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CELL II > Energy > Flashcards

Energy Flashcards

1
Q

Why do we eat?

A

Need energy for metabolism:

  • synthesis of new molecules
  • establishing ion gradients
  • mechanical work
  • keeping warm
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2
Q

Define catabolism?

A

breakdown of complex molecules to release energy or carry out mechanical work

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3
Q

Define anabolism?

A

synthesis of new molecules from less complex components

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4
Q

Why study metabolism?

A
  • Metabolic basis of disease eg diabetes, atherosclerosis, gall stones
  • Diseased state changes way body uses food eg cancer
  • To understand disease need to know how body normally deals with nutrients
  • Can use changes in metabolites to aid diagnosis + to follow treatment
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5
Q

What diff types of metabolic pathways require?

A 
rapid generation (secs) eg exercise
longer (minutes, hours) involving storing molecules (can take months/days)
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6
Q

Describe energy provision

A
  • ATP is central to a cell so bodies energy provision
  • ATP acts as both an acceptor + donator of energy
  • Short term reservoir of energy
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7
Q

How much ATP do we need?

A
  • Total energy available from hydrolysis of ATP = 65kj/mole
  • For rest = 40Kg/24hour
  • For exercise = 0.5Kg/minute
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8
Q

How much ATP does the body have?

A

100g

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9
Q

How does body meet demands for energy?

A

re-synthesise ATP from ADP via oxidative phosphorylation in mitochondria

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10
Q

Major oxidative pathways?

A

Glycolysis
Citric acid cycle
Electron transport coupled to oxidative phosphorylation
FA oxidation

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11
Q

Describe glycolysis

A

-6C glucose -> 2x 3C pyruvate
-glucose phosphorylated (consuming energy) -> G6P
-maintains conc gradient across membrane
-G6P undergoes conformational change -> fructose-6-phosphate
-fructose-6-phosphate phosphorylated -> fructose 1,6
bisphosphate (C6)
-F6BP -> 2x 3C
-each C :
NAD+ -> NADH
ADP -> ATP
phosphoenol pyruvate -> pyruvate
ATP synthesised again

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12
Q

Balance sheet for glycolysis?

A 
Reactants :
1 Glucose
2 NAD+
2 ADP
2 Pi
Products :
2 Pyruvate
2 NADH
2 ATP
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13
Q

What regulates glycolysis?

A

Enzymes catalysing irreversible reactions regulated by:
-reversible binding of allosteric effectors
-covalent modification eg phosporylation
-transcription
Measured in terms of ms, s, hrs

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14
Q

Role of hexokinase?

A

glucose -> G6P

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15
Q

What’s hexokinase under control by?

A

product G6P so negative feedback

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16
Q

Role of pyruvate kinase?

A

phosphoenol pyruvate -> pyruvate (with release of ATP)

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17
Q

What’s pyruvate kinase under control by?

A

product ATP so negative feedback

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18
Q

Role of phosphofructokinase?

A

fructose-6-phosphate -> fructose 1,6 bisphosphate

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19
Q

What’s phosphofructokinase under control by?

A

product ATP, citrate, H+ negative feedback

AMP (product of ATP -> ADP, which gives an indication of energy levels of the cell) positive feedback

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20
Q

Effect of inhibiting phosphofructokinase?

A

-build-up of G6P inhibiting hexokinase
-in liver, we have hexokinase + glucokinase which is not
affected by G6P build up
-glucokinase has a lower affinity for glucose so is
active at higher conc of glucose

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21
Q

How to make AMP?

A

ADP + ADP -> ATP + AMP via adenylate cyclase

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22
Q

Role of AMP?

A

ATP made from 2ADP via adenylate kinase gives ATP + AMP so AMP is a better indicator of energy state

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23
Q

How is phosphofructokinase inhibited?

A

high conc of ATP by lowering the affinity for fructose 6 phosphate, citrate, low pH

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24
Q

How regulation of glycolysis in liver reflects its diverse functions?

A

-Liver has more functions than muscle so regulation of glycolysis more complex
-High conc of ATP inhibit PFK
-Citrate inhibit PFK as indicates precursors of
biosynthesis are abundant
-Low pH in liver irrelevant as liver doesn’t produce lactate
-PFK stimulated indirectly by build-up of F6P.
-Hexokinase inhibited by G6P but liver also has glucokinase which isn’t inhibited by G6P (glucokinase only activated when high glucose)
-Indirect activation by F6P -> F26bisP when high glucose is feed forward regulation

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25
Q

Role of glucokinase?

