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89 Cards in this Set
- Front
- Back
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what is the function and mechanism of glycogen phosphorylase?
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cleaves glucose from nonreducing end of glycogen
PLP + Pi cofactors acid catalyzed glycolsidic bond cleavage: Pi donates H+ to alpha-1,4 bond to cleave it --> oxonium intermediate Pi attacks oxonium at C1 --> glc-1-P |
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What is the function of glycogen debranching enzyme?
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glycosyl transferase action: transfers 3 residues closest to 1,6 branch point to extend the nearest nonreducing end
a-1,6 glucosidase action: cleaves the 1-6 linked glucose from the chain --> glucose |
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How is glucose modified after cleavage from glycogen in muscle cells?
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glc-1-P --Phosphoglucomutase--> glc-6-P
ser-mediated phosphoryl transfer w/glc-1-6-BP intermediate can now enter glycolysis. |
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What is the fate of glucose in the liver?
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glc-6-P --glucose-6 phosphatase--> glucose
P removed to allow export from liver cell. |
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What is the first step in glycogen synthesis?
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glucose-1-P + UTP --UDP-Glucose Pyrophosphorylase--> glucose-UDP + PPi
Glucose's P displaces PPi from UTP. Activates glucose C1 for bond formation b/c UDP = good leaving grp |
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What is the second step in glycogen formation?
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Glucose-UDP + glycogen(n) --Glycogen Synthase--> glycogen(n+1) + UDP
UDP leaves --> oxonium intermediate nonreducing end of glycogen (C4 -OH) attacks oxonium --> alpha-1,4 glycosidic bond. |
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How are glycogen branches formed?
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Branching Enzyme
cuts 7-residue chain of alpha-1,4 linked glucoses attaches to C6 of another glucose 8 to 10 residues away via a alpha-1,6 bond |
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What is the function of glycogenin?
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Glycogen synthase needs a PRIMER
Glycogenin = Tyrosine Glycosyl Transferase makes primer by hooking 8 x Glc-UDP onto a Tyr-OH on itself (autocatalysis, enzyme is also its substrate). |
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What does 1,5 gluconolactone inhibit?
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Glycogen Synthase
Glycogen Phosphorylase 1,5 gluconolactone mimics the structure of the oxonium glucose intermediate involved in both reactions. |
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What is the major difference between photosynthesis in bacteria and in plants?
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Bacteria: no net oxidation of water, only PMF via the Q cycle
cyclic photophosphorylation Plants: oxidation H2O --> O2 + 2H+ + 2e- noncyclic photophosphorylation |
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In which direction are H+ pumped in plants?
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From the stroma into the thylakoid membrane.
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What is the path of electron flow through a plant's photosystems?
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Photosystem II --> Pheophytin a --> Q cycle/Cytochrome b6f --> Plastocyanin --> Photosystem I --> Ferredoxin --> Ferredoxin/NADP+ Reductase
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What is the major difference between NADH and NADPH?
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NADH is used to fuel catabolic cell activities
NADPH is used to fuel biosynthetic reactions (anabolic) |
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How is light energy extracted from pigments?
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Antenna pigments pass energy via e- excitation along until energy reaches rxn center.
At rxn center, "special pair" of chlorophylls becomes excited and photo-oxidized by Pheophytin a. Generates CATIONIC RADICAL. |
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How is chlorophyll able to oxidize water at the Oxygen Evolving Center (OEC)?
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Generation of CATIONIC RADICAL by photo-oxidation. PSII's excited e- gets stolen --> it steals e- from H2O.
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How many H+ are translocated per oxygen molecule produced at the OEC?
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12 H+
4 from breakdown of H2O 8 from Q cycle: 4e- from 2 H2O molecules --> 2 turns of the Q cycle = 8 H+. |
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Why are 4H+ translocated by Cyt.b6f per Q cycle?
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2 Q per Q cycle.
QH2 --> Q- + 2H+ (gives up both H+, gives one e- to cyt.C, gets one e- back) QH2 + Q- --> 2H+ + QH2 + Q (gives up both H+, one e- to cyt.C, one e- to previous Q-) net rxn: QH2 --> 4 H+ + Q |
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Which direction do the electrons from the Special Pair flow?
