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FBS1 > Nutrition and Metabolism > Flashcards

Nutrition and Metabolism Flashcards

1
Q

At what pH is ATP stable?

A

pH 6-9

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2
Q

What are the differences in function between ATP, UTP and GTP?

A

ATP: pumps, transporters, contractile events and movement
UTP: synthesis of complex sugars
GTP: protein synthesis

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3
Q

In glycolysis, what are the steps that use/produce ATP and which step produces NADH + H+?

A

Use ATP:

  1. Hexokinase/glucokinase: glucose –> glucose-6-phosphate
  2. Phosphofructokinase: Fructose-6-phosphate to fructose 1,6-bisphosphate

Produce ATP:

  1. Phosphoglycerate kinase: 1,3-bisphosphoglycerate to 3 phosphoglycerate
  2. Pyruvate kinase: phosphoenolpyruvate to pyruvate

Produce NADH + H+:
1. Glyceraldehyde 3-phosphate dehydrogenase: G3P –> 1,3-bisphosphoglycerate

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4
Q

Which reactions represent activation in glycolysis?

A
  1. Hexokinase
  2. Phosphoglucose isomerase
  3. Phosphofructokinase
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5
Q

Which reaction splits the 6C sugar in glycolysis?

A
  1. Aldolase
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6
Q

Which reaction represents oxidation in glycolysis?

A
  1. glyceraldehyde-3-phosphate dehydrogenase
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7
Q

What are the ATP synthesis stages in glycolysis?

A
  1. Phosphoglycerate kinase*
  2. Phosphoglycerate mutase
  3. Enolase
  4. Pyruvate kinase*
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8
Q

What is the reaction catalysed by lactate dehydrogenase?

A

In muscle:
Pyruvate + NADH H+ –> L-lactate + NAD+
In liver: opposite

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9
Q

How is phosphofructokinase controlled allosterically?

A

ATP and citrate inhibit, AMP activates

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10
Q

What is the link reaction?

A

Conversion of pyruvate to acetyl CoA (pyruvate dehydrogenase, CoA, NAD+)
Cofactors: thiamine pyrophosphate, lipoic acid

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11
Q

What type of bonds does CoA form with carboxylic acids?

A

Thioester bonds

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12
Q

What is the condensation reaction of the Krebs cycle?

A

Citrate synthase:

Acetyl CoA + oxaloacetate –> citrate

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13
Q

What is the isomerisation reaction of the Krebs cycle?

A

Aconitase:

Citrate –> isocitrate

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14
Q

When is the first loss of CO2 in the Krebs cycle?

A

Isocitrate dehydrogenase:

Isocitrate + NAD+ –> alpha-ketoglutarate + NADH H+

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15
Q

When is the second loss of CO2 in the Krebs cycle?

A

Ketoglutarate dehydrogenase:

alpha-ketoglutarate + NAD+ –> succinyl CoA + NADH H+

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16
Q

When does production of GTP occur in the Krebs cycle?

A

Succinate thiokinase:

succinyl CoA + GDP –> succinate + GTP + CoA

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17
Q

When does production of FADH2 happen in the Krebs cycle?

A

Succinate dehydrogenase:

Succinate + FAD –> Fumarate + FADH2

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18
Q

What is the enzyme that converts fumarate to malate?

A

Fumarase

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19
Q

When does the third production of NADH H+ in the Krebs cycle occur?

A

Malate dehydrogenase:

Malate + NAD+ –> oxaloacetate + NADH H+

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20
Q

How many molecules of ATP does the TCA cycle produce?

A

10

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21
Q

Which enzyme steps in the Krebs cycle are irreversible and what inhibits or stimulates these?

A
  1. Citrate synthetase: NADH and succinyl CoA inhibit
  2. Isocitrate dehydrogenase: NADH inhibits, ADP stimulates
  3. Ketoglutarate dehydrogenase: NADH and succinyl CoA inhibit
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22
Q

What are the biosynthetic roles of the TCA cycle?

A

Transaminations:
1. Oxaloacetate –> aspartate
2. Alpha-ketoglutarate –> glutamate
Phosphoenolpyruvate production: by PEP carboxylase from oxaloacetate
Citrate –> FAs
Malate –> pyruvate (malic enzyme –> production of NADPH H+)

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23
Q

What is the activation step of long chain fatty acids?

A

Fatty acid + ATP + CoA –> acyl CoA + AMP + PPi

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24
Q

How are fatty acids transported into the mitochondria?

A

Carnitine palmitoyl-transferase I:
Fatty acyl CoA + carnitine –> CoA + fatty acid-carnitine
Translocase: transports through inner mm
Carnitine palmitoyl-transferase II: opposite reaction

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25
Q

What is the first step of beta oxidation?

A

Acyl-CoA dehydrogenase:

fatty acyl-CoA + FAD –> enoyl CoA + FADH2

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26
Q

What is the second step of b-oxi?

