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NAM Flashcards

1
Q

What are the precursors of steroid hormones?

A

Cholesterol

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2
Q

What is the precursor of prostaglandins?

A

arachidonic acid (C20)

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3
Q

What are the typical body stores in a 70kg adult?

A

11Kg of fat (TG)
150g glycogen
10g glucose

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4
Q

What is the energy efficiency of 1g of fat, protein and carbohydrate?

A 
fat = 38kj 
protein = 21kj 
carbohydrate = 17kj
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5
Q

How is glycerol metabolised in most tissues?

A

enters glycolysis pathway

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6
Q

How is glycerol metabolised in the liver during starvation?

A

undergoes gluconeogenesis

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7
Q

Where does beta-oxidation occur?

A

mitochondrial membrane

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8
Q

How do free fatty acids travel in the blood?

A

bound to albumin

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9
Q

What enzyme breaks down triacylglycerol?

A

lipase

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10
Q

What are the intermediates of the beta-oxidation pathway?

A

CoA thioesters

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11
Q

What is the overall process of beta-oxidation?

A

removal of 2C from fatty acid as acetyl CoA

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12
Q

What is the first step of the beta-oxidation pathway?

A

activation of long chain fatty acids

  • occurs in the cytosol via activating enzyme
  • adds CoA to the fatty acid
  • requires ATP -> AMP
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13
Q

How are fatty acids transported into the mitochondrial matrix?

A

via the carnitine shuttle

  • carnitine acyl-transferase I adds carnitine (+ removes CoA)
  • carnitine acyl-transferase II replaces carnitine with CoA in matrix
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14
Q

What are the 4 enzyme reactions of beta-oxidation in the mitochondria matrix?

A
  1. Removal of 2H
    • by acyl-CoA dehydrogenase
    • requires FAD
    • C=C formation
  2. Addition of water
    • by enoyl-CoA hydratase
    • produces 3-L-hydroxyacyl-
      CoA
  3. Removal of 2H
    • by 3-L-hydroxyacyl-CoA
      dehydrogenase
    • requires NAD+
    • produces B-ketoacyl CoA
  4. Removal of 2C
    • by b-ketoacyl-CoA thiolase
    • addition of CoASH
    • prodcues fatty acyl-CoA
      (-2C), and acetyl CoA
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15
Q

What happens to the products of beta-oxidaiton?

A

actyl-CoA enters the TCA cycle

the fatty acyl CoA undergoes the pathway again

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16
Q

What are the 3 levels of regulation of beta oxidation?

A
  1. adrenaline/glucagon activate lipase for FA activation
  2. rate of mitochondria entry regulated by carnitine shuttle
  3. regulation of rate of NADH and FADH2 reoxidation
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17
Q

What are the main tissues where beta-ox takes place?

A

heart, skeletal muscle and liver

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18
Q

What are the natural sources or carnitine?

A
  • animal and plant sources (diet)

- synthesised in the liver by lysine methylation

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19
Q

How does the beta-oxidation pathway generate ATP?

A

reoxidation of NADH and FADH2 by the electron transport chain

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20
Q

How much ATP is generated from NADH reoxidation?

A

2.5 ATP

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21
Q

How much ATP is generated from FADH2 reoxidation?

A

1.5 ATP

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22
Q

Roughly how many molecules of ATP does acetyl CoA produce in the TCA cycle?

A

10

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23
Q

What vitamin is required for beta-ox of odd-chain fatty acids?

A

cobalamin (B12)

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24
Q

How much glucose is stored in the body?

A

around 10g in plasma

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25
Q

How much glycogen is stored in the body

A

around 400g

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26
Q

What is the function of glycogen in the liver?

A

source of blood glucose

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27
Q

What is the effect of insulin on glycogen?

A

encourages storage and synthesis

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28
Q

What is the effect of glucagon on glycogen?

A

encourages breakdown

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29
Q

How much glycogen is stored in the liver?

A

100-120g

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30
Q

How much glycogen is stored in muscles?

