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Year One: First Things First > Metabolism > Flashcards

Metabolism Flashcards

1
Q

Describe the difference between catabolic and anabolic metabolism

A

· Catabolic is the result of breakdown of larger molecules and anabolic result in formation of complex proteins from precursor molecules
Most of catabolism consists of reactions that extract energy from fuel stuffs and converts it to ATP

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2
Q

What is the total amoung of energy available from the hydrolysis of ATP?

A

65kj/mole

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3
Q

How much ATP do we have in the body?

A

100g

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4
Q

How is the majority of ATP made?

A

By oxidative phsophorylation

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5
Q

What are the cofactors central to metabolism?

A

”
· NAD and FAD are activated carriers of electrons used for oxidation reduction reactions
· NAD- nicotinamide adenine dinucleotide
· FAD- flavin adenine dinucleotide
“

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6
Q

What are the two functions of G6P?

A

“maintains glucose gradient kept low. It traps the glucose within the cell”

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7
Q

Describe the first part of glycolysis

A

Glucose is phosphorylated by ATP to give G6P

2·Then there is a change in the conformation to produce fructose-6-phosphate (isomerization from an aldose to a ketose)
3·then it is phosphorylated again by ATP to give fructose 1,6 bisphosphate which is then cleaved to give the 2 3C units- Dihydroxyacetone phosphate and glyceraldehyde-3 phosphate.

These two molecules are in equilibrium more toward the glyceraldehyde-3 phosphate

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8
Q

Describe the second stage of glycolysis

A

· GA3P is converted into phosphoenol pyruvate. . NADH is formed from NAD+ and Pi reduction

· This is then broken down into pyruvate. ATP is formed.

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9
Q

What are the three enzymes that regulate glycolysis?

A

Hexokinase and phosphofructokinase and pyruvate kinase

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10
Q

Describe the difference between hexokinase and glucokinase(7)

A
  1. Hexokinase is regulated by the product of the reaction.
  2. G6P will inhibit further conversion of G6P
  3. prevents too much glucose being fed into it.
  4. Has a low Km.
    Hexokinase is found in all cells in the body
    glucokinase is found in the liver and is not inhibited by G6P.
  5. Glucokinase: same thing as hexokinase but has a high Km
  6. only active at high concentrations of glucose
  7. found in hepatocytes and beta cells in the pancreas.
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11
Q

Why is glucokinase especially important in the liver?(2)

A
  1. The high Km , high Vmax , and inducibility of glucokinase allow the liver to capture glucose for storage as glycogen and to synthesize triacylglycerols when blood glucose levels are high
  2. to reduce the capture of glucose, thereby conserving it for other tissues that use it as a primary fuel
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12
Q

Why is glucokinase a better glucose sensor?(1)

A

“Its sensitivity to glucose extends over a longer range of glucose concentration

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13
Q

How is glucokinase regulated?(3)

A
  1. Glucokinase gene transcription is repressed by glucagon in response to low blood glucose levels.
  2. When glucose levels are limited existing glucokinase is bound by the Glucokinase Regulatory Protein (GKRP),
  3. This inactivates and sequesters it in the cell nucleus, preventing the glucose produced by gluconeogenesis and glycogenolysis from being rephosphorylated and trapped in the liver
    “
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14
Q

How is phosphofructokinase regulated?(4)

A
  1. ATP- negatively regulated-High concentrations of ATP inhibit PFK by lowering the affinity for Fructose 6 phosphate
  2. H+(low pH) is a negative regulated
  3. Citrate- negatively regulated
  4. AMP- positively regulated-regulate energetic state of the cell. Produced when there are large amounts of ADP.
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15
Q

What inhibits PFK and wh yis this important?(2)

A

· Inhibition of PFK by ATP leads to inhibition of hexokinase because if the enzyme is reduced then increase in glucose.

· Important for muscle to protect them from excessive lactate production during anaerobic respiration

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16
Q

Why doesn’t pyruvate kinase regulate glycolysis in other tissues apart from liver?

