboxylase. Extracts also catalysed the overall conversion of glycerate 3-phosphate into pyruvate in the presence of ADP. 4. Gluconate dehydrogenase, fructose 1,6-diphosphate aldolase and NAD-NADP transhydrogenase were not detected. 5. It is suggested that NAD is the physiological electron carrier in the balanced oxidation-reduction involved in ethanol formation.


Step 1. Glucose is phosphorylated to give glucose-6-phosphate. Thephosphorylation of glucose is an endergonic reaction.

Glucose + Pi - > Glucose-6-phosphate + H2O

∆G° ' = 13.8 kJ mol –1 = 3.3 kcal mol –1

The hydrolysis of ATP is exergonic.

∆G° ' = –30.5 kJ mol –1 = –7.3 kcal mol –1

These two reactions are coupled, so the overall reaction is the sum of the two and is exergonic.

Glucose + ATP - > Glucose-6-phosphate + ADP

∆G° ' = (13.8 + –30.5) kJ mol –1 = –16.7 kJ mol –1 = –4.0 kcal mol –1


Onthou dit ∆G°' is calculated under standard states with the concentration of all reactants and products at 1 M except hydrogen ion. If we look at the actual ΔΓ G in the cell, the number varies depending on cell type and metabolic state,but a typical value for this reaction is –33.9 kJ mol –1 or –8.12 kcal mol –1 . Thus the reaction is typically even more favorable under cellular conditions. Table 17.1 gives the ∆G° ' and G values for all the reactions of anaerobic glycolysis in erythrocytes.


This reaction illustrates the use of chemical energy originally produced by the oxidation of nutrients and ultimately trapped by phosphorylation of ADP to ATP. Recall that ATP does not represent stored energy, just as an electric current does not represent stored energy. The chemical energy of nutrients is released by oxidation and is made available for immediate use on demand by being trapped as ATP.

The enzyme that catalyzes this reaction is hexokinase. Die term kinase is applied to the class of ATP-dependent enzymes that transfer a phosphate group from ATP to a substrate. The substrate of hexokinase is not necessarily glucose rather, it can be any one of a number of hexoses, such as glucose, fructose, and mannose. Glucose-6-phosphate inhibits the activity of hexokinase this is a control point in the pathway. Some organisms or tissues contain multiple isozymes of hexokinase. One isoform of hexokinase found in the human liver, called glucokinase, lowers blood glucose levels after one has eaten a meal. Liver glucokinase requires a much higher substrate level to achieve saturation than hexokinase does. Because of this, when glucose levels are high, the liver can metabolize glucose via glycolysis preferentially over the other tissues. When glu-cose levels are low, hexokinase is still active in all tissues.

A large conformational change takes place in hexokinase when substrate is bound. It has been shown by X-ray crystallography that, in the absence of substrate, two lobes of the enzyme that surround the binding site are quite far apart. When glucose is bound, the two lobes move closer together, and the glu-cose becomes almost completely surrounded by protein (Figure 17.4).


This type of behavior is consistent with the induced-fit theory of enzyme action. In all kinases for which the structure is known, a cleft closes when substrate is bound.

Step 2. Glucose-6-phosphate isomerizes to give fructose-6-phosphate.Glucosephosphate isomerase is the enzyme that catalyzes this reaction. TheC-1 aldehyde group of glucose-6-phosphate is reduced to a hydroxyl group, and the C-2 hydroxyl group is oxidized to give the ketone group of fructose-6-phosphate, with no net oxidation or reduction. (Recall that glucose is an aldose, a sugar whose open-chain, noncyclic structure contains an aldehyde group, while fructose is a ketose, a sugar whose corresponding structure contains a ketone group.) The phosphorylated forms, glucose-6-phosphate and fructose-6-phosphate, are an aldose and a ketose, respectively.


Stap 3. Fructose-6-phosphate is further phosphorylated, producing fructose- 1,6-bisphosphate.

As in the reaction in Step 1, the endergonic reaction of phosphorylation of fructose-6-phosphate is coupled to the exergonic reaction of hydrolysis of ATP, and the overall reaction is exergonic. See Table 17.1.