A

250-300g

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31
Q

What is glycogen in muscles used for?

A

energy for muscle contraction only

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32
Q

What substances affect glycogen in muscle?

A

adrenaline, calcium, AMP, ATP

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33
Q

What type of bonds are in glycogen?

A

a-1,4 glycosidic linkages

a-1,6 links at branches

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34
Q

What is the purpose of having branched glycogen?

A

More efficient as allows several enzymes to attack at once

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35
Q

What are the steps of glycogen synthesis?

A
  1. glucose -> glucose 6-phosphate
  2. glucose 6-p -> glucose 1-p
  3. glucose 1-p -> UDP-glucose + PPi
  4. glucose is added to glycogen chain
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36
Q

What enzyme converts glucose to glucose 6- phosphate?

A

Hexokinase in muscle

glucokinase in liver

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37
Q

What is the difference between hexokinase and glucokinase?

A

Glucokinase has a high km for glucose, so only works when glucose conc is high
- prevents taking glucose from the brain in starvation

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38
Q

what enzyme adds glucose to the glycogen chain?

A

glycogen synthase

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39
Q

What enzyme adds branches to glycogen?

A

branching enzyme

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40
Q

How is glycogen synthase regulated?

A

inactivated by phosphorylation (kinase)

- activated by phosphatase

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41
Q

What enzyme breaks down glycogen?

A

glycogen phosphorylase

- debranching enzyme for branches

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42
Q

What does glycogen phosphorylase produce?

A

glucose 1-phosphate

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43
Q

Why can the liver break glycogen down to glucose and not muscle?

A

only the liver has the enzyme glucose 6-phosphatase which breaks glucose 6-p to glucose

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44
Q

How is glycogen phosphorylase regulated?

A

activated by kinase (phosphorylated)

inactivated by phosphatase

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45
Q

What additional control of glycogen regulation exists in the liver?

A

in high conc, glucose binds glycogen phosphorylase and inactivates it

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46
Q

What additional control of glycogen regulation exists in muscle?

A

Ca2+ from contraction binds calmodulin domain of glycogen phosphorylase -> activated

AMP activates phosphorylase, ATP inhibits it

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47
Q

What is the coordinated regulation of glycogen?

A

Adrenaline/glucagon activate kinase -> synthetase is inactive, phosphorylase is active = glycogen breakdown

Insulin activates phosphatase -> synthetase is active, phosphorylase is inactive = glycogen storage and synthesis

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48
Q

What enzyme is affected in Von Gierke’s disease and the effects?

A

glucose 6-phosphatase

  • enlarged liver
  • hypoglycaemia
  • no muscle effects (lacks enzyme)
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49
Q

What enzyme is affected in Pompe’s disease and its effects?

A

lysosomal glycosidase

  • muscle weakness
  • cardiac failure
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50
Q

What enzyme is affected in McArdle’s disease, and its effects?

A

glycogen phosphorylase

- exercise intolerance

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51
Q

What is the fate of glucose 6-phosphate in the liver?

A
  • free glucose released into blood
  • oxidation to CO2
  • conversion to acetyl CoA then to fat
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52
Q

What is the fate of glucose 6-phosphate in fast muscle fibres?

A

anareobic glycolysis -> lactate

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53
Q

What is the fate of glucose 6-phosphate in slow muscle fibres?

A

glycolysis -> pyruvate -> TCA cycle

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54
Q

Where is protein stored in the body?

A

only in muscle

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55
Q

How much protein is required daily?

A

50-70g

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56
Q

What happens to excess protein intake?

A

it is excreted as urea

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57
Q

What are the essential amino acids?

A 
valine
histamine
lysine
threonine
leucine
isoleucline
methinonine
phenylalanine
arginine
tryptophan
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58
Q

What are the forms nitrogen is excreted as?

A

urea, uric acid, creatinine and ammonia (NH4+)

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59
Q

In what situations is nitrogen intake greater than excretion?

A

growth in childood
illness or trauma recovery
pregnancy

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60
Q

In what situations is nitrogen intake less than excretion?