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To the right: through PheoA and QA.
Why? We don't know. |
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How many NADPH are produced per oxygen molecule?
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2 NADPH
NADP+ can accept 2 electrons and 1 proton. |
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How can plants carry out cyclic electron flow and why is this beneficial?
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Rather than reducing NADP+, Ferredoxin reduces plastoquinone, which reduces cytochrome b6f so that the e- are returned to the Q pool to pump more H+.
Allows plant to change ATP/NADPH synthesis ratio. |
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Where are ATP and NADPH produced?
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In the stroma
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Where does the Calvin Cycle occur and what does it do?
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Occurs in the stroma
Uses ATP/NADPH to reduce CO2 for carbohydrate synthesis. |
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What are the two phases of the Calvin Cycle?
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1. Irreversible Fixation of CO2 by RuBisCO
2. Regeneration of CO2 acceptor molecule, Ribulose Bisphosphate |
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What is the first reaction in the Calvin Cycle?
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RuBisCO
RuBP + CO2 + H2O --> 2 3-Phosphoglycerate + H+ |
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What is the catalytic mechanism of RuBisCO?
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1. abstract H from C3 --> enediolate
2. enediolate attacks CO2 --> carboxylation at C2 3. nucleophilic attack on C3 carbonyl --> tetrahedral dianion (Mg2+ needed to balance charge) 4. tetrahedral intermediate collapses, cleaving C2-C3 bond --> 2 3-PG. |
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How do the light reactions help RuBisCO?
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-plentiful ATP
-plentiful NADPH -slightly basic --> pH optimum = 8 for RuBisCO -Mg2+ (RuBisCO cofactor) efflux from thylakoid to balance charge gradient due to H+ movement. |
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What is the balanced chemical equation for the dark reactions?
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3 CO2 + 3 RuBP + 9 ATP + 6 NADPH -->
6 3-PG + 9 ADP + 9 Pi + 6 NADP+ 1 3-PG --> starch synthesis remaning 5 3-PG --many rearrangements--> 3 RuBP |
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Why are the light reactions coupled to the dark reactions?
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Carbohydrate catabolism yields less ATP/NADPH than is required to synthesize the same amount of carbs.
required input > output --> wasted energy. must generate ATP via light rxns in order to not waste. |
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How do the light reactions help the bisphosphatases involved in the calvin cycle?
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Ferredoxin reduces Thioredoxin
Thioredoxin reduces bisphosphatases to activate them (hydrogenates disulfide bonds: BP-S-S --> BP-(SH)2.) |
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Which enzymes in the Calvin Cycle are major control points?
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-fructose bisphosphatase (Thioredoxin)
-sedoheptulose bisphosphatase (Thioredoxin) -RuBisCO |
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How do plants fight photorespiration?
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Plants combat by concentrating CO2 around RuBisCO using Malate/Pyruvate shuttle:
pyruvate + ATP --PK--> PEP + AMP + PPi + CO2 --> OAA --malate DH--> malate malate passes into cell with RuBisCO then releases CO2: malate --malic enzyme--> pyruvate + CO2 |
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What is the net ATP yield per oxygen molecule produced?
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12 H+ --> 4 ATP
2 NADPH --> 6 ATP net 10 ATP. 10 mol ATP = ~70kcal 30% efficiency vs. energy of the 4 photons absorbed by photosystems to make that O2. |
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What is the dG cutoff for reaction reversibility?
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dG = -30 kJ/mol
dG = -7 kcal/mol below this, can change rxn direction with reactant/product concentrations any more negative and you must couple it to ATP hydrolysis to reverse it. |
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What is so wasteful about photorespiration?
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RuBisCO reduces O2 --> 2 H2O.
2 RuBP + O2 --> 2 3-PG + 2 Phosphoglyoxylate 2 Phosphoglyoxylate must be salvaged: 2 Phosphoglyoxylate --> 2 glycine 2 gly --> ser + CO2 ser --> glycerate + ATP --> 3-PG + ADP "unfix" a carbon and WASTE ENERGY! |
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What is the function of the Pentose Phosphate Pathway?