The reaction in which fructose-6-phosphate is phosphorylated to give fructose-1,6-bisphosphate is the one in which the sugar is committed to gly-colysis. Glucose-6-phosphate and fructose-6-phosphate can play roles in other pathways, but fructose-1,6-bisphosphate does not. After fructose-1,6-bisphos-phate is formed from the original sugar, no other pathways are available, and the molecule must undergo the rest of the reactions of glycolysis. The phos-phorylation of fructose-6-phosphate is highly exergonic and irreversible, and phosphofructokinase, the enzyme that catalyzes it, is the key regulatory enzymein glycolysis.

Phosphofructokinase is a tetramer that is subject to allosteric feedback regu-lation of the type we discussed. There are two types of subunits, designated M and L, that can combine into tetramers to give different per-mutations (M4, M3L, M2L2, ML3, and L4). These combinations of subunits are referred to as isozymes, and they have subtle physical and kinetic differences (Figure 17.5). The subunits differ slightly in amino acid composition, so the two isozymes can be separated from each other by electrophoresis. The tetrameric form that occurs in muscle is designated M4, while that in liver is designated L4. In red blood cells, several of the combinations can be found. Individuals who lack the gene that directs the synthesis of the M form of the enzyme can carry on glycolysis in their livers but experience muscle weakness because they lack the enzyme in muscle.


When the rate of the phosphofructokinase reaction is observed at varying concentrations of substrate (fructose-6-phosphate), the sigmoidal curve typical of allosteric enzymes is obtained. ATP is an allosteric effector in the reaction. High levels of ATP depress the rate of the reaction, and low levels of ATP stimulate the reaction (Figure 17.6). When there is a high level of ATP in the cell, a good deal of chemical energy is immediately available from hydrolysis of ATP. The cell does not need to metabolize glucose for energy, so the presence of ATP inhibits the glycolytic pathway at this point. There is also another, more potent, allosteric effector of phosphofructokinase. This effector is fructose-2,6-bisphosphate we shall discuss its mode of action when we consider general control mechanisms in carbohydrate metabolism.

Stap 4. Fructose-1,6-bisphosphate is split into two three-carbon fragments. Thecleavage reaction here is the reverse of an aldol condensation the enzyme that catalyzes it is called aldolase. In the enzyme isolated from most animal sources (the one from muscle is the most extensively studied), the basic side chain of an essential lysine residue plays the key role in catalyzing this reaction. The thiol group of a cysteine also acts as a base here.


Step 5. The dihydroxyacetone phosphate is converted to glyceraldehyde-3- phosphate.


The enzyme that catalyzes this reaction is triosephosphate isomerase. (Both dihydroxyacetone and glyceraldehyde are trioses.)

One molecule of glyceraldehyde-3-phosphate has already been produced by the aldolase reaction we now have a second molecule of glyceraldehyde-3-phosphate, produced by the triosephosphate isomerase reaction. The original molecule of glucose, which contains six carbon atoms, has now been converted to two molecules of glyceraldehyde-3-phosphate, each of which contains three carbon atoms.

The ∆ G value for this reaction under physiological conditions is slightly positive (+2.41 kJ mol –1 or +0.58 kcal mol –1 ). It might be tempting to think that the reaction would not occur and that glycolysis would be halted at this step. We must remember that just as coupled reactions involving ATP hydrolysis add their G values together for the overall reaction, glycolysis is composed of many reactions that have very negative G values that can drive the reaction to completion. A few reactions in glycolysis have small, positive ∆ G values (see Table 17.1), but four reactions have very large, negative values, so that the ∆ G for the whole process is negative.


Essay on Metabolism (For School and College Students) | Biologie

Are you looking for an essay on ‘Metabolism’? Find paragraphs, long and short essays on ‘Metabolism’ especially written for school and college students.

1. Essay on the Introduction to Metabolism:

The term metabolism is defined as ‘the chemical processes by which nutritive material is built up into living matter, or by which complex molecules are broken down into simpler substances during the performance of special functions’. The various reactions which involve the synthesis of complex molecules are grouped under anabolism, whereas the breakdown of complex molecules is known as catabolism.