A

starvation
serious illness e.g. cancer
injury or trauma

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61
Q

How are cellular proteins degradated?

A

by the ubiquitin breakdown system

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62
Q

How are exogenous proteins degraded?

A

by lysosomes

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63
Q

What is oxidative deamination?

A

removal of an amino group from an AA:

AA + H20 + coenzyme -> keto acid + ammonia + coenzyme-2H

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64
Q

What is transamination?

A

Transfer of an amino group to another molecule:
AA 1 + keto acid 2 -> keto acid 1 + AA 2
- often first step in AA breakdown

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65
Q

What is the purpose of transamination?

A

production of non-essential AAs

intermediate for removing amino group from AAs

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66
Q

What is transdeamination?

A

When transdeamination of an AA produces glutamate

- glutamate can then be degraded to produce ammonia which enters the urea cycle -

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67
Q

What are glucogenic amino acids?

A

amino acids that can be converted to glucose by the liver

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68
Q

What are ketogenic amino acids?

A

amino acids that are degraded to acetyl CoA (fats)

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69
Q

Which amino acids are exclusively ketogenic?

A

lysine and leucine

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70
Q

Which amino acids are ketogenic and glucogenic?

A

phenylalanine and tyrosine

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71
Q

Where does degradation of proteins occur?

A

in liver and muscle

- but only liver can degrade amino acids to urea

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72
Q

How are amino acids transported to the liver?

A
  • mainly glutamine from muscle

- also alanine, glutamate and aspartate

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73
Q

What is the order of the urea/ornithine cycle:

A

ammonia + Co2 -> carbonyl phosphate
carbonyl phosphate + ornithine -> citrulline
citrulline + carbonyl phosphate -> arginosuccinate
arginosuccinate -> fumerate + arginine
arginine -> urea + ornithine

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74
Q

why does ammonia need to be excreted?

A

it is neurotoxic

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75
Q

What is the concentration of circulating glucose?

A

3.9-6.7mM

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76
Q

What is the normal fasting glucose concentration?

A

4.4-4.5mM

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77
Q

What glucose concentration causes coma/death?

A

<2.5.>

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78
Q

What are the advantages of glucose as a fuel?

A
  • water soluble (travels unbound)
  • crosses the blood brain barrier
  • can be oxidised anaerobically
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79
Q

What are the disadvantages of glucose as a fuel?

A
  • relatively low ATP yield
  • osmotically active
  • high concentrations can damage cells
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80
Q

What are the sources of blood glucose?

A

diet
glycogen
gluconeogenesis

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81
Q

When does gluconeogenesis occur?

A

in carbohydrate deprivation

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82
Q

Can fatty acids be used for gluconeogenesis?

A

no

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83
Q

What sources can be used for gluconeogenesis?

A

lactate, glycerol, monosaccharides, glucagonic amino acids

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84
Q

What 3 steps of glycolysis need to be bypassed in gluconeogenesis?

A
  1. glucose -> glucose 6-p
    - via hexokinase
  2. fructose 6-p -> fructose 1,6- bisp
    - via phosphofructokinase
  3. phosphoenolpyruvate -> pyruvate
    - via pyruvate kinase
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85
Q

Where do the irreversible steps of glycolysis happen?

A

in the cytosol

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86
Q

What enzymes are used to bypass irreversible steps in gluconeogenesis?

A

glucose 6-phosphatase
fructose 1,6-bisphosphatase
pyruvate carboxylase
PEP carboacylkinase

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87
Q

What 2 levels is gluconeogenesis regulated at?

A

mobilisation of substrate

enzyme activation

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88
Q

What activates gluconeogenesis enzymes?

A

low insulin/glucagon

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89
Q

What activates pyruvate carboxylase for gluconeogenesis?

A

acetyl CoA

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90
Q

What is the glucose-alanine cycle?