A

Enoyl CoA hydratase:

enoyl CoA + H2O –> 3-L-hydroxyacyl CoA

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27
Q

What is the third step of b-oxi?

A

3-L-hydroxyacyl CoA dehydrogenase:

3-L-HA CoA + NAD+ –> beta-ketoacyl CoA + NADH H+

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28
Q

How does the removal of 2C unit in b-oxi happen?

A

beta-ketoacyl CoA thiolase:

beta-ketoacyl CoA + CoASH –> fatty acyl CoA + acetyl CoA

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29
Q

What do odd-chain fatty acids require?

A

Enzyme requiring cobalamin (VitB12)

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30
Q

What activates lipase enzyme?

A

Adrenaline and glucagon

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31
Q

What are the first stages of glycogen synthesis from glucose?

A
  1. Hexokinase (muscle), glucokinase (liver) –> glucose-6-phosphate
  2. Phosphoglucomutase –> glucose-1-phosphate
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32
Q

How is UDP glucose formed?

A

Transferase:

Glucose-1-phosphate + UTP –> UDP glucose + PPi

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33
Q

Which enzyme adds glucose to protein primer (glycogenin)?

A

Glycogen synthase

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34
Q

How is glycogen synthase regulated?

A

Protein kinase phosphorylates and inactivates glycogen synthase
Protein phosphatase dephosphorylates and activates glycogen synthase

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35
Q

Which enzymes are required to degrade glycogen?

A

Glycogen phosphorylase and debranching enzyme

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36
Q

Which enzyme converts glucose-6-phosphate to glucose?

A

Glucose phosphatase (only present in liver)

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37
Q

How is glycogen phosphorylase regulated?

A

Protein phosphatase deactivates

Protein kinase activates

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38
Q

Which enzyme converts cAMP to AMP?

A

Phosphodiesterase

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39
Q

What stimulates protein kinase?

A

Adrenaline and glucagon

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40
Q

What stimulates protein phosphatase

A

insulin

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41
Q

What are other control mechanisms in the liver and muscle?

A

Liver: high glucose –> glucose binds to glycogen phosphorylase and inactivates it
Muscle: high calcium concentrations –> calcium binds to calmodulin domain on glycogen phosphorylase kinase and activates it
Prolonged exercise: AMP activates glycogen phosphorylase –> no need for hormonal interaction (ATP is an inhibitor)

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42
Q

What is von Gierke’s disease?

A

Defective glucose-6-phosphatase

43
Q

What is Pompe’s disease?

A

Defective lysosomal glycosidase

44
Q

What is McArdle’s disease?

A

Defective glycogen phosphorylase

45
Q

How are most cellular proteins and foreign exogenous proteins broken down?

A

Most cellular proteins: ubiquitin pathway
Foreign exogenous proteins: taken into vesicles by endocytosis, or autophagocytosis, vesicle fuses with lysosome –> proteolytic enzymes degrade protein

46
Q

What are the two pathways responsible for amino acid degradation?

A

Transamination: produces non essential aa
Amino acid 1 + keto acid 2 keto acid 1 + amino acid 2
Oxidative deamination: only glutamate by glutamate dehydrogenase
Amino acid + H2O + NADP+ –> keto acid + ammonia + NADPH H+

47
Q

What do all aminotransferases require?

A

vitamin B6

48
Q

Which are the ketogenic amino acids?

A

Leucine and lysine

49
Q

Which aa are both ketogenic and glucogenic?

A

phenylalanine, tyrosine, tryptophan and isoleucine

50
Q

How are amino groups transported in the blood?

A

As glutamine

51
Q

How is glutamine converted to glutamate and vice versa?

A

Glutaminase: glutamine –> glutamate

Glutamine synthetase: glutamate + ATP + NH3 –> glutamine

52
Q

Where do the nitrogens in urea come from?

A

One from glutamate and one from aspartate

53
Q

What is the physiologically normal glucose concentration?

A
  1. 9-6.2 mM

4. 4-5.0 mM average fasting

54
Q

Which are the irreversible reactions in glycolysis and how are they bypassed?

A
  1. Hexokinase –> glucose-6-phosphatase
  2. Phosphofructokinase –> fructose-1,6-bisphosphatase
  3. Pyruvate kinase –> pyruvate carboxylase + PEP carboxylase
55
Q

What is the estimated average requirement (EAR)?

A

mean of bell curve; the notional mean requirement of a nutrient

56
Q

What is the reference nutrient intake (RNI)?

A

two standard deviations above the EAR: sufficient of a nutrient to meet the needs of most of the population

57
Q

What is the lower reference nutrient intake (LRNI)?

A

2 sd below EAR: intake of a nutrient below this level are almost certainly inadequate for most individuals

58
Q

What are the Vitamin C values for EAR, RNI and LRNI?

A

EAR: 25 mg
RNI: 40 mg
LRNI: 10 mg

59
Q

What do energy requirements depend on?