Both anabolic and catabolic proc­esses include a vast number of different chemical reactions, but there are number of common features. Most of the metabolic processes occur inside the cells of the body, mainly in the cytoplasm, but also inside intracellular organelles such as the mitochondria. Anabolic and catabolic reactions involve the action of enzymes and the utilization of energy.

Metabolism, a vital process for all life forms, is a constant process that begins when an organism being conceived and ends when it dies. In case the metabolism stops, results in death. The process of metabolism is really a balancing act involving two kinds of activities that go on at the same time the building up of body tissues and energy stores (anabolism or constructive metabolism) and the breaking down of energy stores to generate more fuel for body functions (catabolism or destructive metabolism).

Almost all of the chemical reactions in the living body require the expenditure of energy, which is made available mainly by the catabolism of the ‘macronutrients’ fats and carbohydrates (particularly glucose), and proteins (to a small extent). According to the law of conservation of energy, the total energy of a system remains constant, though energy may transform into another form. In the body’s metabolism, the energy released from the oxidation of the macronutrients is used for a series of chemical reactions, instead of being released only as heat.

A fundamental feature of both anabolic and catabolic processes is the utilization of energy. The ultimate source of energy for all living system is solar energy. Thus, the meta­bolic process on earth begins with the producers, the plants. First, a green plant takes energy from sunlight. The plant uses this energy and the molecule chlorophyll (which gives plants their green color) to build sugars from water and carbon dioxide in a process known as photosynthesis.

The men and the animals when eat the plants, they take this energy (in the form of sugar), along with other vital cell-building chemicals. The body’s next step is to break the sugar down so that the energy released can be distributed to, and used as fuel by the body’s cells. These reactions are made easy by biological catalysts, (enzymes) and they break down proteins into amino acids, fats into fatty acids and carbohydrates into simple sugars (e.g., glucose).

During these processes, the energy from these compounds can be re­leased by the body for use or stored in body tissues, especially the liver, muscles, and body fat. During anabolism, small molecules are changed into larger, more complex molecules of carbohydrate, protein and fat.

2. Essay on Carbohydrate Metabolism:

In animals, especially in human the major source of dietary carbohydrate is starch from con­sumed plant material and a small amount of glycogen from animal tissue as well as disaccharides such as sucrose from products containing refined sugar and lactose in milk. Digestion in the gut converts all carbohydrate to monosaccharides which are transported to the liver and converted to glucose. The liver has a central role in the storage and distribution within the body of all fuels, including glucose.

Carbohydrate metabolism begins with digestion in the small intestine here monosaccharides are absorbed into the blood stream.

Blood sugar concentrations are controlled by three hormones: .

When the concentration of glucose in the blood increases, insulin is secreted by the pancreas, which stimulates the transfer of glucose into the cells, especially in the liver and muscles, although other organs are also able to metabolize glucose.

Glucose in the body undergoes catabolism in all peripheral tissues, particularly in brain, muscle and kidney to produce ATP. Excess glucose is changed into glycogen by the process of glycogenesis (anabolism) and stored as glycogen in liver and muscle or converted to fatty acids and is stored in adipose tissue as triglycerides. Eqinephrine and glucagon hormones are secreted to stimulate the conversion of glycogen to glucose when blood glucose level be­comes low. This process is called glycogenolysis (catabolism).

Glucose metabolism begins with the process called glycolysis (catabolism). The end products of glycolysis are pyruvic acid and ATP. Since glycolysis releases relatively little ATP, further reactions continue to convert pyruvic acid to acetyl CoA and then citric acid in the citric acid cycle. The majority of the ATPs are made from oxidations in the citric acid cycle in connection with the electron transport chain. During strenuous muscular activity, pyruvic acid is converted into lactic acid rather than acetyl CoA. During the resting period, the lactic acid is converted back to pyruvic acid. The pyruvic acid in turn is converted back to glucose by the process called gluconeogenesis (anabolism).