A

glucose is made by gluconeogensis in the liver
glucose undergoes glycolysis in muscle
produces alanine and lactate
alanine and lactate travel to liver and produce pyruvate
pyruvate is then used in liver to undergo glucogenogenesis

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91
Q

What enzymes maintain blood glucose?

A

insulin, glycogen and adrenaline

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92
Q

What are the effects of insulin on the liver?

A

inhibits gluconeogenesis

increases glycogen, fatty acid and protein synthesis

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93
Q

What are the effects of insulin on muscle?

A

increases glucose uptake via GLUT4

increases protein and glycogen synthesis

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94
Q

What are the effects of glucagon?

A

increases glycogen breakdown and gluconeogenesis = increases blood glucose
- increases circulating fatty acids and ketone bodies
increases amino acid uptake by the liver

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95
Q

what is the estimated average requirement (EAR)?

A

intake that will be sufficient for 50% of the population

- mid point in bell graph

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96
Q

What is the reference nutrient intake (RNI):

A

intake that is sufficient for the majority of the population
= EAR + 2SD

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97
Q

What is the lower RNI?

A

intake that is inadequate for the majority of people

= EAR - 2SD

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98
Q

What is the EAR, RNI and LRNI for vitamin C?

A 
EAR = 25mg
RNI = 40mg
LRNI = 10mg
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99
Q

How is BMI calculated?

A

weight/height^2

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100
Q

what are the categories of bmi?

A 
normal = 18.5-24.9
overweight = 25-29.9
obesity grade 1 = 30-34.9
obesity grade 2 = 25-29.9
obesity grade 3 = >40
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101
Q

What is the recommended daily salt intake?

A

6g

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102
Q

What methods can be used to measure body composition?

A 
body density, body water 
total body potassium
creatinine excretion
skinfold measurements
mid-arm circumference 
bioelectrical impedence
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103
Q

How much energy is derived from 1 gram of carbohydrate?

A

4kcal

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104
Q

How much energy is derived from 1 gram of fat?

A

9.2kcal

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105
Q

How much energy is derived from 1 gram of protein?

A

5.4kcal

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106
Q

How much energy is derived from 1 gram of alcohol?

A

7kcal

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107
Q

What is the metabolisable energy?

A

Digestible energy - energy lost in urine and sweat

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108
Q

What does energy requirements depend on?

A 
metabolic rate 
diet induced thermogenesis 
physical activity 
temperature of environment
growth, pregnancy, lactation
age
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109
Q

What does leptin signal in appetite?

A

signals the state of fat stores

increases satiety via hypothalamus

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110
Q

What does insulin signal in appetite?

A

signals the state of carbohydrate stores

increases satiety via hypothalamus

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111
Q

What signals stimulate hunger?

A

NPY and ghrelin

112
Q

What does POMC signal?

A

suppresses appetite

113
Q

Where do short term signals for satiety come from?

A

GI, hepatic portal vein and liver

114
Q

What are genetic causes of obesity?

A

leptin deficiency

115
Q

What are endocrinological causes of obesity?

A

adrenal hyperactivity

hypothyroidism

116
Q

What drug is licensed for treating obesity in the UK?

A

orlistat

- decreases fat absorption

117
Q

What is the problem with treating obestiy with leptin?

A

obese people often have leptin resistance

118
Q

What surgical options can treat obesity?

A

liposuction, intestine resection, stomach banding and stapling

119
Q

What is the average daily intake of fat?

120
Q

What percentage of the average diet is fat?

A

40% of energy intake

121
Q

What are 2 essential fatty acids?

A

linolenic acid and linoleic acid

122
Q

What are essential fatty acids required for?

A

membrane phospholipids and eicosanoid precursors

123
Q

What percentage of the average diet is carbohydrate?

A

40% of energy intake

124
Q

What are common monosaccharides in the diet?

A

glucose, fructose, sorbitol, inositol

125
Q

How much sucrose is consumed on average?

126
Q

What percentage of the average diet is protein?

127
Q

How much protein is recommended daily?

A
  1. 75g per kg of body weight
    - 55g for men
    - 44g for women
128
Q

How much protein do newborns require?