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1. generate NADPH for anabolic pathways
2. make PENTOSES for nucleotide/ATP synthesis 3. incorporate pentoses from food into biological molecules. |
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Where is the PPP most active?
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Liver
Adipose Tissue (fatty acid synthesis) Actively Dividing cells (need pentoses for DNA replication) Cancerous tissue |
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What stage of the PPP is irreversible?
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Oxidation of glucose:
glc-6-P + 2 NADP+ + H2O --> Ru5P + CO2 + 2 NADPH + 2 H+ |
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PPP Step 1
Glucose-6-P --> ? |
glc-6-P Dehydrogenase + NADP+ --> 6-Phosphogluconolactone + NADPH
oxidation of C1 hydroxyl to a ketone group. |
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PPP Step 2
6-Phosphogluconolactone --> ? |
(lactonase) + H2O --> 6-Phosphogluconate
lactone hydrolysis. may also occur without enzyme (just straight hydrolysis) |
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PPP Step 3
6-Phosphogluconate --> ? |
(6-Phosphogluconate Dehydrogenase) + NADP+ + H+ --> Ribulose-5-P + CO2 + NADPH
6-P-Gluconate DH makes Keto group at C3 --> beta-keto acid intermediate Decarboxylation to RuBP. |
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What reactions are carried out by transketolase?
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Xfer of C2 unit from ketose to an aldose
Xylulose-5-P + Ru-5-P --> Sedoheptulose-7-P + GAP Xylulose-5-P + Erythrose-4-P --> Fructose-6-P + GAP |
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What reactions are carried out by transaldolase?
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Xfer of C3 unit from ketose to an aldose.
Sedoheptulose-7-P + GAP --> Erythrose-4-P + Fructose-6-P |
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What is the reaction mechanism of transketolase?
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TPP cofactor
TPP attacks ketose C=O --> tetrahedral intermediate alpha-OH collapses to carbonyl --> ejects aldose; C2 group still attached to TPP run rxn in reverse: attack aldose to attach C2 unit to aldose. |
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What is the reaction mechanism of transaldolase?
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Lys-NH3+ on enzyme attacks carbonyl --> schiff base + H2O
schiff base gets protonated, beta-OH collapses to eject LG aldose. C3 unit remains attached to Enz-Lys run rxn in reverse to attach to aldose substrate: C=C double bond attacks aldose, then deprotonate and hydrolyze schiff base to detach from lys. |
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What determines which pathway glucose enters when it gets to the cell?
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Ratio of NADPH/NADP+
Products of PPP are normally abundant --> only runs if NADPH is depleted. NADPH/NADP+ = 100 NAD+/NADH = 1000, NADH very scarce |
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What is the importance of the Pentose Phosphate Pathway in combating oxidative stress?
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NADPH is critical for reducing radical oxygen species with Glutathione.
Glutathione reduces radical O species; when oxidized forms disulfide S-S with another molecule of itself NADPH (only made in PPP) must re-reduce Glutathione to restore its functionality. |
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Why is debranching a 3-step process? Why not just remove the 1,6 bond and make a new 1,4 bond?
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Break/Reform 1,4 bond: dG = 0
Break 1,6 bond: dG = -7.1 Only break 1,6 and form 1,4: dG = -7.1 + 15.5 = +8.4, endergonic! needs to be 3-step to be exergonic. |
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What is the structure of glycogen phosphorylase and how is it regulated?
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Homodimer structure
Phosphorylate by Phosphorylase Kinase --> activate Allosteric effectors AMP --> activate (low E signals) ATP, Glucose-6-P --> deactivate (high E signals) |
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What is the structure of Phosphorylase Kinase?
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4 x 4 subunits: a, b, gamma, delta
gamma = catalytic subunit a, b = regulatory subunits that sit on gamma; phosphorylate to remove delta = calmodulin (CaM), binds 4 x Ca2+ and activates gamma |
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Aside from alpha/beta phosphorylation, how is the gamma subunit of Phos Kinase regulated?