3. Essay on Glycolysis (Catabolism):

Glycolysis (Embden-Meyerhof pathway) is the initial metabolic pathway of carbohydrate catabolism. It is the most universal process by which cells of all types derive energy from sugars. Glucose is oxidized by all tissues to synthesize ATP. The first pathway which begins the complete oxidation of glucose is called glycolysis. This pathway cleaves the six carbon glucose molecule (C6H12O6) into two molecules of the three carbon compound pyruvate (C3H3O3 – ). This oxidation is coupled to the net production of two molecules of ATP per glu­cose. Glycolysis converts one molecule of glucose into two molecules of pyruvate, along with “reducing equivalents” in the form of the coenzyme NADH.

The global reaction of gly­colysis is:

Glucose + 2 NAD + + 2 ADP + 2 Pi –> 2 NADH+ 2 pyruvate + 2 ATP + 2 H2O + 4 H +

In eukaryotes, glycolysis takes place within the of the cell. Glucose gets into the cell through facilitated diffusion. The first step in glycolysis is phosphorylation of glucose by hexokinase (in liver the most important hexokinase is glucokinase). This reaction con­sumes 1 ATP molecule. Although the cell membrane is permeable to glucose because of the presence of glucose transport proteins, it is impermeable to glucose 6-phosphate.

Glucose 6- phosphate is then rearranged into fructose 6-phosphate by phospho-glucose isomerase. (Fructose can also enter the glycolytic pathway at this point.). Phosphofructokinase-1 then consumes 1 ATP to form fructose 1, 6-bisphosphate. The energy expenditure in this step is justified in 2 ways- the glycolytic process is now irreversible, and the energy supplied to the molecule allows the ring to be split by aldolase into 2 molecules – dihydroxyacetone phos­phate and glyceraldehyde 3-phosphate. (Triosephosphate isomerase converts the molecule of di-hydroxy-acetone phosphate into a molecule of glyceraldehyde 3-phosphate.) Each mole­cule of glyceraldehyde 3-phosphate is then oxidized by a molecule of NAD + in the presence of glyceraldehyde 3-phosphate dehydrogenase, forming 1, 3-bisphosphoglycerate.

Phosphoglycerate kinase then generates a molecule of ATP while forming 3- phosphoglycerate. At this step, glycolysis has reached the break-even point- 2 molecules of ATP were consumed and 2 new molecules have been synthesized. Phosphoglyceromutase then forms 2-phosphoglycerate enolase then forms phosphoenolpyruvate and another sub- strate-level phosphorylation later forms a molecule of pyruvate and a molecule of ATP by means of the enzyme pyruvate kinase (Fig. 3.45).

NAD is used as the electron acceptor in the oxidation reaction. This cofactor is present only in limited amounts and once reduced to NADH, as in this reaction, it must be reoxidised to NAD to permit continuation of the pathway.

Methods of Glycolysis:

This re-oxidation occurs by one of two methods:

(i) Anaerobic Glycolysis:

In the absence of oxygen, pyruvate is reduced to lactate that is ideally suited to utilization in heavily exercising muscles where oxygen supply is often insufficient to meet the demands of aerobic metabolism. The reduction of pyruvate to lactate is coupled to the oxidation of NADH to NAD.

The lactate formed is transported to other tissues and dealt with by one of the two mecha­nisms such as converted back to pyruvate or converted back to glucose in the liver. The process of conversion of lactate to glucose is called gluconeogenesis, uses some of the reac­tions of glycolysis (but in the reverse direction) and some reactions unique to this pathway to re-synthesize glucose.

The majority of the enzymes responsible for gluconeogenesis are found in the cytoplasm the exception is pyruvate carboxylase which is located in the mito­chondria. This pathway requires ATP but has the role of maintaining a circulating glucose concentration in the bloodstream (even in the absence of dietary supply) and also maintain­ing a glucose supply to fast twitch muscle fibres.

The Cori cycle, named after its discoverers, Carl Cori and Gerty Cori, refers to the meta­bolic pathway in which lactate produced by anaerobic glycolysis in the muscles moves to the liver and is converted to glucose, which then returns to the muscles and is converted back to lactate (Fig. 3.46). It can be shown by a complex calculation of energy yields that this proc­ess of partially oxidizing glucose to lactate in muscle, transporting it to the liver for conver­sion back to glucose and then re-supplying it to muscle, actually has a much higher energy yield than the 2 ATP/glucose produced by glycolysis alone.