129
Q

What can happen with excess protein consumption?

A

Renal damage and bone demineralisation

130
Q

What are the different forms of PEM?

A

growth failure
marasmus
kwashiorkor
marasmic kwashiorkor

131
Q

What disease has no oedema and 60-80% of expected weight?

A

underweight

132
Q

What disease has oedema and 60-80% of expected weight?

A

kwashiorkor

133
Q

What disease has no oedema and <60% of expected body weight?

134
Q

What disease has oedema and <60% of expected body weight?

A

marasmic kwashiorkor

135
Q

What are the features of marasmus?

A 
emaciation
muscle wasting, fat loss, loss of protein from organs
impaired immunity and absorption 
diarrhoea
apathy
136
Q

What additional features to marasmus does kwashiorkor have?

A 
oedema
enlarged and fatty liver 
hair changes 
dermatitis 
mental retardation (possible)
137
Q

What causes kwashiorkor?

A

usually food deficiency + infection

138
Q

What vitamins are water soluble?

139
Q

What vitamins are fat soluble?

A

A, D, E, K

140
Q

What are differences between water and fat soluble vitamins?

A

water - not stored, generally not toxic

fat - stored, not easily absorbed or excreted, can be toxic in excess

141
Q

What are the functions of B vitamins

A

coenzymes in metabolic pathways

142
Q

What is vitamin B1 known as?

143
Q

What does thiamin/B1 deficiency result in?

A

Beri-Beri:
- infantile, wet (oedema, cardiac) and dry (chronic, neuropathy)

Werniche-Korsahoff syndrome - in alcoholics, memory loss/dememtia

144
Q

What foods are anti-thiamin factors?

A

coffee and tea

145
Q

What reaction does thiamin act on?

A

pyruvate -> acetyl CoA

pyryvate dehydrogenase complex

146
Q

What is vitamin B2 known as?

A

riboflavin

147
Q

What is riboflavin found in?

148
Q

What is the function of riboflavin?

A

FAD and FMN

149
Q

What is B3 known as?

A

Niacin, nicotinic acid nicotinamide

150
Q

What is a vitamer?

A

different structural forms of a vitamin

151
Q

Why do alcoholics get vitamin B deficiencies?

A

empty calories from alcohol - inadequete level of vitamins and nutrients
GI tract malfuncitons
Cirrhosis affects storage, transport and metabolism of vitamins

152
Q

What is the function of niacin (B3)?

A

NAD and NADP

153
Q

What are the sources of niacin?

A

cereals, can be formed from tryptophan

154
Q

What does deficiency of niacin (B3) result in?

A

Pellagra
Casal’s necklace (photosensitive dermatitis)
diarrhoea
dementia

155
Q

What is vitamin B6 known as?

A

pyridoxine

156
Q

What is the function of pyridoxine (b6)?

A

amino acid metabolism and haem synthesis

157
Q

What is pyridoxine (B6) deficiency?

A

usually secondary

in isoniazid treatment for TB

158
Q

What are some theraputic uses of B6 (pyridoxine)?

A

siezures, Down’s syndrome, autism, PMS

159
Q

What is vitamin B12 known as?

160
Q

What is the function of cobalamin (b12)?

A

carrier of methyl groups

161
Q

What defect does b12 deficiency cause?

A

pernicious anemia

162
Q

what are the sources of b12?

A

animal tissues

163
Q

How is vitamin b12/cobalmin transported?

A

by intrinsic factor

164
Q

What is the function of folate (b9)?

A

carries 1C units

- active form = tetrahydrofolate

165
Q

Where is folate found?

A

green vegetables liver, whole grains

166
Q

What do folate and B12 do?

A

involved in amino acid metabolism

167
Q

What does folate/B12 deficiencies cause?

A

megaloblastosis
inadequate myelin synthesis
neural tube defects

168
Q

What can cause folate/B12 deficiency?