A
  1. They contains no allosteric sites and so does not contribute to the regulation of glycolysis in these tissues
  2. these tissues also do not undergo significant gluconeogenesis.
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17
Q

Why does pyruvate kinase regulate glycolysis in the liver?

A

PK can be regulated by phosphorylation by cAMP-dependent protein kinases activation and a number of allosteric regulators (fructose 1,6 bis phosphate which ties the rate of activity to PFK-1 and inhibited by ATP)

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18
Q

how is glycolysis regulated in the muscle?(4)

A
  1. under anaerobic conditions lactic acid is produced which will decrease blood pH.
  2. If there is a high concentration of ATP in the cell phosphofructokinase (PFK) is inhibited by lowering its affinity to fructose-6-phosphate so pyruvate cannot be formed.
  3. PFK is also inhibited by low pH which means too much lactic acid is forming.
  4. High AMP or ADP levels activate PFK to synthesize more ATP.
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19
Q

Recall the formula relating ADP and AMP

A

ADP+ADP–>ATP +AMP using adenylate kinase

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20
Q

What happens in the liver when glucose concentration is high?(2)

A
  1. glucokinase increases the rate of glycolysis
  2. · Indirect activation by F6P which is converted to F26bisP when blood glucose is high – example of feed forward regulation
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21
Q

Summarise the meabolism of fructose in adipose tissue

A
  • In muscle and adipose tissue, fructose can be phosphorylated by hexokinase (which is capable of phosphorylating both glucose and fructose) to form fructose 6-phosphate which then enters glycolysis.
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22
Q

Summarise the metabolism of fructose in the liver. (3)

A
  1. In liver, the cells contain mainly glucokinase instead of hexokinase and this enzyme phosphorylates only glucose.
  2. Thus in liver, fructose is metabolized instead by the fructose 1-phosphate pathway
  3. Fructose 1-phosphate is then split into glyceraldehyde and dihydroxyacetone phosphate by fructose 1-phosphate aldolase”
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23
Q

How is galactose metabolised?(1)

A

Galactose is first converted into glucose and then undergoes glycolysis

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24
Q

Describe exercising in muscle cells

A

(1) In exercising muscle when the need for ATP exceeds the capacity of the of the mitochondria the pyruvate is converted to lactic acid.
(2) lactate is acidic so there is acid build up and low pH which has adverse effect on fructose 1,6 phosphate

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25
Q

How does hypoxia stimulate tumour growth?(3)

A
  1. Low oxygen stimulates the activity of HIF1 (hypoxia induced factor). HIF1 has several effects in stimulating blood vessel growth.
  2. the low oxygen stimulates the TF (stabilizes it) which express enzymes in the glycolytic pathway, it regulates glucose transporters (GLUT), hexokinase, PFK and aldolase are also used.
  3. Many enzymes are stimulated by low levels of oxygen in glycolysis so tumours can survive even if oxidative phosphorylation cannot take place”
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26
Q

Where does TCA cycle take place and in what presence?

A

• Occurs only in the presence of oxygen
• Takes place in the mitochondria
“

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27
Q

Summarise the balance sheet for TCA cycle for each glucose molecule

A

6 NADH +2 NADH before the actual cycle2 FADH22 GTP4CO2 +2CO2

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28
Q

Describe the generation of Acetyl CoA(3)

A
  1. Formation of acetyl CoA from pyruvate is irreversible
  2. In the presence of oxygen, pyruvate is converted into acetyl CoA
  3. The enzyme involved is pyruvate dehydrogenase
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29
Q

Describe the enzymes involved in the TCA and their regulation(4)

A
  1. Pyruvate dehydrogenase- -vely by NADH, ATP and ACA, +vely by ADP and pyruvate
  2. citrate synthase- -vely by citrate
  3. isocitrate dehydrogenase- -vely by NADH and ATP, +vely by ADP
  4. a-ketogluterate dehydrogenase- -vely by NADH, ATP and succinyl CoA
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30
Q

Describe Ca2+ in muscle and liver (4)