(ii) Aerobic Glycolysis:

In aerobic condition pyruvate is transported inside mitochondria and oxidized to acetyl coen­zyme A (abbreviated to “ acetyl CoA ). This is an oxidation reaction and uses NAD as an electron acceptor. Further, acetyl CoA is oxidized ultimately to CO2 by citric acid cycle. These reactions are coupled to a process known as the electron transport chain which has the role of harnessing chemical bond energy through a series of oxidation/reduction reactions to the synthesis of ATP and simultaneously re-oxidizing NADH to NAD.

The Krebs cycle, also known as the tri-carboxylic acid cycle (TCA), was first recognized in 1937 by the man for whom it is named, German biochemist Hans Adolph Krebs, the winner of Nobel Prize in 1953. In short, the Krebs cycle constitutes the discovery of the major source of energy in all living organisms. The Krebs cycle reactions take place in the matrix of the mitochondria. Some of the final steps of intermediate metabolism take place there, as well.

For example, in the matrix as well as the cytoplasm, glutamate (the amino acid glu­tamic acid) loses its amino group and is oxidized to alpha-ketoglutarate. Under aerobic con­ditions the end product of glycolysis is pyruvic acid converted to acetyl coenzyme A (acetyl CoA) which is the initiator of the citric acid cycle. In carbohydrate metabolism, acetyl CoA is the link between glycolysis and the citric acid cycle. The citric acid cycle contains the final oxidation reactions, coupled to the electron transport chain, which produce the majority of the ATP in the body.

For each glucose molecule that enters glycolysis, two pyruvate molecules are produced and have gained two NADH and two ATPs, while in the Calvin cycle approximately 54 ATPs are utilized by the plant to synthesize one glucose molecule. ATP is generated by breaking the bonds in glucose and capturing as much as possible of the energy stored in that molecule. The CA cycle produces very little ATP directly, but generates many molecules of reduced coenzymes NAD and FAD as NADH and FADH2.

The Krebs cycle begins with oxalo-acetate and combines with Acetyl CoA to cycle through one complete turn. After Acetyl CoA is oxidized to CO2 en H2O, the electrons drive proton pumps which generate ATP that is greatly needed by the cell. Remember that the NADH molecules are important because they contain extracted electrons which ultimately reduce NAD + .

However, when the electrons do not have enough energy to reduce NAD + , they are stored temporarily in the FADH2 molekule. Each NADH molecule is responsible for the production of three ATP molecules, while FADH2 is responsible for the production of two ATP molecules. In prokaryotic cells, the citric acid cycle occurs in the cytoplasm in eukaryotic cells the citric acid cycle takes place in the matrix of the mitochon­dria.

The overall reaction for the citric acid cycle is:

2 acetyl groups + 6 NAD + + 2 FAD + 2 ADP + 2 Pi –> 4 CO2 + 6 NADH + 6H + + 2 FADH2 + 2 ATP

The citric acid cycle provides a series of intermediate compounds that donate protons and electrons to the electron transport chain by way of the reduced coenzymes NADH and FADH2. The electron transport chain then generates additional ATPs by oxidative phos­phorylation.

The TCA cycle involves 8 distinct steps, each catalyzed by a unique enzyme:

ek. The citric acid cycle begins when Coenzyme A transfers its 2-carbon acetyl group to the 4- carbon compound, oxalo-acetate, to form the 6-carbon molecule, citrate.

ii. The citrate is rearranged to form an isomeric form, isocitrate (Fig. 3.47).

iii. The 6-carbon isocitrate is oxidized and a molecule of CO2 is removed producing the 5- carbon molecule α-ketoglutarate. During this oxidation, NAD + is reduced to NADH + H + .