A 
low intake
coeliac disease 
Crohn's
drugs/alchol
lack of intrinsic factor
169
Q

What is B5 known as?

A

pantothenic acid

170
Q

what is the function of pantothenic acid (B5)?

A

component of coenzyme-A (CoASH)

171
Q

What is B7 known as?

172
Q

Where is biotin (B7) found?

A

in most food and gut flora synthesis

173
Q

What is the function of biotin (B7)?

A

prosthetic group for carboxylations

174
Q

When can biotin/B7 deficiency occur?

A

eating raw egg whites

long term antibiotic use

175
Q

What is vitamin C also called?

A

ascorbic acid

176
Q

What is the function of vitamin C?

A

antioxidant
collagen formation
iron absorption

177
Q

What disease results from vitamin C deficiency?

A

scurvy

- impaired wound healing, haemorrhage and anemia

178
Q

What people are likely to have vitamin C deficiency?

A

elderly, alcoholics, adolescents that eat junk food

179
Q

What is the RNI for vitamin C?

A

40mg

- smokers is 80mg

180
Q

What sources does vitamin A come from?

A

in form of retinol

- liver, fish liver oils, milk, eggs, green yellow & orange fruit and vegetables

181
Q

What are the active forms of vitamin A?

A

retinoic acid - hormone
retinal - vision
B-carotene - antioxidant

182
Q

What are the risks of vitamin C megadoses?

A

kidney stones
diarrhoea
systemic conditioning

183
Q

How is potency of vitamin A expressed?

A

retinol equivalents

1 RE = 1 microgram of retinol

184
Q

What are the functions of vitamin A?

A

binding chromatin to control protein synthesis

conversion of light energy in retina

185
Q

How is vitamin A transported?

A

From gut to liver = chylomircons

from liver to tissues = retinol bindng protein and pre-albumin

186
Q

What happens in vitamin A deficiency?

A

night blindness -> xerophthalmia -> keratomalacia -> irreversible blindness

187
Q

What happens in vitamin A toxicity?

A

teratogenic (in pregnancy)

dermatitis, hair loss, liver dysfunction, bone thinning

188
Q

What are the sources of vitamin E?

A

vegetable oils, nuts, green vegetables

189
Q

What type of molecules are vitamin E (and the most potent)?

A

tocapherols

most potent is alpha-tocepherol

190
Q

What is the function of vitamin E?

A

antioxidant for PUFAs and circulating lipoproteins

191
Q

What is vitamin E deficiency in humans?

A

haemolytic anaemia in premature infants

192
Q

What are the 2 main types of vitamin D?

A

D3 - cholecalciferol (from UV on skin)

D2 - ergocalciferol (from plants)

193
Q

What is the function of vitamin D?

A

rickets in children

osteomalacia in adults

194
Q

What are the toxic effects of vitamin D?

A

hypercalcaemia, calcification of soft tissue

195
Q

What are the sources of vitamin K?

A

green leafy vegetables, eggs, milk, meat , cereal, gut flora

196
Q

Why are babies susceptible to vitamin K deficiency?

A
  • levels in human milk are low
  • vitamin K doesn’t cross placenta easily
  • neonatal gut is sterile
    = haemorrhage disease of the new born
197
Q

what happens in vitamin K deficiency?

A

defective blood clotting

- in long term antibiotic therapy

198
Q

What hormone stimulates fatty acid synthesis?

A

insulin in the fed state

199
Q

How are fatty acids synthesised?

A
  1. acetyl CoA + bicarbonate -> Malonyl CoA
    - requires biotin
  2. chain is extended by fatty acid synthetase
    - adds 3C and removes 1 each time
    - requires NADPH
200
Q

Where is TAG synthesised?

201
Q

How is TAG synthesised?

A

3 fatty acids are joined to glycerol phosphate (from glycolysis)
phosphate disappears

202
Q

What is the structure of lipoproteins?

A

inner core of TAG and cholesterol esters

outer shell of phospholipids, cholesterol and apoproteins

203
Q

Why are lipoproteins needed?