A
  1. In muscle pyruvate dehydrogenase phosphatase is stimulated by Ca2+
  2. Calcium is involved in muscle contraction which uses ATP. In the absence of phosphate, the active form is active so ATP synthesis occurs
  3. In liver adrenalin increases Ca2+ through the activation of a adrenergic receptors and IP3
  4. In liver and adipose tissue, insulin (which signifies the fed state) stimulates the phosphatase which funnels glucose to Fatty Acid synthesis
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31
Q

Describe Beriberi(3)

A

Is a deficiency in thiamine (Vit B1)

  1. Characterised by cardiac and neurological symptoms because of glucose being the most common substrate for neurological tissue
  2. Thiamine is a prosthetic group for pyruvate and a-ketoglutarate dehydrogenase
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32
Q

Describe the process of oxidative phosphorylation(5)

A
  1. NADH is accepted by protein complex 1 in the inner membrane. FADH 2 is accepted by complex 2
  2. NADH and FADH2 are oxidised and their electrons enter the electron transfer chain through the electron carrier proteins.
  3. Electrons are carried from one complex to another. Energy is lost as the electrons move along the transfer chain, moving from a high energy state to a low energy state.
  4. Energy lost is used to produce an electrochemical gradient across the inner membrane through actively pumping protons from the matrix and into the intermembrane space, facilitated by membrane proteins.
  5. The hydrogen ions travel back to the matrix, along the gradient, through ATP synthase, which uses the potential energy created by the proton gradient to catalyse the addition of ADP and Pi to produce ATP”
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33
Q

How many ATPs and protons are produced and pumped respectively by NADH and FADH2?(2)

A

• NADH can produce 3ATPs and pumps out about 10 protons

  1. FADH2 produces 2ATP and pumps about 6 H+ across the membrane
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34
Q

Describe ATP synthesis in ETC transport(4)

A
  1. Proton gradient is used to generate ATP. As electrons pass down the chain, protons are pumped from matrix to intramembrane space and forms a sig gradient.
  2. The gradient is dissipated by the passage of protons through ATP synthase which is a molecular engine.
  3. As protons pass through it, ATP is formed
  4. Generation of proton gradients and synthesis of ATP is not always the same- not directly linked
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35
Q

Describe the difference between brown and white fat(2)

A
  1. In white fat, majority of space within cell is lipid.
  2. In brown, large numbers of mitochondria is present. Mitochondria contain cytochromes and cytochromes are coloured due to the haem the contain.
36
Q

How does brown fat generate heat in babies?(3)

A
  1. used to generate heat some infants do not have shiver reflex. Brown fat is used to generate heat
  2. In brown fat, they express a protein called UCP1 which diverts flow of protons away from generation of ATP to generation of heat.
  3. This short-circuits the ATP synthase, allowing H ions to cross and generates heat.
37
Q

What is OXPHOS disease?(3)

A
  1. Caused by mutations in genes encoding proteins of ETC
  2. Symptoms, including fatigue, epilepsy, dementia
  3. Dependent on the mutation, symptoms may be evident near birth to early adulthood Metabolic consequence can be congenital lactic acidosis
38
Q

What are symptoms of hypoglycaemia?(5)

A 
– Muscle weakness 
– Loss of coordination 
– Mental confusion 
– Sweating
– Hypoglycaemic coma and death
39
Q

What are the symptoms of hyperglycaemia?(3_

A

– Non enzymatic modification of proteins
– Cataracts
– Hyperosmolar coma

40
Q

Describe the process of glycogenesis(6)

A
  1. Glucose 6 phosphate is converted into glucose 1 phosphate using phosphoglucomutase enzyme.
  2. Glucose 1 phosphate is activated (made readier for reactions) by adding UDP from UTP.
  3. Makes UDP-Glucose, which more readily reacts with glycogenin.
  4. Glycogen synthase adds glucose residues to glycogenin in 1-4 formation up to 11 residues.
  5. This stimulates branching enzyme to form a 1-6 bond with the next residue, forming a branch
  6. Regulated by insulin
41
Q

Why is glycogen important? (5)

