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Metabolism Flashcards

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1
Q

Glycolysis location

A

Cytoplasm

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2
Q

Glycolysis equation

A

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

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3
Q

What is substrate level phosphorylation

A

Direct transfer of a phosphate group onto ADP
From a molecule with higher phosphoryl transfer potential
So free energy released is higher than free energy of hydrolysis of atp

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4
Q

Importance of glycolysis

A

Energy production in anaerobic conditions

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5
Q

3 control points in glycolysis

A

Hexokinase (glucose to G6P)
Phosphofructokinase (PFK) (makes fructose 1.6 bp)
Pyruvate kinase (PEP to pyruvate)

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6
Q

Isoenzymes of PFK (glycolysis)

A

2 different forms of an enzyme that catalyse the same reaction
Can be regulated differently
Different isoenzymes in muscle and liver
In muscle decreasing pH decreases enzyme activity
In liver, citrate is an Allosteric inhibitor and fructose 2,6 BP is an Allosteric activator

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7
Q

Allosteric regulation of PFK (glycolysis)

A

Regulated by need for atp in muscles
ATP inhibits
AMP activates
ATP decreases affinity for fructose-6-P

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8
Q

Regulation of pyruvate kinase in liver (glycolysis)

A

Regulated by phosphorylation
Usually stimulated by hormones
Phosphorylated form less active
Phosphorykated by Cyclic AMP dependent kinase (PKA)
Activated by phosphoprotein phosphatase
PKA stimulated by glucagon
Can phosphorylate serine residue

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9
Q

Function of tca cycle

A

Final common pathway for oxidation of all fuel molecules
Complete oxidation of acetyl-coA
Produces reduced cofactors that carry e- to ETC
Directly generates atp by substrate level phosphorylation

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10
Q

Net reaction of TCA cycle

A

Acetyl-coA + 3NAD+ + FAD +ADP (GDP) + Pi + 2H2O —> 2CO2 + 3NADH + FADH2 + ATP (GTP) + CoA

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11
Q

How many ATP from NADH

A

2.5 ATP

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12
Q

How many ATP from FADH2

A

1.5 ATP

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13
Q

How is ATP generated in oxidative phosphorylation

A

NADH and FADH2 reoxidised in ETC
E- passed to ETC components then finally to O2
Process coupled to ATP production

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14
Q

Bio synthetic reactions of tca cycle

A

Citrate —> FAs/ sterols
Alpha-keto glutarate —> aas —> purines
Succinyl-CoA —> porphyrins —> haem
OAA —> glucose / aas/ purines/pyrimidines

Reactions happen in cytoplasm so must be carriers in IMM for intermediates to move out

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15
Q

Replenishing OAA for TCA

A

Carboxylation of pyruvate by pyruvate carboxylase
Has biotin attached
Bicarbonate + pyruvate —> OAA

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16
Q

Control of TCA cycle

A

Allosterically regulated
Responds to energy charge ( ATP/ADP ratio)
Controlled enzymes:
Pyruvate dehydrogenase
Isocitrate dehydrogenase
Alpha keto glutarate dehydrogenase

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17
Q

Allosteric control of pyruvate dehydrogenase ( TCA)

A

ATP inhibits, NADH inhibits, acetyl-CoA inhibits
ADP activates, pyruvate activates

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18
Q

Allosteric control of isocitrate dehydrogenase (TCA)

A

ATP inhibits, NADH inhibits
ADP activates

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19
Q

Allosteric control of alpha keto glutarate dehydrogenase (TCA)

A

NADH inhibits, ATP inhibits

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20
Q

Control of pyruvate dehydrogenase by phosphorylation (TCA)

A

Inactivated by phosphorylation on serine residue in E1 subunit
Phosphorylated by pyruvate dehydrogenase kinase
Dephosphorylated by pyruvate dehydrogenase phosphatase
Kinase and phosphatase controlled by Allostery and hormones
Kinase:
Activated by NADH, ATP Acetyl-CoA
Inhibited by NAD+, CoA, ADP, Ca2+ (muscle)
Phosphatase:
Activated by Ca2+ in muscles
Activated by insulin in liver