A

to transport lipids as they are not water soluble

204
Q

What do chylomicrons transport?

A

dietary TAG

205
Q

What does VLDL transport?

A

endogenous TAG

206
Q

What does LDL transport?

A

cholesterol to tissues

207
Q

What does HDL transport?

A

cholesterol to the liver

208
Q

How is exogenous fat transported?

A
  1. Packaged with ApoB in small intestine
  2. Form chylomicrons with addition of ApoC-11 and ApoE in blood
  3. lipoprotetin lipase removes free fatty acids from TAG
  4. FFAs enter adipocytes and are re-esterifed to TAG
  5. Remaining glycerol goes to liver and chylomicron remenant is taken up by ApoE receptors on liver
209
Q

How is endogenous fat transported?

A
  1. Packaged with ApoB-100 in the liver
  2. Becomes VLDL in blood with apoC-II and apoE
  3. lipoprotein lipase takes free fatty acids, leaving IDL
  4. IDL is converted to LDL which transports cholesterol to tissues
  5. cholesterol is taken up by B-100 receptors
210
Q

Where is HDL synthesised?

A

in the liver and small intestine

211
Q

What enzyme converts cholesterol to cholesterol esters?

212
Q

How is the number of LDL receptors regulated?

A

by cholesterol

- receptor mediated enodcytosis

213
Q

What are the steps in cholesterol synthesis?

A

acetyl CoA + acetoacetyl CoA -> HMG-CoA

-> mevalonate -> cholesterol

214
Q

What enzyme do statins inhibit?

A

HMG-CoA reducatse

215
Q

What do LDL receptors recognise?

216
Q

What is the purpose of LDL receptors?

A

to remove LDL from circulation

217
Q

What is familial hypercholesterolaemia?

A

defective LDL receptors

218
Q

How does atherosclerosis develop?

A

foam cell accumulation ->
fatty streak formation ->
plaque

219
Q

What are foam cells?

A

macrophages filled with lipid

220
Q

How do foam cells develop?

A

oxidised LDL is taken up by scavenger receptors on macrophages as they are not down-regulated

221
Q

what are the essential minerals?

A

Na, Mg, Ca, K

222
Q

What are the normal Na+ concentrations?

A

inside cell = 12mM

outside cell = 140mM

223
Q

What are the normal K+ concentrations?

A

inside cell = 140mM

outside cell = 5mM

224
Q

What is Mg2+ required for?

A

cofactor for ATP and enzyme complexes

225
Q

What is cobalt used in the body for?

A

component of B12/cobalamin

226
Q

What is molybdenum (Mo) used for?

A

cofactor for molybdopeterin

227
Q

What does manganese overload cause?

A

form of parkinson’s disease

228
Q

What is the daily requirement of iron?

229
Q

WHat is the daily requirement of copper?

230
Q

What is the daily requirement of zinc?

231
Q

What controls iron export?

A

ferroportin

- regulated by hepcidin

232
Q

What is the distribution of iron in the body?

A 
muscle - 300mg
bone marrow - 300mg
liver - 1000mg 
RBCs - 1800mg 
-> lost in blood loss
233
Q

How is iron taken up by cells

A

in Fe2+ form

bu DMT1

234
Q

How is iron stored in cells?

A

as Fe3+ in ferretin

235
Q

How is iron transported?

A

by transferrin

236
Q

What is HFE1?

A

genetic iron overload

treated by phlebotomy

237
Q

How can iron overload be treated?

A

with deferoxamine

- chelating agent

238
Q

How is zinc taken up by cells?

239
Q

How is zinc exported from cells?

240
Q

How is zinc transported?

A

by metallothioneins

241
Q

What are signs of zinc deficiency?

A

suppressed immunity, loss of appetite, growth retardation, dermatitis, alopecia, delayed sexual maturation

242
Q

What is acrodermatitis enteropathica?

A

severe skin lesions caused by zinc deficiency

- ZIP4 mutation

243
Q

What is transient neonatal zinc deficiency

A

mutation in ZNT2 due to lack of zinc from mother

244
Q

How is zinc deficiency treated?

