Energy Production (carbohydrates And Lipids) Flashcards

1
Q

Why is glycolysis separated into the different stages

A

More efficient
More versatile
Easier to control

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2
Q

What 2 enzymes would be used in the liver to regulate glycolysis

A

3-phosphofructokinase (would be high when high insulin:glycogen)
Pyruvate kinase (same reason)

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3
Q

What regulator of glycolysis would be a covalent modifier and what does it do

A

Pryruvate kinase
Dephosphorylate

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4
Q

What levels would hyperlactemia occur

A

2-5nm

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5
Q

What levels would lactic acidosis occur

A

Over 5nm

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6
Q

What would be used to produce lactate

A

Glucose (and alanine) via pyruvate

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7
Q

What is the equation that would involve LDH

A

lactate + NAD+ —————- Pryuvate + NADH + H+

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8
Q

What are the two important intermediates of glycolysis

A

Glycerol phosphate: would be produced in the adipose tissue of the liver
2,3 BPG would be used in the red blood cells and would allow the regulation of oxygen

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9
Q

How would fructose be broken down

A

FRUCTOSE — FRUCTOSE-1-PHOSPHATE — GLYCERATE-3-PHOSPHATE (G-3-P)

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10
Q

What causes fructosuria and what causes fructose intolerance

A

Fructosuria: when would not have enough fructokinase (would break down fructose to F-1-P)
Fructose intolerance: when would not have enough aldolase (f1p to 2-gyceraldehyde-3-p)

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11
Q

What is galactosemia

A

When the body is unable to metabolise galactose.
Leads to an excess galactose in the blood, toxic
Can cause sepsis, cataracts (when produced galaticol) and anemia

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12
Q

What would be the difference in the rare and the common forms of galactosemia

A

Rare: a kinase deficiency (no galactose to galactose-1-p so build of galactose
Common: a transferase deficiency (build of galactose and galactose-1-p) and no glucose produced for glycolysis

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13
Q

Where would the accumulated galactose go

A

Galactose —— galacitiol
Via NADPH TO NADP+
enzyme: Aldose reductase

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14
Q

What so the issue with fructose intolerance and how would you solve it

A

Fructose would accumulate in the liver and this could cause liver damage
Would need to remove fructose form your diet

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15
Q

How does galactosemia lead to cataracts

A

The lens would need NADPH
Galactose going through the alternative pathways would convert NADPH to NADP+
Then none would be available for the lens’

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16
Q

What is the difference between the GALK in carbohydrates and the GALT in the lymph tissue

A

GALT - GUT ASSOCIATED LYMPHOID TISSUE
GALT- GALACTOSE-1-PHOSPHATE URIDYLTRANSFERASE

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17
Q

What does glycerol phosphate produce

A

DHAP (dihydroxyacetone phosphate)
In the liver and the adipose tissue (where most likely would then go on to be stored)
DHAP can also produce glycerol phosphate too (reversible)

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18
Q

How could the levels of ADP help to regulate oxidative phosphorylation

A

When levels of ADP are low, no substrate
No activity working atp synthase
No hydrogen can move through

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19
Q

How would molecules like cyanide, hydrogen sulphide and carbon monoxide act as inhibitor

A

Bind to cytochrome oxidase
Oxygen would not be able to accept an electron and produce water
No ETC

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20
Q

What is an uncoupling molecule

A

Increases the inner membrane permeability to hydrogen
Hydrogen moves back into the matrix and not through the ATP synthase
No ATP produced

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21
Q

What is a natural uncoupling molecule

A

Brown adipose tissue (fatty acids)
Lipase release fatty acids
Fatty acids would stimulate the UCP1
Moves hydrogen back into the matrix
Not through the atp synthase