iv. Alpha-ketoglutarate is oxidized, carbon dioxide is removed, and coenzyme A is added to form the 4-carbon compound succinyl-CoA. During this oxidation, NAD + is reduced to NADH + H +

v. CoA is removed from succinyl-CoA to produce succinate. The energy released is used to make guanosine triphosphate (GTP) from guanosine diphosphate (GDP) and Pi by sub- strate-level phosphorylation. GTP can then be used to make ATP.

vi. Succinate is oxidized to fumarate. During this oxidation, FAD is reduced to FADH2.

vii. Water is added to fumarate to form malate.

viii. Malate is oxidized to produce oxaloacetate, the starting compound of the citric acid cycle. During this oxidation, NAD + is reduced to NADH + H +

In addition to their roles in generating ATP by catabolism, the citric acid cycle also sup­plies precursor metabolites (anabolic) for various biosynthetic pathways (Fig. 3.48).

(b) Electron Transport Chain:

It is the final part of the phase-II of aerobic respiration. In respiration, oxidation of the sub­strate occurs by dehydrogenation (i.e., removal) of hydrogen atoms (2H) from the substrate. Most of these hydrogen atoms are accepted by NAD to form reduced co-enzyme NADH. In the aerobic respiration 10 NADH2 are formed (2NADH2 in glycolysis + 8 NADH2 in Krebs cycle) from one molecule of glucose. Also, in Krebs cycle, hydrogen is accepted by FAD to form FADH2 in one step a total of 2 FADH2 are formed by aerobic respiration of each glucose molecule.

Each molecule of reduced co-enzyme thus formed in aerobic respiration (glycolysis and Krebs cycle) is finally oxidized by the free molecular oxygen through a process called termi­nal oxidation (Fig. 3.49).

The respiratory chain (or the ETS) is present in the inner membrane of mitochondrion (i.e., in the cristae membrane). It consists of various enzymes and co-enzymes which act as electron carriers. Embedded in the inner membrane are proteins and complexes of molecules that are involved in the process called electron transport. The electron transport system (ETS), as it is called, accepts energy from carriers in the matrix and stores it to a form that can be used to phosphorylate ADP.

Two energy carriers are known to donate energy to the ETS, namely nicotine adenine di-nucleotide (NAD) and flavin adenine di-nucleotide (FAD). NADH binds to complex -I. It binds to a prosthetic group called flavin mononucleotide (FMN), and is immediately re-oxidized to NAD. NAD is recycled, acting as an energy shuttle. FMN receives the hydrogen from the NADH and two electrons. It also picks up a proton from the matrix. In this reduced form, it passes the electrons to iron-sulfur clusters that are part of the complex, and forces two protons into the inter-membrane space. Reduced NAD carries energy to complex I (NADH-Coenzyme Q Reductase) of the electron transport chain. FAD is a bound part of the succinate dehydrogenase complex (complex II).

Electrons cannot pass through complex-l without accomplishing proton translocation. Electron transport carriers are specific, in which each carrier accepts electrons (and associ­ated free energy) from a specific type of preceding carrier. Electrons pass from complex I to a carrier (Coenzyme Q) embedded by itself in the membrane. From Coenzyme Q electrons are passed to a complex -III which is associated with another proton translocation event.

Complex-II, the succinate dehydrogenase complex, is a separate starting point, and is not a part of the NADH pathway. From succinate, the sequence is Complex II to Coenzyme Q to Complex III to cytochrome C to Complex IV. Thus, there is a common electron transport pathway beyond the entry point, either Complex I or Complex II. Protons are not translocated at Complex II. There is not sufficient free energy available from the succinate dehydrogenase reaction to reduce NAD or to pump protons at more than two sites. From Complex III the pathway moves to cytochrome C then to a Complex IV (cytochrome oxi­dase complex). More protons are translocated by Complex IV, and it is at this site that oxy­gen binds, along with protons, and using the electron pair and remaining free energy, oxygen is reduced to water.

Oxygen serves as an electron acceptor, clearing the way for carriers in the sequence to be re-oxidized so that electron transport can continue. The purpose of elec­tron transport is to conserve energy in the form of a chemiosmotic gradient. The gradient, in turn, can be exploited for the phosphorylation of ADP as well as for other purposes. With the cessation of aerobic metabolism cell is damaged immediately and irreversibly.