245
Q

How is copper imported?

A

as Cu+ by crt1

246
Q

How is copper imported to golgi?

247
Q

What is Wilson’s disease?

A

Copper accumulation in liver and brain

  • ATP7B mutation
  • get kayser-fleischer rings
248
Q

What is Menkes disease?

A

ATP7A mutation

  • defective absorption of copper
  • no cure, 2 year life expectancy
249
Q

How is copper overload (wilson’s disease) treated?

A

chelation therapy - D-penicillanmire and with zinc

250
Q

What are the main hormones that control metabolism?

A

insulin and glucagon

251
Q

What stimulates insulin secretion?

A

increased blood glucose and amino acid concentration
glucagon
secretin

252
Q

What can inhibit insulin secretion?

A

adrenaline

253
Q

How is insulin secreted from pancreatic beta cells?

A

stimulus causes closure of K+ channels
leads to opening of Ca2+ channels for influx
triggers secretion

254
Q

How insulin activated in pancreatic cells?

A

proinsulin is cleaved to c-peptide and insulin

255
Q

What stimulates glucagon secretion?

A

low blood glucose
high blood amino acid conc
adrenaline

256
Q

What are the metabolic effects of insulin?

A

promotes growth and fuel storage

- glycogen, TAG and protein synthesis

257
Q

What type of receptor is the insulin receptor?

258
Q

What is the main pathway downstream of insulin receptor activation?

A

activation of AKT/PKB

259
Q

How does insulin receptor activation affect glucose?

A
  • AKT/PKB increases GLUT4 translocation to membrane

- also inactivates glycogen synthase kinase to promote glycogen synthesis

260
Q

How does insulin receptor activation inhibit lipolysis?

A
  • AKT/PKB activates phosphodiesterase

- inhibits lipase to prevent TAG breakdown

261
Q

How does insulin receptor activation affect gene expression?

A

SHC causes Ras -> Raf

activates MAPK cascade to activate transcription factors

262
Q

What are the effects of glucagon on metabolism?

A
  • maintains blood glucose in fasting
  • activates glycogen breakdown and gluconeogenesis
  • promotes FA oxidation and ketone body formation in the liver
263
Q

What effect does adrenaline have on metabolism?

A

mobilises fuel during stress

264
Q

What effect does cortisol have on metabolism?

A

maintains long term requirements

265
Q

What is used as fuel in the fasting state?

A

1st - glycogen

2nd - lactate, glycerol and amino acids are used in gluconeogenesis

266
Q

How is conversion to glucose favoured in the fasting state?

A

pyruvate dehydrogenase is inhibited to prevent pyruvate being converted to acetyl CoA

267
Q

What is released in ketone body formation?

A

acetoacelate and beta-hydroxybutyrate

268
Q

What change happens in prolonged starvation?

A

ketone body formation is increased to spare protein

urea production decreases

269
Q

What fuels do the brain and muscle use in prolonged starvation?

A

brain uses more ketone bodies

muscle uses fatty acids

270
Q

How is protein breakdown reduced in prolonged starvation?

A

ketone bodies stimulate insulin release

271
Q

How does type 1 diabetes occur?

A

autoimmune destruction of beta cells -> no insulin production

272
Q

How is type 1 diabetes treated?

A

insulin administration after meals

273
Q

what are the characteristics of type 1 diabetes?

A

hyperglycaemia and ketoacidosis

274
Q

How does type 2 diabetes occur?

A

insulin resistance

275
Q

What is the characteristics of type 2 diabetes?

A

hyperglycaemia but no ketoacidosis

276
Q

What are the major complications of diabetes?

A

microangiopathy, retinopathy, nephropathy, neuropathy

277
Q

What is metabolic syndrome?

A

type 2 diabetes/insulin resistance + any 2 of:

  • hypertension
  • dyslipidaemia
  • central obesity
  • microalbuminuria

FBS1 (9 decks)

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