A
  1. Cannot store glucose as it is osmotically active
  2. 400mM glucose is stored as 0.01µM glycogen so significant reduction in osmotic power of the molecule when compounded this way
  3. The branched structure of glycogen means it can be rapidly mobilised
  4. Glucose can be metabolised in the absence of oxygen, whereas fats cannot.
  5. Fat cannot be converted back to glucose. At least the bulk of the molecule cannot be used to generate glucose
42
Q

Describe the process of glycogenolysis(8)

A
  1. Removal of residue and breaking of alpha1,6 links by enzyme called debranching enzyme
  2. The phosphorylase acts until it gets to 4 residues
  3. Debranching transferase removes 3 residues and put on the nonreducing end of a neighbouring a1-4 chain- transferase activity
  4. Debranching a-glucosidase enzyme then removes the branch point by breaking the alpha 1-6 bond.
  5. Phosphorylase continues to break down the alpha1,4 chain links and second enzyme activity associated with debranch enzyme breaks down link and gives G1P and is phosphorylated to G6P
  6. Phosphorylase continues to break down chain- G1P-G6P by phosphoglucomutase enzyme.
  7. If in liver then enzyme glucose 6 phosphatase will convert G6P using hexokinase, to trap glucose in the cell, then to glucose and then transported to general circulation. If it is muscle, then G6P is used in glycolysis
  8. Occurs when glucose levels are low”
43
Q

What are the four enzymes specifically involved in glycogenolysis?

A

– Phosphorylase breaks the a1-4 links
– Transferase moves 3 residues to an existing chain
– Debranching enzyme a1-6
– Phosphoglucomutase converts G1P to G6P

44
Q

Describe glycogen phosphorylase (4)

A

Phosphorylase is a large, multi-subunit enzyme that plays a key role in glycogenolysis

  1. Exists in two isoforms: Inactive isoform is phosphorylated and requires phosphorylase b kinase,Phosphorylase a is the active
  2. It is regulated by allosteric interactions that signal the energy state of the cell
  3. Many phosphorylase molecules are bound to each glycogen particle, so glycogenolysis can be switched on very rapidly (less than a second in muscle
45
Q

Describe the cascade reactions that leads to activation of phosphorylase by adrenaline(hormone)(5)

A
  1. Adrenaline binds to b-adrenal receptors on muscle cells, activating the g-protein to dissociate. The alpha subunit binds to adenylate cyclase which converts ATP into cyclic AMP.
  2. Cyclic AMP activates protein kinase A, which phosphorylates phosphorylase kinase.
  3. Phosphorylase kinase phosphorylates phosphorylase b into phosphorylase a
  4. Protein kinase A also phosphorylates glycogen synthase a, which inactivates it to glycogen synthase b.
  5. Hormonal regulation as insulin inhibits, glucagon stimulates in the liver, adrenaline stimulate in muscle and cortisol is a weak stimulus.
46
Q

Recall the hormonal regulations of glycogenolysis(3)

A
  1. insulin inhibits
  2. glucagon stimulates in the liver, adrenaline stimulate in muscle
  3. cortisol is a weak stimulus.
47
Q

Describe activation and deactivation of phosphorylase in liver and muscle(6)

A
  1. In the liver the activated phosphorylase a is inhibited by glucose.
  2. glycogen breakdown by phosphorylase is inhibited by the presence of glucose, even after the enzyme has been activated to the a form by being phosphorylated
  3. In muscle, glycogen phosphorylase b can also be activated without being phosphorylated. 5
  4. ´-AMP (which forms when ATP is depleted) binds to separate allosteric site, the nucleotide-binding site.
  5. ATP will bind to the same site, blocking the activation.
  6. Glucose-6-phosphate also blocks 5´-AMP activation.
48
Q

Describe the activation of phosphorylase b Kinase by Ca2+(3)

A
  • Ca2+ ions activate phosphorylase b kinase in muscle, mediating glycogenolysis during muscle contraction
  • Only get max activity with Ca2+ and phosphorylation
  • in liver α-adrenergic activation stimulates Ca2+ release
49
Q