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22
Q

What is pyruvate dehydrogenase

A

Enzyme that would convert pryruvate to acetyl Co a

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23
Q

What activates and inhibits pyruvate dehydrogenase

A

Activates: ADP NAD+ insulin pyruvate
Inhibits: ATP NADH acetyl Co a

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24
Q

What molecules does oxaloacetate make

A

Glucose
Amino acids

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25
Q

What molecules can alpha ketoglycerate make

A

Amino acids

26
Q

What molecules does succinate produce

A

Haem
Amino acids

27
Q

What molecule does Malate make

A

Amino acids

28
Q

How many ATP molecules are produced overall

A

32

29
Q

What is a PTC

A

protein translocating complex
Basically electron carriers

30
Q

What electron carrier produced NAD+

A

Coenzyme q

31
Q

What electron carrier would produce FAD2+

A

Cytochrome p

32
Q

What carrier would produce water

A

Cytochrome oxidase

33
Q

What is isocitrate dehydrogenase

A

Converts isocitrate to alpha ketoglycerate
Release CO2 and NADH

34
Q

What is the difference between NADH and FAD2H

A

Electrons in NADH have more energy then that of FAD2H
Oxidation of 2 molecules of NADH produces 5 ATP molecules
Oxidation of 2 molecules of FAD2H produces 3 ATP molecules

35
Q

What are ketone bodies

A

Water soluble molecules
Would be produced from the liver
Made when there is low glucose levels or when there is a low insulin to glucagon ratio (e.g in starvation)

36
Q

What organs would metabolise lactate

A

Heart and the lungs

37
Q

What factors can lead to the production of lactate

A

Strenuous excersise
Shock
Congestive heart disease

38
Q

What is lactate broken down into

A

Glucose (in liver) and CO2 (in muscle)

39
Q

What are he three main ketone bodies

A

Acetone
Acetoacetone
Beta hydroxybutyrate

40
Q

What is ketonuria

A

Ketone levels would be above the renal threshold
Need to be excreted by the body

41
Q

Where would the ketone bodies be produced

A

In the liver

42
Q

What is the level of ketone bodies when the body is starved

A

2-10 mM

43
Q

What are the levels of ketone bodies for untreated diabetes

A

Above 10mM

44
Q

What enzyme would produce acetone from acetoacetone

A

Lyase

45
Q

What is ketoacidosis

A

Levels of insulin on the body would be so low
Fatty acids would be broken down by the ketone bodies
Build of ketones in the blood

46
Q

What form would lipids be stored in

A

Triacylglycerides in the adipose tissues

47
Q

What moves the lipids to the adipose tissues

A

Chylomicrons (lipoproteins)

48
Q

What moves the fatty acids to the functional tissues

A

Albumin (plasma protein)

49
Q

How are fatty acids activated

A

Conversion to fatty acyl CO A
Via fatty acyl CO A synthase
Adding Coa and ATP

50
Q

How would fatty acids be transported into the mitochondrias matrix

A

Carnitine shuttles

51
Q

What as the equations for the carnitine shuttles

A

CAT (carnitine acyltransferase)
Acyl CO A + carnitine ——-(cat 1)———- acyl carnitine + CO A
acyl carnitine + CO A ——— (cat 2) ——— acyl CO A + carnitine

52
Q

What is beta oxidation

A

Metabolism of the fatty acids in the mitochondria
Requires oxygen
Release of 2 carbons each unit (an acetate)
No direct production of ATP
Produced NADH, FAD2H

53
Q

What is glycerol metabolised to in the liver

A

First glycerol phosphate (via glycerol kinase needing ATP)
Can produce triglycerides (used or stored)
Produce DHAP (NAD+ TO NADH) can be used for glycolysis

54
Q

What enzyme metabolises glycerol

A

Glycerol kinase

55
Q

What would stop beta oxidation

A

Absence of oxygen

56
Q

What molecule would inhibit the transfer of fatty acids to the mitochondrial matrix

A

Malonyl CO A

57
Q

What carbon number can double bonds not be formed after

A

C9

58
Q

What does amiphipatic mean

A

Contains the hydrophilic and hydrophobic areas

59
Q

What vitamins are lipid based

A

A K D E

60
Q

What lipids are hydroxy-methyl-glutaric acid derived

A

Cholesterols
Ketone bodies

61
Q

What lipids are fatty acid derivatives

A

Triglycerides
Phospholipids

62
Q

What is produced during starvation and in the fed state

A

Starved: ketone bodies, levels of insulin would be low, low glucose, high break down of fatty acids
Fed: high levels of insulin as would have lots of glucose. Cholesterol produced (reductase)