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Gamma has SUBSTRATE ANALOG (Ala-6 rather than Ser-6) that sticks to active site
CaM-Ca2+ (muscle contraction) binds to move substrate analog out of the way. --> need phos AND Ca2+ to be fully active! |
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What enzyme regulates Phosphorylase Kinase and how is it structured?
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PKA, Protein Kinase A
R2C2 inactive holoenzyme complex bind cAMP to release 2 x C catalytic subunits. |
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How is cAMP regulated in the cell?
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ATP --(adenylate cyclase)--> cAMP + PPi
cAMP --(phosphodiesterase)--> AMP a.cyclase activated by nor/epinephrine and glucagon PDE repressed by caffeine |
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How is glycogen synthase regulated?
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Allosteric activator = Glucose-6-P excess, insulin hormone
Phosphorylase Kinase and PKA phosphorylate GS to deactivate |
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What does insulin do and where is it active?
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activates phosphatase: removes P's
turn OFF PKA, Glycogen Phosphorylase turn ON Glycogen Synthase --> STORE GLUCOSE. secreted by pancreatic beta cells active in muscle and fat tissue to stimulate glucose uptake |
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What do epinephrine/norepinephrine do and where are they active?
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secreted by adrenal medulla
active in liver and muscle activates adenylate cyclase --> make cAMP --> activate PKA --> activate phos kinase --> activate glycogen phosphorylase --> release glucose. |
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What does glucagon do and where is it active?
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activates adenylate cyclase --> --> mobilize glucose from glycogen
active in liver only |
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What organ is responsible for detecting blood glucose levels?
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pancreas
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Where is the only place gluconeogenesis occurs?
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in the liver.
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What are the precursors for glucose synthesis during exercise? During starvation?
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Exercise: lactate
Starvation: amino acids (taken from muscle) |
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How is pyruvate converted to PEP for gluconeogenesis?
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in mitochondrion: Pyruvate + CO2 + ATP --(pyruvate carboxylase)--> Oxaloacetate
OAA exported to cytosol in cytosol: Oxaloacetate + GTP --(PEPCK)--> PEP + CO2 + GDP |
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What is the mechanism of Pyruvate carboxylase?
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ATP + HCO3- --> carboxyphosphate transfers CO2 to biotin prosthetic grp.
biotin loses CO2, then deprotonates pyruvate to form enolate enolate attacks CO2 --> pyruvate is carboxylated at C3 to yield OAA. |
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Why is pyruvate carboxylase a mitochondrial enzyme?
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Anapleurotic: it generates OAA, which can be used to replenish intermediates in the TCA cycle.
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How is oxaloacetate converted to PEP?
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OAA + GTP --> GDP + CO2 + PEP
OAA decarboxylates; C-C double bond forms + disrupts carbonyl group, which steals P from GTP to form phosphoanhydride bond of PEP. |
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How is oxaloacetate transported into the cytosol from the mitochondrion?
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1. OAA + NADH --(malate deHase)--> malate + NAD+
malate --> cytosol, convert back to OAA (same enzyme) **NADH co transported 2. OAA + amino acid --(asp aminotransferase)--> asp + a-keto acid asp --> cytosol, converted back to OAA (same enzyme) |
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How is PEP transported into the cytosol from the mitochondrion?
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PEP passes from mitochondrion --> cytosol via transport proteins.
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How does pyruvate get into the mitochondrion?
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H+ symporter
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Once in the cytosol how is PEP converted to glucose?
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Run glycolysis in reverse except for PFK, PK, and hexokinase rxns
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Which enzymes reverse the Pyruvate Kinase reactions?
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1. pyruvate carboxylase
converts pyruvate --> OAA 2. PEP carboxykinase (PEPCK) converts OAA --> PEP using energy of OAA decarboxylation |
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Which enzyme reverses the Phosphofructokinase reaction?
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Fructose 1,6-Bisphosphatase
F1,6BPase hydrolyzes the P from C1 |
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Which enzyme reverses the hexokinase reaction?
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glucose-6-phosphatase
hydrolyzes phosphate from C6 |
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Why do muscle cells have pyruvate carboxylase enzyme if they don't carry out gluconeogenesis?