Compare glycogen synthase, and glycogen phosphorylase(4)

A

“1. glycogen synthaseActivated by ATP and G6P in times of plenty, whereas glycogenphosphorylaseInactivated by ATP and G6P

  1. glyogen synthaseInactivated by phosphorylation (by protein kinase A), whereas glycogenphosphorylaseActivated by phosphorylation
  2. glycogen synthaseActivated by dephosphorylation (by protein phosphatase-1), whereas glycogenphosphorylaseInactivated by dephosphorylation
  3. glycogen synthaseStimulated by insulin, whereas glycogenphosphorylaseStimulated by Glucagon, Adrenalin and noradrenalin
50
Q

When is pentose phosphate pathway activated?

A

When G6P is in high demand

51
Q

What is the role of pentose phosphate pathway?

A
  1. Pathway is activated when G6P is in high supply

2. Ribose 6Phosphate is involved in several biosynthesis pathway leading to nucleotide and nuclei acids

52
Q

What are the by-products of pentose phosphate pathway?

A

2x NADPH1x CO2(H+) from H2O

53
Q

Where does gluconeogenesis?

A

Liver, kidney, and small amounts in intestines

54
Q

Describe the porportion of gluconeogenesis in the liver and kidney

A

Takes place mostly in the liver and a little in the kidney but during starvation kidney productions rises to 40%”

55
Q

Describe the process of gluconeogenesis(6)

A
  1. Pyruvate is transported into the mitochondria through a pyruvate carrier and is converted into oxaloacetic acid using pyruvate carboxylase (mitochondrial enzyme)
  2. Oxaloacetate is converted into malate and transported through a malate transporter into the cytosol and oxaloacetate is resynthesized.
  3. Phosphoenol pyruvate is produced from oxaloacetate, using Phosphoenolpyruvate carboxykinase (glucagon is inhibitory).
  4. Reversible reaction to produce glyceraldehyde-3-phosphate.
  5. Fructose bisphosphate produces G6P from F6P. (inhibited by glucose)
  6. Glucose-6-phosphatase produces glucose from G6P.
56
Q

Describe the brains need for glucose(6)

A
  1. Brain- uses 100-120g glucose daily
  2. Over half the energy consumed is used for Na+-K+ transport to maintain membrane potential and the synthesis of neurotransmitters
  3. Lacks energy stores
  4. Glucose is transported by GLUT3 which has a low Km – saturated under most conditions
  5. Danger point when plasma glucose drops to below 2.2mM
  6. Normally fatty acids are used not for energy but for membrane biosynthesis
57
Q

What are the main source of energy for cardiac muscle?

A

· Fatty acids are the main source of energy followed by lactate and ketone bodies

58
Q

Describe the strage of triglycerides in adipose tissue(6)

A
  1. Adipose tissue store triglycerides
  2. A 70kg man will have 15kg of TG
  3. TG come either from the diet and delivered by chylomicrons
  4. Synthesised by the liver and transported by VLDL to the adipocytes
  5. Glucose is transported by GLUT4
  6. GLUT4 is insulin sensitive”
59
Q

Describe the role of kidney in metabolism (2)

A
  • Although only 0.5% body mass they consume 10% of the energy because of the transport mechanism
  • During starvation, the kidney may contribute half of the blood glucose through gluconeogenesis
60
Q

Describe the role of the liver in regulating metabolism

A
  1. – Most compounds absorbed by gut pass through the liver except lipids which are delivered through the lymphatic system
  2. Provides fuel for brain, muscle and other peripheral organs
  3. Takes its own energy from α-ketoacids
  4. GLUT2 is bidirectional
61
Q

Desribe the control of blood glucose by the liver(6)

A
  1. If blood glucose rises above the norm, glucose enters the hepatocytes using gLUT2(not insulin sensitive) which is a transporter where the movement is dependent on glucose concentration.
  2. To maintain glucose, it is phosphorylated into G6P. Glucokinase has a low Km.
  3. G6P is then stored in the hepatocytes as glycogen
  4. When glucose is low, glycogen is broken down into G6P or through glycogenolysis.
  5. For G6P to move out of cell, it is converted into glucose using G6P-ase.
  6. The glucose leaves cell down concentration gradient using GLUT2
62
Q

Describe glucose regulation in muscles(3)

A
  1. Glucose stored in muscle is exclusively for use and generation of ATP.
  2. When Glucose high it is converted into G6P by hexokinase (Km 0.1mM for glucose). G6P is used either as glycolysis and glycogen
  3. Glycolysis of the G6P is a rapid source of ATP
63
Q

How is a 100m sprint powered?