A

activated when high glucose in liver not inhibited by G6P

26
Q

Function of glycolysis?

A
  • Degrades glucose to generate ATP

- Provides building blocks for synthesis of cellular components

27
Q

Why’s rate of conversion of glucose to pyruvate regulated?

A
  • 3 non-reversible steps phosphofructokinase inhibited by ATP + citrate, activated by AMP + fructose 2-6 bisphosphate
  • In liver bisphosphate signals glucose is abundant. PFK active when either energy or building blocks needed.
  • hexokinase inhibited by G6P
  • ATP + alanine inhibit PK
  • PK activity max when energy charge is low + glycolytic intermediates accumulate
28
Q

What do exercising muscles and tumours have in common?

A

Their energy needs are met through anaerobic respiration

29
Q

Why do tumours use glycolysis?

A
  • tumours outgrow their blood supply
  • O2 reduced
  • activation of transcription factor HIF-1α
  • HIF-1α regulates expression of enzymes in glycolytic pathway
30
Q

Why’s lactate produced?

A 
-C3 undergo es areaction where NAD+ ->
NADH 
-enables ATP to be produced
-to allow reaction to continue, pyruvate -> lactate 
-NADH -> NAD+ 
-NAD+ fed back to earlier reaction
-enables more molecules to flow through this part of glycolysis
-replenish NAD+ 
-but muscle can’t cope with lactate
-lactate exported via blood to liver
31
Q

Summary of energy I?

A

-Glycolysis is 6C glucose ->2x 3C pyruvate
-1st part of glycolysis consumes energy
-2nd part generates 2NADH + 2ATP
-ATP used as direct source of energy
-NADH used to generate energy via oxidative phosphorylation (which needs O2 to occur)
-In muscle O2 delivered insufficient so 3C pyruvate -> lactate allowing 2nd part of glycolysis to occur as replacing the NAD+
-Tumours use glycolysis as they grow faster than a blood supply can form around it so insufficient O2
-In a liver cell or less active muscle, pyruvate -> Acetyl
CoA which fed into the Krebs cycle

32
Q

What does aerobic respiration require?

A

Requires O2,citric acid cycle, oxidative phosphorylation.

33
Q

Where does aerobic respiration occur?

A

mitochondria

34
Q

Where does TCA cycle occur?

A

matrix

35
Q

Where does oxidative phosphorylation occur?

A

inner mitochondrial membrane

36
Q

Product of TCA cycle?

A 
for each glucose:
6NADH (+2 from before)
2FADH 
2GTP
4CO2 (+2 from before)
37
Q

Describe citric cycle

A

-in presence of O2
-pyruvate -> ACoA (2C) + enters citric acid cycle
-ACoA + oxaloacetic acid (4C) -> citrate (6C)
-citrate undergoes series of reactions –> loss of 2CO2
3 NADH + 1 FADH2 formed per cycle
1 GTP molecule is formed
ATP not produced in citric acid cycle

38
Q

Key facts about citric acid cycle?

A
  • Krebs cycle provides electrons for mitochondrial oxidative phosphorylation
  • Integrates carbohydrate, lipid, protein metabolism
  • Aerobic
  • Oxidizes ACoA to generate NADH H, FADH2, CO2
39
Q

Role of Kreb’s cycle?

A
  • Oxidation (electron harvesting) producing NADH, FADH2 which become substrates for electron transport chain
  • Source of building blocks for vital bio-molecules
40
Q

What regulates entry into citric acid cycle?

A
  • formation of ACoA from pyruvate is irreversible via pyruvate dehydrogenase
  • this commits glucose C skeleton to either oxidation to CO2 + energy production or FA synthesis
41
Q

Role of pyruvate dehydrogenase?

A

pyruvate -> ACoA

42
Q

What’s pyruvate dehydrogenase regulated by?

A
  • Inhibited by products NADH + ACoA

- Regulated by phosphorylation by a kinase + phosphatase (covalent modification)

43
Q

What regulates entry into the citric acid cycle?

A
  • In muscle pyruvate dehydrogenase activated again via phosphatase – stimulated by Ca2+
  • In liver adrenalin increases Ca2+ via activation of a adrenergic receptors + IP3
  • In liver + adipose tissue, insulin stimulates phosphatase which funnels glucose to FA synthesis
44
Q

Sig of build up of NADH + ACoA?

