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MCD > Metabolism 2 > Flashcards

Metabolism 2 Flashcards

1
Q

Give 2 methods of synthesising acetyl coA

A

glycolysis + link reaction

Fatty acid oxidation

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2
Q

What can acetyl coA be used for

A

sterols and fatty acids
TCA
ketone bodies
protein acetylation

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3
Q

Compare unsaturated to saturated fatty acids

A

both are hydrocarbon chains with -COOH at the end
unsaturated= 1 or more double bonds, liquids e.g. plant oils
saturated= no double bonds, solids e.g. animal fat

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4
Q

What is the structure of a triglyceride

A

1 glycerol and 3 fatty acids bonded together by ester bonds

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5
Q

How are fatty acids stored

A

stored as triglycerides in adipocytes

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6
Q

compare the caloric yield of fat to glucose

A

38 ATP vs 129 ATP

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7
Q

How much of energy is from fat in the human body

A

50%, except for in the brain where only glucose and ketone bodies are used

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8
Q

What can fatty acids be involved in metabolically

A

conversion to acyl coA
transport to the mitochondrial matrix
bet oxidation
acetyl coA production

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9
Q

What is acyl coA used for and how is it synthesised

A

used for beta oxidation
outer mitochondrial membrane
acyl coA synthetase converts the fatty acid to any cop while ATP is converted to AMP (2 high energy bonds broken)

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10
Q

How is acyl coA transported to the mitochondria

A

carnitine shuttle
carnitine is converted to acyl carnitine via acyl coA by carnitine acyltransferase I
acyl carnitine transported into the matrix via translocase
acyl carnitine converted to carnitine via coA

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11
Q

What are the 4 main reactions of beta oxidation

A

oxidation
hydration
oxidation
thiolysis

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12
Q

Explain the process of beta oxidation

A
  1. Acyl coA is oxidised by FAD via Acyl coA dehydrogenase
  2. 3-hydroxyacyl hydrolase hydrates the product
  3. oxidation of the product via L-3-hydroxyacyl coA dehydrogenase
  4. Splitting of the product into acyl CoA -2C + Acetyl coA by beta-ketothiolase

this repeats until the fatty acid is broken down (no. of cycles = /2,-1)

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13
Q

When can acetyl coA enter the TCA cycle

A

beta oxidation and carb metabolism is balanced (oxaloacetate needed for entry)

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14
Q

What occurs when fat metabolism > carb metabolism and when may this occur

A

occurs during fasting

acetyl coA forms acetoacetate, D-3 hydrocybutyrate and acetone (ketone bodies)

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15
Q

Explain how ketone bodies are formed from acetyl coA

A
  1. acetyl coA -> acetoacetyl coA
  2. acetoacetyl coA -> 3-hydroxy-3-methyl glutaryl coA
  3. 3-hydroxy-3-methyl glutaryl coA -> acetoacetate
  4. acetoacetate -> D-3 hydroxy butyrate + acetone
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16
Q

What are the 4 main reactions of fatty acid synthesis

A

decarboxylative condensation
reduction
dehydration
reduction

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17
Q

Explain the process of decarboxylative condensation in fatty acid synthesis

A

Aims to make a donator malonyl coA (3C)

  1. acetyl coA is converted to malonyl coA by acetyl coA carboxylase, using ATP
  2. malonyl coA binds to ACP (acyl carrier protein) which swings from one domain to another
  3. another acetyl coA binds to ACP
  4. condensation of malonyl coA and acetyl coA, releasing CO2 and forming acetoacyl ACP (2C)
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18
Q

Explain the process of reduction, dehydration and reduction in fatty acid synthesis

A 
Reduction of acetoacyl ACP using NADPH
Dehydration
Reduction of the product using NADPH
Repeated until the desired molecule is made 
Product is hydrolysed to release ACP
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19
Q

What is the role of fatty acid synthase in fatty acid synthesis

A

Catalyses all reactions except the 1st reaction

Composed of 7 smaller enzymes

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20
Q

Give the reaction for the synthesis of palmitate

A

acetyl coA + 7 malonyl coA + 14 NADPH + 14H+
->
palmitate + 7CO2 + 6 H20 + 8 coA + 14 NADP

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21
Q

Compare metabolism of fatty acids to synthesis of fatty acids

A

met - coA, FAD/NAD, mitochondrial matrix

syn - ACP, NADPH, cytoplasm

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22
Q

Give two examples of inborn errors of lipid metabolism

A

MCAD

Primary carnitine deficiency

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23
Q

What occurs in MCAD

A 
Medium chain acyl coA dehydrogenase deficiency
Required for the oxidation of acyl coA
tested for via heel prick
Autosomal recessive inheritance
Fat cannot be burnt 
No fasting + increase glucose intake
SIDS
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24
Q

What occurs in primary carnitine deficiency

A

unable to shuttle acyl coA
mutation in a gene that takes up carnitine
supplement or carnivore given
Autosomal recessive inheritence

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25
Q

How many carbons are in cholesterol

A

27

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26
Q

Give the overall mechanism for the synthesis of cholesterol

A
  1. Make IPP (isopentyl pyrophosphate)
  2. condense 6 IPP into squalene
  3. modification via cyclisation in the ER
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27
Q

Explain how IPP is made in cholesterol synthesis

A

cytoplasm

  1. 2x acetyl coA combined to form acetoacetyl coA via bet ketothiolase
  2. add another acetyl coA to form HMG-coA via HMG-CoA synthase
  3. reduction of the product to mevalonate via HMG-coA reductase and 2 NADH
  4. conversion of mevalonate by sequential phosphorylation and decarboxylation
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28
Q

