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Fundamentals of the Living Cell > Energy, Metabolism, ATP, Glycolysis, Acetyl CoA, Mitochondria, OXPHOS > Flashcards

Energy, Metabolism, ATP, Glycolysis, Acetyl CoA, Mitochondria, OXPHOS Flashcards

1
Q

what is anabolism?

A

the synthesis of new molecules from less complex compounds

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2
Q

what is catabolism?

A

the breakdown of complex molecules into simpler molecules for the release of energy

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3
Q

why do people study metabolism?

A
  • to understand the metabolic basis of diseases like diabetes
  • to understand how the diseased state changes how body uses food
  • to understand diseases
  • changes in metabolites can aid diagnosis
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4
Q

what is ATP in terms of energy?

A
  • is the body’s energy provision
  • it can act as both an acceptor or donator of energy
  • it is a short term reservoir of energy
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5
Q

what regulates glycolysis?

A
  • reversible binding of allosteric effectors
  • covalent modification
  • transcription
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6
Q

how much ATP do we use at rest?

A

40kg/24hours

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7
Q

how much ATP does the body have?

A

100g

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8
Q

what are the major oxidative pathways?

A
  • glycolysis
  • citric acid cycle
  • ETC to OXPHOS
  • fatty acid oxidation
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9
Q

how is glucose converted to pyruvate?

A
  • glucose is phosphorylated by hexokinase to form G6P using ATP
  • phosphofructokinase (PFK) converts G6P to fructose-6-phospahte using ADP
  • fructose-6-kinase is converted to fructose-1,6-bisphosphate by PFK
  • fructose-1,6-bisphosphate is converted to two C3 molecules (dihydroxy acetone phosphate and gylceraldehyde-3-phosphate (GAP))
  • GAP is converted to phosphoenol pyruvate using reduced NADH
  • phosphoenol pyruvate is converted to pyruvate by pyruvate kinase using ADP to form ATP
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10
Q

what are the products formed in glycolysis?

A
  • net of 2 ATP per glucose
  • 2 NADH
  • 2 pyruvate
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11
Q

what are the enzymes involved in glycolysis and how are they inhibited?

A
  • hexokinase: converts glucose to G6P and inhibited by G6P
  • phosphofructokinase: converts G6P to fructose-6-phosphate and inhibited by ATP
  • pyruvate kinase: forms pyruvate from phosphoenol pyruvate and inhibited by ATP
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12
Q

which enzymes are present in the liver?

A
  • glucokinase
  • has a higher Km so requires higher [glucose] to be functional
  • not inhibited by G6P

-liver is responsible for storing excess glucose so when [glucose] high, glucokinase increases rate of glycolysis

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13
Q

what types of respiration does glycolysis occur at?

A

aerobic and anaerobic

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14
Q

how are tumours and exercising muscles similar?

A

both generate ATP where there is very little oxygen

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15
Q

how do tumours respond to low oxygen?

A

-hypoxia induced factor (HIF1) senses low [O2] and stimulates transcription factors that express enzymes in the glycolytic pathway (hexokinase, PFK, glucose transporters)

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16
Q

why is glycolysis in the liver inhibited by citrate?

A
  • liver uses glucose and glycolysis as a source of carbon skeletons
  • high levels of citrate means there precursors of biosynthesis are abundant
17
Q

what are the steps in the citric acid cycle?

A
  • pyruvate (C3) is converted into acetyl CoA (2C) by pyruvate dehydrogenase, forming CO2 and NADH
  • acetyl CoA (2C) is joined to oxaloacetate (4C) to form citric acid (6C) by citrate synthase
  • citric acid (6C) is then converted to isocitrate (6C).
  • isocitrate (6C) is then converted to α-ketoglutarate (5C) by isocitrate dehydrogenase, releasing a molecule of CO2 and NADH.
  • α-ketoglutarate (5C) is converted to succinyl CoA (5C) by α-ketoglutarate dehydrogenase, releasing a molecule of CO2 and NADH.
  • succinyl CoA (5C) is converted to succinate (4C), releasing GTP.

→-succinate (4C) is then converted to fumarate (4C), releasing FADH2.

-fumerate (4C) is converted to malate (4C).

→-malate (4C) is finally converted to oxaloacetate (4C), releasing NADH.

18
Q

what does pyruvate dehydrogenase do and what is it stimulated and inhibited by?

A
  • converts pyruvate to acetyl CoA
  • stimulated by ADP and pyruvate
  • inhibited by acetyl CoA, NADH, ATP
19
Q

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

A
  • joins oxaloacetate and acetyl CoA together

- inhibted by citrate

20
Q

what does isocitrate dehydrogenase do and what is it stimulated and inhibited by?

A
  • it converts Isocitrate to α-ketoglutarate
  • it is stimulated by ADP
  • inhibited by NADH and ATP
21
Q

what does α ketoglutarate dehydrogenase do and what is it inhibited by?

A
  • catalyses the conversion of α ketoglutarate to succinyl-CoA
  • inhibited by NADH, ATP and succinyl-CoA
22
Q

how many molecules of FADH2, NADH and GTP are produced per glucose molecule?

A
  • FADH2 = 2
  • NADH = 6
  • GTP = 2
23
Q

how is pyruvate dehydrogenase stimulated in muscles?

A
  • stimulated by Ca2+

- causes increase in CoA production

24
Q

how is [Ca2+] increased in liver?

A

adrenalin increases Ca2+ by activating α-drenergic receptors and IP3

25
Q

what regulates pyruvate dehydrogenase in liver and adipose?

A

insulin

26
Q

what is beri beri?

A
  • a disease caused by deficiency in thiamine (fit B1)
  • common where rice is staple food
  • causes neurological and cardiac problems
  • thiamine isa prosthetic group for pyruvates and α-ketoglutarate dehydrogenase
27
Q

what is NADH and FADH2 used in?

A

OXPHOS

28
Q

what happens to the H+ on FADH2 and NADH?

A

dropped off at the ETC to build up proton gradient

29
Q

how is ATP generated in OXPHOS?

A
  • H+ moves down proton gradient into the matrix of mitochondria
  • creates proton motive force which provides energy for ATP synthase to phosphorylate ADP into ATP
30
Q

how many molecules of ATP are produced from each NADH and FADH2?

A
  • 1 NADH: 3ATP molecules

- 1 FADH2: 2ATP molecules

31
Q

why do newborn babies need brown fat and where are they located?

A
  • newborns cannot shover so the have brown fat
  • brown fat have high [mitochondria] so provides alternative way to regulate heat
  • located in shoulders and down the back
  • as the babies grow, [brown fat] decreases
32
Q

why are mitochondria in brown fat different to other mitochondria?

A

they express uncoupling proteins

33
Q

what do uncoupling proteins do?

A
  • they uncouple a generation of proton gradient from generation of ATP
  • they get the H+ to take different route instead of going into the matrix which causes a generation of heat
34
Q

what are OXPHOS diseases and what are the symptoms?

A
  • common degenerative diseases
  • caused by mutations in genes encoding for proteins in the ETC
  • depending on the mutation, the symptoms may be evident near birth to early childhood
  • metabolic consequence can be congenital lactic acidosis

symptoms:fatigue, epilepsy, dementia

Fundamentals of the Living Cell (31 decks)

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