A

inform enzyme that energy needs of cell are meet or FA are broken down to produce NADH + ACoA - sparing glucose.

45
Q

Control points of citric acid cycle?

A

-ACoA -> citrate via citrate synthase
-Isocitrate -> α-ketogluterate via isocitrate dehydrogenase
-α-ketogluterate -> succinyl CoA via α-ketogluterate
dehydrogenase

46
Q

Role of citric synthase?

A

ACoA -> citrate

47
Q

What inhibits citric synthase?

A

product citrate so when enough ATP, ACoA directed to other ways eg FA synthesis (if you can’t use it store
it)

48
Q

Role of isocitrate dehydrogenase?

A

Isocitrate -> α-ketogluterate

49
Q

What regulates isocitrate dehydrogenase?

A

inhibited by NADH, ATP + stimulated by ADP

50
Q

Role of α-ketogluterate dehydrogenase?

A

α-ketogluterate -> succinyl CoA

51
Q

What regulates α-ketogluterate dehydrogenase?

A

inhibited by NADH, ATP, Succinyl CoA.
(note that the control of entry into TCA spoken of earlier (pyruvate -> ACoA) is inhibited by NADH, ATP, ACoA. It is stimulated by ADP and pyruvate)

52
Q

Effect of inhibiting isocitrate dehydrogenase +

α-ketogluterate dehydrogense?

A
  • build up of citrate
  • citrate transported out of mitochondria
  • where it inhibits PFK
  • stops glycolysis
  • citrate also act as a source of ACoA for FA synthesis
53
Q

Describe what Beriberi is?

A
  • Def in thiamine (Vit B1)
  • Common where rice common
  • Characterised by cardiac + neurological symptoms
  • Thiamine is a prosthetic group for pyruvate + α-ketogluterate dehydrogense
  • Neurological disorders common as glucose is primary source of energy
54
Q

Fate of NADH + FADH2?

A

-electron transport coupled to ATP synthesis
-needs 3H+ to make 1ATP
-1H+ used to transport ATP out of matrix so 4H+
generates 1ATP
-ETC removes hydrogen from oxidisable substrates : NADH + FADH2 .
-hydrogen enter ETC
-hydrogen -> elctron + H+
-electron passed via series of cytochromes going from high to low energy state powering proton pumps
-proton + O2 -> water
-proton pumped across inner mitochondrial membrane into IMS
-generates pH gradient transmembrane potential (proton motive force)
-membrane act as a barrier to reestablishment of gradient
-gradient harnessed to produce ATP

55
Q

How many protons generate ATP?

A

-needs 3H+ to make 1ATP
-1H+ used to transport ATP out of matrix so 4H+
generates 1ATP

56
Q

How much ATP produced from NADH + FADH2?

A

-each NADH produces 3ATP
-each FADH2 produces 2ATP
(these are approximations, not always 100% efficient)

57
Q

How many protons pumped out for each NADH + FADH2?

A

10H+ pumped out for every NADH

6H+ pumped out for every FADH2

58
Q

Describe ATP synthesis

A
  • ATP synthase is transmembrane protein
  • acts as motor
  • H+ pumped out into IMS will be able to drop back down their pH gradient via ATP synthase
  • generates ATP from ADP
59
Q

How neonates generate heat?

A

proton movement across inner mitochondrial membrane no longer coupled with ATP synthesis.

  • neonates cannot shiver so no heat
  • lose heat from their surface
  • possess brown fat around neck + shoulders
  • brown fat has many mitochondria
  • brown from cytochromes which has iron in structure
  • baby mitochondria has uncoupling protein
  • uncouples proton gradient with ATP synthesis
  • uncoupling protein is an alternative route where H+ moves down its conc gradient
  • so it doesn’t generate ATP but heat!
60
Q

Describe OXPHOS diseases?

A
  • Common degenerative diseases
  • Caused by mutations in genes encoding proteins of ETC
  • Symptoms : fatigue, epilepsy, dementia
  • Dependent on the mutation, symptoms near birth to early adulthood
  • Metabolic consequence can be congenital lactic acidosis
61
Q

What regulates ETC?

A
  • Governed by need for ATP
  • Electron transport coupled to phosphorylation : ADP to ATP
  • EXCEPTION : regulated uncoupling leads to the generation of heat

CELL II (9 decks)

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