A

Creatine phosphate

Relatively small but rapidly mobilised ATP store lasting only a few seconds

The build up of lactate and the fall in pH ultimately limits performance

64
Q

How is a marathon powered?(4)

A
  • Initially glycogen is used but later fat is mobilised from the adipose tissue.
  • Fats are a large source of ATP, but metabolism is x10 slower than creatine phosphate
  • The combined use of both glycogen and fats is the efficient

• The result is approximately half of the glycogen stores remain
“

65
Q

What are the priorities when we are not eating?(3)

A

· 1st priority to maintain glucose levels

· 2nd priority to preserve protein

· To achieve this metabolism shifts from glucose to fatty acids and ketone bodies

66
Q

What are the reactions that occur in the post absorptive phase?(4)

A
  • blood glucose falls insulin levels fall and glucagon levels rise
  • phosphorylase a activity increases as does glycogen breakdown
  • drop in insulin reduces glucose uptake by muscle and adipose tissue early starvation. Tis preserves circulation levels of glucose.
  • Pathways altered in this state will be the laying down of storage molecules- they will be inhibited. Pathways that increase glucose to the brain increase incl. gluconeogenesis and glycogenolysis
67
Q

What happens during early starvation?(4)

A
  • Glucose released from the liver due to gluconeogenesis and glycogenolysis
  • Mobilisation of FA from adipose tissue
  • Glucose use falls as muscle switches to FA oxidation

• Insulin drops causing GLUT4 expression by muscle to fall reducing glucose uptake
After 12hrs 45% of resting energy from FA and 40% from glucose”

68
Q

What happens during intermediate starvation(3-20)?(6)

A
  • Glycogen stores depleted
  • Increased lipolysis and ketogenesis
  • Increased gluconeogenesis to maintain blood glucose
  • 60hrs FA account for ¾ energy provision
  • After 8 days β-hydroxybutyrate is raised 50-fold
  • Further starvation sees the kidney take over gluconeogenesis from the liver. As starvation prolongs, rise in ketone is prominent and FA is low because they are being converted into ketone bodies.
69
Q

What happens during prolonged starvation-3wks+?(6)

A
  • β-hydroxybutyrate plateaux at 20 days
  • As brain starts to move to using ketone bodies the need for glucose falls from 100g to 40g/day
  • Other sources of gluconeogenic precursors are lactate and glycerol
  • Lactate is recycled by the Cori cycle
  • Glycerol and amino acids are oxidized

• Proteins are broken down by the muscle forming amino acid precursors- Loss of proteins is last results

70
Q

What is the equation for creatine?

A

creatine phosphate + ADP—> ATP+ Creatine

enzyme: creatine kinase

71
Q

What is the role of the liver in metabolism?

A

Plays a central role in regulating metabolism
Carbohydrate
Fatty acid
Amino acids

Most compounds absorbed by gut pass through the liver except lipids which are delivered through the lymphatic system

Provides fuel for brain, muscle and other peripheral organs

Takes its own energy from α-ketoacids

GLUT2 is bidirectional

72
Q

what is half the energy supplied to the brain used for?

A

→Na-K transports to maintain membrane potential

→ synthesis of neurotransmitter

73
Q

What does the brain lack and how is glucose transported in cardiac muscle?
Comment on the km of the transporter

A

→ Lacks energy stores
→ glucose is transported by GLUT3
→ has a low Km
→ meaning the transporter is active at most times

74
Q

List the three enzymes involved in glycolysis, and list what they are inhibited by.