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Anapleurotic function: pyruvate carboxylase makes OAA --> enters TCA cycle
improves efficiency of metabolizing acetyl-CoA |
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How many ATP does it cost to convert 2 pyruvate back into a glucose molecule?
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6 ATP:
1 for pyruvate carboxylase rxn 1 GTP = ATP for PEPCK rxn 1 for phosphorylating 3-PG to 1,3BPG by PG kinase = 3 ATP/pyruvate x 2 pyruvate/glucose = 6 ATP |
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How is the Phosphofructokinase/Fructose Bisphosphatase system regulated?
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PFK-1 activated mainly by F2,6BP from PFK-2
AMP formation: 2 ADP --> AMP + ATP PFK-2 activated, FBPase-2 repressed by F6P from PFK-1 inactivity --> increase F2,6BP |
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When is it beneficial to turn off FBPase-2?
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When you want increased F2,6BP --> increased glycolysis.
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When is PFK-2 turned off?
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in absence of F-6P --> signals no incoming glucose
PFK-2 off --> no F2,6,BP --> PFK-1 inactive --> GLUCONEOGENESIS, not glycolysis. |
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How do epinephrine and glucagon affect PFK-2 and FPBase-2 in the liver?
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Epi/Glucagon phosphorylate PFK-2/FBPase-2 complex --> phosphorylase on --> inhibits glycolysis in liver
epi/glucagon signal need for glucose; liver carries out gluconeogenesis to furnish glucose to body. |
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When and where does gluconeogenesis occur?
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when glycogen has been degraded and there is no external source of glucose (food)
mostly in liver but also in kidney. |
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How does the body prevent pyruvate kinase from eating up all the PEP during gluconeogenesis?
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high [coA] and [amino acid] inhibits Pyruvate Kinase --x--> no pyruvate to PEP conversion
phosphorylate to turn off also during GN, PFK-1 is off --> no F1,6BP for feed-forward activation of PK |
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Why is it important to coordinate regulation of glycolysis and gluconeogenesis?
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To avoid a futile cycle: glycolysis produces 2 ATP but gluconeogenesis consumes 6 ATP for a net loss of 4 ATP if you were to let the two processes cycle back and forth freely.
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How does the body prevent PDH from eating up all the pyruvate destined for gluconeogenesis?
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high [acetyl-CoA] ihibits PDH
activates P carboxylase xs acetyl-CoA from fatty acid oxidation stimulates formation of OAA from pyruvate to initiate gluconeogenesis. |
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How does the body prevent PDH from eating up all the pyruvate destined for gluconeogenesis?
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high [acetyl-CoA] ihibits PDH
activates P carboxylase xs acetyl-CoA from fatty acid oxidation stimulates formation of OAA from pyruvate to initiate gluconeogenesis. also: glycogen/epinephrine: PDH kinase phos. PDH to turn on |
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What is the difference between pyruvate kinase regulation in muscle and liver?
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Muscle: only inhibited by ATP b/c doesn't need to worry about gluconeogenesis
Liver: regulated by epinephrine/glucagon so it can carry out gluconeogenesis. |
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What activates PDH Kinase?
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Ca2+
pyruvate low energy signals turn on PDH Kinase in liver --> no glycolysis, pyruvate used for GNG |
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What inactivates PDH Kinase?
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Acetyl CoA
NADH high energy --> liver can do glycolysis. |
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What activates PDH Phosphatase?
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insulin
PDHPase on --> PDH dephosphorylated --> PDH on --> make acetyl coA for fatty acids |
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Which enzymes are only hormonally regulated in the liver but allosterically regulated in muscle?
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-PDH
-Pyruvate Kinase -FBPase-2/PFK-2 |
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What is the immediate end product at the end of the irreversible segment of the Pentose Phosphate Pathway?
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Ribulose-5-Phosphate, a ketose.
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What is the immediate product of the first stage of the Calvin Cycle?
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2 x 3-phosphoglycerate.
reverse glycolysis to GAP: 3-PG + ATP --> 1,3 BPG + NADPH --> GAP + NADP+ + Pi |
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What is the catalytic subunit of phosphorylase kinase?
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gamma subunit
has pseudosubstrate. |