What process in cholesterol synthesis is the target of statins

A

reduction of HMG-coA using HMG-coA reductase in the production of IPP

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29
Q

Explain how 6 IPPs are combined during cholesterol synthesis

A

cytoplasm
IPP + dimethylallyl pyrophosphate -> geranyl pyrophosphate (10C)
geranyl PP -> farnesyl PP (15C)
farnesyl PP x 2 -> squalene (30C)

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30
Q

Explain the process of cyclisation in cholesterol synthesis

A

ER
squalene is converted to squalene epoxide and then cyclase causes it to form lanosterol (methyl and hydride shifts)
19 step conversion from lanosterol to cholesterol + x3 demethylation

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31
Q

What is the significance of pregnenolone

A

building block for enzymes

All 5 steroid hormone classes derive from pregnenolone

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32
Q

What can cholesterol be used for

A

synthesis of pregnenolone synthesis of taurocholate

synthesis of glycocholate (primary bile salt) via breakdown

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33
Q

Where are bile salts synthesised and stored

A

synthesised in the liver and stored in the gall bladder

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34
Q

What are bile salts required for

A

fat and fat soluble vitamin digestion
Released into the SI to emulsify fats
a lack of bile salts = steatorrhea

35
Q

How is vitamin D synthesiserd

A

7- dehydrocholesterol converted to pre vit D (UV) then converted to vit D then calcitrol
lack = ricketts

36
Q

Where are lipid rafts found and what is their function

A

found in the plasma membrane

Used for movement of cell-surface receptors

37
Q

Explain the process of absorption of triglycerides

A
  1. TAGs -> MAGs/DAGs + fatty acids via lipases
  2. emulsification by bile salts and addition of cholesterol -> mixed micelle
  3. mixed micelle passes through the intestine wall via enterocytes
  4. MAG + fatty acids -> TAGs
  5. TAGs incorporated into chylomicron with cholesterol and apoproteins
  6. enters lymphatic system via lacteal
38
Q

Describe the structure of a chylomicron

A

core of TAGs, cholesterol esters
apoproteins on the surface
phospholipid monolayer with free cholesterol
hydrophobic core

39
Q

What is the function of cholesterol acyltransferase

A

synthesis of cholesterol esters so they are more hydrophobic and pack more tightly

40
Q

What are the 5 forms of lipoproteins

A 
chylomicrons
very low density lipoproteins (VLDL)
intermediate density lipoproteins (IDL)
Low density lipoproteins (LDL)
High density lipoproteins (HDL)
41
Q

What is the function of apoproteins

A

Act as receptors

Different apoproteins are taken up into different cells

42
Q

What is the purpose of the chylomicron

A

Allows transport from the lymphatic system to the blood

lipoprotein enzyme recognises the apoprotein and breaks down the TAGs to form glycerol and fatty acids

43
Q

What are lipoproteins

A

“leftovers” of the CM

44
Q

Compare LDL to HDL

A

LDL - bad, takes cholesterol from the liver to peripheral tissue, leads to athersclerosis
HDL - good, takes cholesterol from peripheral tissues to the liver

45
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

46
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)

47
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

48
Q

Describe the synthesis of proteins and how they become free or bound

A

All ribosomes begin in a common pool
Translation of mRNA
protein produced has a signal peptide which directs the protein to the correct area in the cell

49
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

50
Q

What happens to a protein with no signal peptide

A

ribosome remains in the cytoplasm

51
Q

What happens to a protein that is compartment specific

A

ribosome remains

Protein moves to the compartment

52
Q

Why are there multiple ribosome per peptide

A

1 ribosome = too slow

polyribosome used instead

53
Q

What happens to incorrectly folded proteins

A

blocked form the ER exit

Exported and degraded

54
Q

Which disorder is associated with membrane trafficking

A

cystic fibrosis

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

55
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
56
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

57
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
58
Q

What are the 3 types of endocytosis

A

Receptor mediator endocytosis
Pinocytosis (fluid intake)
phagocytosis

59
Q

Describe gated transport

A

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

60
Q

Describe vesicular transport

A

Proteins move between organelles via microtubules

vesicles bud on one organelle and move to fuse with others

61
Q

How far apart do membranes have to be for fusion

A

1.5nm

62
Q

What are the 3 types of intracellular transport

A

Gated transport
Transport across membranes
Vesicular transport

63
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

64
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

65
Q

What does skeletal muscle and cardiac muscle rely on for energy

A

carb metabolism and fatty acid oxidation

66
Q

What does the brain and nervous tissue rely on for energy

A

carb and ketone body metabolism (no fatty acids)

67
Q

How are carbs stored

A

glycogen in the liver

68
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

69
Q

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

A

hyperglycaemia - irreversible dameg

hypoglycaemia - faintness and coma

70
Q

What does the heart use for energy

A

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

71
Q

Give the metabolic features of the liver

A

highly metabolically active
can interconvert nutrients
glucose storage
lipoprotein metabolism

72
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

73
Q

What are the metabolic responses to short term fasting

A

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

74
Q

What are the metabolic responses to prolonged fasting

A

pancreas secretes more glucagon

when the glycogen store runs out, gluconeogenesis occurs

75
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

76
Q

Describe aerobic respiration

A

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

77
Q

What is the effect of adrenline

A

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

78
Q

Describe anaerobic respiration

A

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

79
Q

Describe product inhibition

A

as levels of product increases, the rate of reaction decreases

80
Q

What are the 2 forms of hexokinase

A

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

81
Q

Which hormones increase blood glucose

A

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

82
Q

Which hormone decreases blood sugar

A

Insulin

83
Q

What are the 2 types of diabetes

A

type 1 - beta cell dysfunction, not enough insulin

type 2 - insulin resistance

84
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

MCD (13 decks)

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