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21
Q

Glycogen synthesis

A

UDP glucose synthesised from Glucose-1-P and UTP
Made from UDP-glucose
Initiation by glycogenin
Tyr 194 nucleophilic attack onto UDP sugar (glucosyltransferase activity)
Chain extending activity adds a glucose at non-reducing end (where CH2 is)
Repeats x6
Glycogen synthase catalyses formation of alpha-1,4 glycosidic linkage
UDP displaced by OH group in C4
Branching by Glycosyl 4-6 transferase
Breaks 1-4 bond and moves chain to create 1-6 linkage
Transfers terminal 6/7 residues from non-reducing end
Need chain of at least 11 residues

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22
Q

Glycogen breakdown

A

Glycogen phosphorylase adds a phosphate across the 1-4 bond and removes a residue from non-reducing end by phospholytic cleavage
Releases glucose-1-P
Pyridoxal phosphate co factor involved in acid base catalysis
Can take off residues until within 4 residues of a branch
Transferase activity of debranching enzymes moves 3 residues to non reducing end
1-6 glucosidase activity of debranching enzyme hydrolyses 1-6 bond and releases free glucose
Glucose 1-p converted to glucose-6-p via glucose-1,6-bp by phosphoglucomutase
Glucose-6-p used in muscle for glycolysis for a higher net atp or liver hydrolyses back to free glucose

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23
Q

Regulation of glycogen phosphorylase

A

2 forms, phosphorylase a and phosphorylase b
A is double phosphorylated and favours R state
B is less active and favours T state
Interconverted by phosphorylase b kinase and phosphoprotein phosphatase 1
Phosphorylase b kinase activated by glucagon and adrenaline
Phosphoprotein phosphatase 1 activated by insulin
Also Allosteric regulation
In muscle:
Phosphorylase b inhibited by glucose-6-p and ATP, only active if AMP high
In liver:
Phosphorylase a inhibited by glucose, enzyme acts as glucose sensor

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24
Q

Regulation of glycogen synthase

A

2 subunits
Each one is triple phosphorylated
Phosphorylated form is glycogen synthase b, less active
Dephosphorylated form is glycogen synthase a, more active
Interconverted by phosphoprotein phosphatase (PP1) and glycogen synthase kinase (GSK1)
Glucagon and adrenaline activate kinase
Insulin activates PP1 in liver and muscle
Insulin can inactivate GSK3
Allosteric regulation:
G6P is an Allosteric regulator of glycogen synthase b