A

→Hexokinase: - converts glucose to G6P - inhibited by G6P

→Phospho-fructokinase: - converts fructose-6-phosphate - inhibited by ATP, citrate and H+ (acids) - stimulated by F16BP and AMP (the inhibition of PFK leads to the inhibition of G6P)

→Pyruvate Kinase: - converts phosphoenol pyruvate to pyruvate - inhibited by ATP

–

75
Q

What difference in the TCA cycle occurs when the respiration is anaerobic?

A

→Instead of pyruvate being converted to Acetyl CoA, in anaerobically respiring muscle, it is converted to lactate (using NADH, making NAD+).

→The lactate is then sent to the liver to be converted back into glucose (so that the build-up of acid doesn’t inhibit PFK), and put back into the cycle.

→The making of lactate uses NADH to make NAD+. This NAD+ is used in the conversion of GALP to phosphoenol pyruvate.

→continues until NAD+ is a limiting factor.

76
Q

how is glycolysis regulated in the liver?

A

→In the liver high levels of ATP inhibit PFK, it is also inhibited by citrate.

→ The liver has glucokinase which has a higher Km so it needs a higher concentration of glucose to be functional and is not inhibited by G6P unlike hexokinase.

→The liver is responsible for storing excess glucose, so when glucose levels are high glucokinase increases the rate of glycolysis.

77
Q

Why ia glycolysis in the liver inhibited by citrate?

A

→The liver uses glucose and glycolysis as a source of carbon skeletons glycolysis in the liver is inhibited by citrate.
→High levels of citrate indicate the precursors of biosynthesis are abundant

78
Q

what does citrate synthase do and what is it inhibited by?

A

→joins Oxaloacetate and Acetyl CoA to make Citrate

→ inhibited by citrate

79
Q

what regulates entry into the citric acid cycle?

A

→ formation of Acetyl CoA from Pyruvate (by Pyruvate Dehydrogenase) is irreversible.
→This commits the glucose carbon skeleton to either oxidation to CO2 and energy production or fatty acid synthesis.

80
Q

how is pyruvate dehydrogenase activated in muscles

A

→In muscles, Pyruvate Dehydrogenase is activated again via the action of a phosphatase; this enzyme is stimulated by Ca2+ (this increases CoA production)

81
Q

what are the four enzymes needed to break down glycogen and what do they do?(3)

A

→phosphorylase breaks the α 1-4 links
→translocase transports G-6-P to ER for further modification
→ debranching enzyme - debranches (acts on 1-6 links) →phosphoglucomutase - converts G1P to G6P
Transferase moves 3 residues to an existing chain

82
Q

what are the five enzymes needed to form glucose?

A 
→phosphorylase
→translocase
→debranching enzyme
→phosphoglucomutase
→glucose 6 phosphatase converts G6P to glucose (present in the liver and kidney, but not muscle)
83
Q

what hormones control the regulation of glycogenolysis in the liver and in the muscle?

A

→Different hormones stimulate it in different places.

→in the liver, it is stimulated by Glucagon

→ in the muscle, it is stimulated by Adrenaline (Cortisol is a weak stimulus of glycogenolysis, and Insulin inhibits it.)

84
Q

how does pyruvate get converted to oxaloacetate in the liver?

A

1) Pyruvate is brought into the mitochondria (in the liver) via a Pyruvate carrier.
2) Pyruvate is converted to Oxaloacetate by Pyruvate Carboxylase.
3) To leave the liver, the Oxaloacetate is converted to Malate.
4) The Malate is then brought out of the mitochondria.
5) Now outside, it is converted back to Oxaloacetate and then the process continues.

–

85
Q

how is G6P made during glycogen breakdown?

A

The residues are removed till you get to a certain length (an end portion of a particular branch).

→This portion left is then broken off and moved onto the end of the main chain.

→This is done by the first kind of debranching enzyme, Translocase.

→Glucosidase is the second kind of debranching enzyme which removes the final residue left on the branch, releasing it as G6P (that could be converted to glucose in the liver)

Year One: First Things First (27 decks)

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