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Metabolism Flashcards

1
Q

What does a deficiency in TPP lead to

A

Beri Beri syndrome

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2
Q

Describe the process of pyruvate dehydrogenase action

A
  1. decarboxylation -> hydroxyethyl TPP
  2. oxidation and transfer to lipoamide -> acetyl lipoamide
  3. transfer of acetyl -> acetyl coA
  4. regeneration of oxidase lipoamide + FAD -> NADH
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3
Q

Describe the glycerol phosphate shuttle

A

Skeletal muscle, brain
glycerol-3-phosphate dehydrogenase transfers electrons to DHAP to generate G-3-P
The same enzyme in the membrane transfers electrons to FAD, then passed to co-enzyme Q in the ETC

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4
Q

Describe the malate aspartate shuttle

A

Liver, kidney, heart
2 membranes, 4 enzymes
H- transferred from NADH to oxaloacetate to give malate (malate dehydrogenase)
Malate transported into the mitochondria, re-oxidation by NAD+
Refer to notes

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5
Q

Compare anabolic to catabolic reactions

A

anabolic - creating molecules using NADPH

catabolic - breaking down molecules using NADH

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6
Q

What can NADPH be used for

A 
thymidine synthesis (DNA)
Cholesterol synthesis
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7
Q

Explain the proposed evolutionary origins of the mitochondria

A

Evolutionary descendants of a prokaryote that established an endosymbiotic relationship
Only arises from pre-existing mitochondria
Own circular genome
Own protein-synthesising machinery
First amino acid of transcripts is a fMet (bacteria) and not Met (eukaryotes)
Antibiotics that affect bacterial protein synthesis can also affect mitochondria (but not eukaryotes)

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8
Q

Define the chemiosmotic theory

A

Translocation of protons from within the matrix is controlled by the electron transport or respiratory chain
Pumping of a proton through ATP synthase creates a gradient. The proton motive force that drives h+ consists of both a pH and a transmembrane electrical potential

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9
Q

Summarise the ETC

A

Proteins accept electrons and a proton
Electrons pass through complexes so that protons are pumped into the inter membrane space
Cytochrome oxidase receives 4 electrons before the cycle repeats
Electrons passed to oxygen to generate water

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10
Q

What is the order of units in the ETC

A

NADH dehydrogenase complex
Cytochrome b-c complex
Cytochrome oxidase complex

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11
Q

Explain how ATP synthase can generate and utilise ATP

A

Contains F0 and F1
F0 - a,b,c
F1 - 𝛼,β,𝛾
Protons passing through causes rotation with transition states with altering affinities for ATP and ADP
Generation or utilisation depends on direction of flow

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12
Q

Explain the process of ATP synthase action in the ETC

A
  1. proton flow
  2. C and gamma rotate
  3. alpha and beta remain stationary (fixed by b)
  4. ATP generation/utilisation
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13
Q

How does malonate work as a poison

A

competitive inhibitor of succinate dehydrogenase, slowing flow to ubiquinone

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14
Q

How does oligomycin work as a poison

A

produced by streptomycin that binds to the ATP synthase stalk to inhibit oxidative phosphorylation

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15
Q

How does cyanide/azides work as a poison

A

bind to the ferric form (Fe3+) of the hame group in cytochrome oxidase and blocking electron flow

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16
Q

How does DNP work as a poison

A

proton ionophore that can shuttle protons
Uncouples oxidative phosphorylation from ATP production
Heat is released from the ETC
Leads to weight loss, increase in temp. and metabolic rate

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17
Q

Which enzyme is used to form cholesterol esters

A

cholesterol acytransferase

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18
Q

What occurs in familial hypercholesterolaemia

A

Normally LDL is taken up by the liver via the LDL receptor by receptor mediated endocytosis
Mutant LDL receptor means LDL is left in circulation
Dominant inheritance
Atherosclerosis and heart attacks

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19
Q

Give some drugs used to treat familial hypercholesterolaemia

A

statins - inhibits HMG-coA reductase (lovastatin)

resins - inhibits absorption of bile salt and cholesterol in the small intestine by binding (cholestyramine)

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20
Q

What is the difference between ribosomes bound to the ER and free

A

free - proteins for cellular use

bound - for secretion or within plasma membrane or lysosome

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21
Q

What happens to a protein with a signal peptide specific to the ER

A

translation halts
ribosome moves to the ER membrane
Translation restarts with the peptide entering the lumen