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25
Signalling pathway for glucagon and adrenaline
GCPR receptor Conformational change as GDP exchanged for GTP Alpha subunit disssociates Binds adenylate cyclase ATP—> cAMP Activates PKA Phosphorylates phosphorylase b kinase and glycogen synthase a
26
Insulin signalling pathway
Tyrosine kinase receptor Heterodimer When insulin binds, 2 intracellular tyrosine kinases phosphorylate each other Activates protein kinase Inactivates SK 3 Activates PP1
27
Gluconeogenesis net reaction
2 pyruvate + 4 ATP + 2GTP + 2NADH + 2H+ + 4H2O —> glucose + 4ADP + 4Pi + 2GDP + 2Pi + 2 NAD+ Energetically very costly but essential 6 ATP for each glucose made
28
Precursors of glucose
Lactate —> pyruvate Some amino acids e.g. alanine —> pyruvate Glycerol from triacylglycerols —> G3P
29
Cori Cycle
In liver: 2 lactate —> 2 pyruvate —> glucose Lactate oxidised to pyruvate Travels in blood In muscle: Glucose —> 2 pyruvate —> 2 lactate Pyruvate reduced to lactate in anaerobic conditions Travels in blood Cycle shifts metabolic burden of glucose synthesis from RBC and muscles to liver
30
Why do we need reciprocal regulation of glycolysis and gluconeogenesis
If both reactions happened at the same time you would get a futile cycle Hydrolysis of atp with no useful metabolic reaction occurring is wasteful
31
Regulation of fructose-6-p to fructose-1,6-bp
F6p-f16bp by phosphofructose kinase Activated by F2,6BP, AMP Inhibited by ATP, citrate, H+ F1,6BP to F6P by fructose 1,6 bisphosphatase Activated by citrate Inhibited by F2,6BP and AMP Synthesis of fructose 2,6 BP from fructose 6 p is controlled by hormones
32
Regulation of PEP —> pyruvate interconversion
PEP—-> pyruvate by pyruvate kinase Activated by F 1,6 BP Inhibited by ATP and alanine Pyruvate —> OAA by pyruvate carboxylase Activated by acetyl-CoA Inhibited by ADP OAA—> PEP by PEP carboxykinase Inhibited by ADP
33
Regulation of PFK2 and FBPase 2 by hormones
Catalyse interconversion of fructose - 6 -p and fructose -2,6 bp Both in one bifunctional enzyme Regulated by phosphorylation Phosphorylated form has inactive PFK 2 and active FBPase 2 Phosphorylated by cAMP dependent kinase Glucagon stimulates production of cAMP so activates the kinase Phosphatase activated by insulin
34
Processes of lipid breakdown
Mobilisation of Fas from TGs in adipose tissue Transport to tissues by serum albumin Activation of FAs by CoA Transport into matrix - requires conjugation to carnitine Beta oxidation of FAs produces acetyl coA Acetyl coA oxidised in TCA cycle
35
Control of release of FAs from adipose tissue
Controlled by hormones Glucagon and adrenaline bind GCPR receptors Cascade CAMP activates PKA which phosphorylates TRIACYLGLYCEROL LIPASE Releases a free fatty acid from TG Diacylglycerol and monoacylglyceol lipase act on diacylglycerol to release free FAs and glycerol Free FAs diffuse through membrane into blood Very hydrophobic so once in blood they bind to serum albumin which has many hydrophobic binding sites
36
Conjugation of FAs to carnitine and transport into matrix
Acyl-coA + carnitine undergo transesterification reaction to swap thiol for carnitine group Acyl-coA can go through pore in OMM Carnitine acyltransferase I in OMM catalyses formation of Acyl-carnitine in IMS Carnitine in IMS Acyl-carnitine travels into matrix through translocase in IMM Carnitine acyltransferase II in IMM catalyses conversion of Acyl-carnitine to Acyl-coA in matrix Carnitine travels back through translocase to IMS
37
Beta oxidation of FAs
Series of 4 reactions Releases Acetyl-coA Oxidation by FAD of beta carbon to create double bond Hydration across double bond Oxidation with NAD+ so hydroxyl —> keto Thiolytic cleavage as CoA reacts with 2C For odd number chains: Carboxylation produces D-methylmalonylcoA Isomerisation to L isomer Mutase converts to succinyl CoA that enters TCA
38
Net reaction for beta oxidation of palmitate (C16)
Palmityl-CoA + 7CoA + 7FAD + 7NAD+ + 7H2O —> 8 acetyl-coA + 7FADH2 + 7NADH + 7H+
39
Hormonal control of TG lipase (FA degradation)
Activated by glucagon or adrenaline Inhibited by insulin
40
Control of Transport of FAs into mitochondria
Carnitine acyltransferase I inhibited by malonyl coA High malonyl coA corresponds to high acetyl-coA so dont need more FAs can’t move into matrix
41
FA synthesis committed step
Acetyl-coA + bicarbonate + ATP —> malonyl coA By acetyl-coA carboxylase
42
Elongation phase of FA synthesis