22
Q

What happens to a protein with no signal peptide

A

ribosome remains in the cytoplasm

23
Q

What happens to incorrectly folded proteins

A

blocked form the ER exit

Exported and degraded

24
Q

Which disorder is associated with membrane trafficking

A

cystic fibrosis

CTFR mutation means that chloride channels become affected which leads to CF

25
Q

Explain the process of exocytosis

A
  1. vesicles containing protein which have been modified in the ER bud
  2. fusion with the golgi
  3. further modification (usually sugar addition)
  4. vesicle buds
  5. fusion with the palms membrane for secretion
26
Q

What are the 2 types of secretion

A

constitutive vs regulated
C - all cells, steady stream of vesicles, from TGN, fuse with the membrane, replenishes the membrane
R - Excitable cells, concentrated products, stored in secretory vesicles until a signal stimulates secretion e.g. insulin release

27
Q

Explain the process of endocytosis

A
  1. membrane invaginate and pinches off
  2. vesicle formation
  3. vesicle surrounded by clathrin which is removed after complete formation
  4. dynamic helps pinch from the membrane
28
Q

What are the 3 types of endocytosis

A

Receptor mediator endocytosis
Pinocytosis (fluid intake)
phagocytosis

29
Q

Describe gated transport

A

Import receptors around the nucleus recognise nuclear localisation signals on nuclear proteins
Movement is via nuclear pores

30
Q

Describe vesicular transport

A

Proteins move between organelles via microtubules

vesicles bud on one organelle and move to fuse with others

31
Q

How far apart do membranes have to be for fusion

A

1.5nm

32
Q

What are the 3 types of intracellular transport

A

Gated transport
Transport across membranes
Vesicular transport

33
Q

Give a disease associated with endocytosis

A

familial hypercholesterolaemia

LDL receptor is not produced or is not functional so LDL is not taken up leaving a high level in the blood

34
Q

Give a disease associated with exocytosis

A

Cytic fibrosis

CTFR mutation leads to a deltaFSO8 mutation and degradation. Chloride channels being affected lead to CF

35
Q

What does skeletal muscle and cardiac muscle rely on for energy

A

carb metabolism and fatty acid oxidation

36
Q

What does the brain and nervous tissue rely on for energy

A

carb and ketone body metabolism (no fatty acids)

37
Q

How are carbs stored

A

glycogen in the liver

38
Q

What occurs to skeletal muscle during exercise, both light and heavy contraction

A

Large and rapid increase in ATP demands
light - ATP consumption = oxidative phosphorylation
heavy - ATP consumption > oxidative phosphorylation
glycogen store breaks down
lactate is transported to the liver and then remade into pyruvate

39
Q

Why must the amount of glucose in the brain be carefully controlled

A

hyperglycaemia - irreversible dameg

hypoglycaemia - faintness and coma

40
Q

What does the heart use for energy

A

TCA cycle substrates e.g. fatty acids and ketone bodies

41
Q

Give the metabolic features of the liver

A

highly metabolically active
can interconvert nutrients
glucose storage
lipoprotein metabolism

42
Q

What are the metabolic responses to eating

A

Increase in insulin from eh beta cells in the pancreas
Increase in glucose uptake
Increase in glycogen synthesis
Increase in glycolysis

43
Q

What are the metabolic responses to short term fasting

A

pancreas secretes glucagon from the alpha cells of the pancreas
Gluconeogenesis
Glycogenolysis

44
Q

What are the metabolic responses to prolonged fasting

A

pancreas secretes more glucagon

when the glycogen store runs out, gluconeogenesis occurs

45
Q

Explain the process of gluconeogenesis and what can it be used for

A

uses 4 ATP (G=-38)
pyruvate -> oxaloacetate -> phosphophenol pyruvate -> fructose-6-p -> glucose

glycogenic amino acids from the TCA
glycerol
Lactate

46
Q

Describe aerobic respiration

A

ATP demands can be met by oxidative phosphorylation using glucose and other fuels

47
Q

What is the effect of adrenline

A

rate of glycolysis increases
muscle glycolysis increases
liver gluconeogensis increases
increase in lipolysis in adipocytes

48
Q

Describe anaerobic respiration

A

ATP demands > oxygen delivered
glycogen breaks down in muscle
increase in lactate
liver converts lactate to glucose

49
Q

What are the 2 forms of hexokinase

A

HK1 in muscle and HK IV in the liver (sensitive to glucose)

50
Q

Which hormones increase blood glucose

A

Glucagon
Adrenaline
Glucocorticoid (cortisol) (increases enzymes concerned with glucose availability)

51
Q

What does Diabetes lead to

A 
hyperglycaemia 
diabetic retinopathy
nephropathy
neuropathy 
increase in fatty acids and lipoproteins
increase in ketone bodies -> acidosis risk increases

?? (14 decks)

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