Malonyl coA/ acetyl-coA transferases swap coA for same group attached to ACP Condensation - malonyl-CoA is activated donor of 2C units, release of CO2 drives reactions, forms 4CFA-ACP Reduction reaction to reduce ketone to hydroxyl using NADPH Dehydration to create double bond Reduction to reduce C=C using NADPH Repeated cycle of 4 reactions with malonyl-acp each time 2C added Can repeat up to 7 times Hydrolysis of thio-ester bond to release FA from ACP
43
Overall reaction for palmitate synthesis
Acetyl-ACP + 7 malonyl-ACP + 14 NADPH + 14 H+ —> palmitate + 7CO2 + 14 NADP+ 8ACP + 6H2O To make malonyl-coA: 7acetyl-coA + 7CO2 + 7ATP —> 7malonyl-CoA + 7ADP + 7Pi Overall: 8 acetyl-coA + 7ATP + 14 NADPH + 14H+ —> palmitate + 14 NADP+ + 8CoA + 7ADP + 7Pi + 6H2O Energetically costly
44
Transport of acetyl-coA out of mitochondria
No carrier in IMM so citrate acts as a carrier of acetyl coA In matrix: Malate oxidised to OAA OAA + acetyl-coA —> citrate Citrate moves to cytoplasm when atp high Citrate —> OAA + acetyl coA using 1 ATP OAA reduced to malate Malate —> pyruvate Pyruvate moves to matrix
45
Control of acetyl-coA carboxylase (FA synthesis) by phosphorylation
Phosphorylated form is inactive Phosphatase activated by insulin Kinase is AMP dependent, activated by AMP and inhibited by ATP Also activated by glucagon and adrenaline in cascade
46
Allosteric control of acetyl-coA carboxylase (FA synthesis)
Phosphorylated form is allosterically activated by citrate to make it partially active Citrate conc high when TCA cycle is slow Effect of citrate inhibited by palmitoyl-coA
47
Glucogenic amino acids
Can make glucose in gluconeogenesis and be oxidised in TCA cycle Gly, Cys, Ser, Ala, The, Arg, Pro, His, Glu, Val, Ile, Met, Asp, Trp, Tyr, Phe
48
Ketogenic amino acids
Broken down into acetyl-coA, can’t synthesise glucose Ile, Lys, Leu, Tyr, Trp, Phe
49
Removal of alpha amino group in aa breakdown
Transfer of NH2 to alpha keto acid Aspartame + alpha keto glutarate —> OAA + glutamate Alanine + alpha keto glutarate —> pyruvate + glutamate Catalysed by aminotransferases with pyridoxal phosphate cofactor Occurs in liver Reversible
50
Removal of alpha amino group from glutamate
Glutamate dehydrogenase reaction In mitochondrial matrix Glutamate oxidised to schifi base intermediate then hydrolysed to alpha keto glutarate and NH4+ Oxidative deamination reaction NH4+ —> urea, driving reaction forwards
51
Urea cycle net reaction
Co2 + NH3 + 3ATP + Aspartate + 2H2O —> urea + 2ADP + Pi + AMP + PPi + fumarate Urea cycle linked to TCA cycle by fumarate
52
Control of urea cycle
Carbamoyl phosphate synthetase 1 (CPS1) activated allosterically by N-acetyl glutamate N-acetyl glutamate synthesised by reaction of glutamate and acetyl-coA Enzyme synthesising this is activated by arginine Arg is an intermediate in urea cycle so if its conc increases not enough carbamoyl is entering the cycle
53
Role of glutamine in nitrogen metabolism
Some ammonium needed for synthesis of nucleotides and aas Glutamine acts as non toxic carrier of nitrogen and can be used as a nitrogen donor Glutamine synthase: Glutamate + NH4+ + ATP —> glutamine + ADP + Pi + H+ Glutamine neutral so can be moved in blood
54
Ketone body synthesis
2 acetyl-coA —> acetoacetate —> beta hydroxybutyrate / acetone Occurs in liver mitochondrial matrix
55
Ketone body degradation
Beta-hydroxybutyrate —> acetoacetate —> 2 acetyl-coA 1st step reduces NAD+
56
Glyoxalate cycle
Can produce glucose precursors with acetyl-coA as animals can’t make glucose from acetyl-coA Isocitrate —-> glyoxalate + succinate By Isocitrate Lyase Glyoxalate —> malate By malate synthase Malate — OAA by malate dehydrogenase OAA —> PEP —> glucose
57
uses of ketone bodies
Some acetyl-coA —> ketone bodies when not enough OAA to enter TCA cycle Alternative fuel source Heart muscle uses ketone bodies In starvation we get a high conc of ketone bodies Brain can adapt to use them
58
Cholesterol synthesis
2 acetyl coA —> acetoacetyl-coA —-> beta hydroxyl beta methylglutaryl coA —-2NADPH—-> mevalonate —-> cholesterol
59
Key junctions in metabolism
Glucose-6-P Pyruvate Acetyl-coA
60
How is Pentose phosphate pathway regulated
NADP+ activates glucose-6-phosphate dehydrogenase Acts as e- acceptor in dehydrogenase reaction Competes with NADPH for space in the active site
61
Glycogen phosphorylase cofactor
PLP

Enzymes And Metabolism (4 decks)

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