A

Basal metabolic rate, diet induced thermogenesis, physical activity, environmental T, growth, pregnancy and lactation, age

60
Q

What are the functions of leptin and insulin?

A

Satiety signals; act on hypothalamus to inhibit hunger pathways and stimulate satiety pathways

61
Q

What do pro-opiomelanocortin (POMC) related peptides (PYY 3-36) do?

A

Suppress appetite; secreted by the intestine

62
Q

Where are satiety and hunger signals integrated?

A

Arcuate nucleus of hypothalamus

63
Q

What stimulates/inhibits NPY/AgRP producing neurons and POMC neurons?

A 
NPY/AgRP producing neurons:
1. Inhibited by: PPY 3-36, leptin and insulin
2. Stimulated by: ghrelin
POMC neurons:
1. Stimulated by: leptin, insulin
64
Q

What is the formula for BMI?

65
Q

What does orlistat do?

A

Decreases fat absorption

66
Q

Define kwashiorkor, marasmus and marasmic kwashiorkor?

A

Kwashiorkor: 60-80% of expected weight for age + oedema (changes in colour and texture of hair, dermatitis)
Marasmus: less than 60% of weight and no oedema
Marasmic kwashiorkor: less than 60% + oedema

67
Q

Which are the water soluble vitamins and which are the fat soluble ones?

A

Water soluble: B and C

Fat soluble: A, D, E and K

68
Q

What is beri-beri?

A

Deficiency of thiamin (B1)

69
Q

What is Wernicke-Korsakoff syndrome due to?

A

Thiamin deficiency, associated with alcoholism

70
Q

Where can you find thiaminases?

71
Q

What is the biochemical role of thiamin?

A

Thiamin pyrophosphate coenzyme in pyruvate dehydrogenase

72
Q

What is the function of riboflavin?

A

B2; functions as FAD and FMN in redox reactions

Deficiency: rare except in alcoholics

73
Q

What is the function of niacin and what is its deficiency?

A

B3

NAD and NADP in redox reactions; pellagra, dermatitis, diarrhoea, dementia

74
Q

What is the importance of vitamin B12 and folate?

A

Needed for purine, pyrimidine and amino acid synthesis

Pernicious anemia: deficiency in intrinsic factor –> no B12 absorption (secondary deficiency)

75
Q

What is the function of biotin?

A

B7; prosthetic group for carboxylations (pyruvate –> oxaloacetate; acetyl CoA –> malonyl CoA)
Rare unless eating raw eggs or long term antibiotic treatment

76
Q

What is the function of vitamin C?

A

Collagen formation (hydroxylation of lysine and proline); reduction of dietary Fe for absorption

77
Q

What is the function of vitamin A?

A

Control of protein synthesis and in scotopic vision (low light intensity)

78
Q

What is the function of vitamin E?

A

Includes family of tocopherols –> antioxidants; prevents oxidation of PUFA and apoB in LDL

79
Q

What is the function of vitamin D?

A

Cholecalciferol (D3), ergocalciferol (D2); act to mantain correct levels of calcium and phosphate in the blood so that proper mineralisation of the bone is achieved
Deficiency: rickets (children), osteomalacia (adults)

80
Q

What are deficiencies associated with vitamin K?

A

Defective blood clotting in long term antibiotic therapy

Haemorrhagic disease in newborns due to poor placental transfer

81
Q

What is the rate limiting step of fatty acid synthesis and what is it activated by?

A

Acetyl CoA carboxylase (activated by insulin):

Acetyl CoA + ATP + CO2 –> malonyl CoA + ADP + Pi

82
Q

What does malonyl CoA inhibit?

A

Carnitine transferase

83
Q

Which pathway is source to NADPH?

A

Hexose monophosphate shunt

84
Q

What is the structure of lipoproteins?

A

Inner core: triglycerides and cholesterol esters

Outer shell: single layer of phospholipids, cholesterol an apoproteins

85
Q

Which apoproteins are present on chylomicrons?

A

Apo B-48, apo C-II and apoE

86
Q

Which apoproteins are present on VLDLs?

A

Apo B100, apo C-II and apoE

87
Q

Where are the B100 receptors situated?

A

Peripheral tissue and liver

88
Q

What is the function of apo C-II?

A

Activate lipoprotein lipase

89
Q

Where is HDL synthesised and how does it work?

A

Synthesised in gut and liver; has apo A-1 –> activates LPC and LCAT these provide acids for esterification of cholesterol from phospholipids

90
Q

How is cholesterol synthesised?

A

Acetyl CoA + acetoacetyl CoA –> HMG-CoA
HMG CoA + HMG-CoA reductase –> mevalonate I (rate limiting step)
Mevalonate I –> cholesterol
*Statins inhibit HMG-CoA reductase

91
Q

What is familial hypercholesterolaemia caused by?

A

Deficiency in B100 receptors

92
Q

Which are the essential minerals?

A

sodium, magnesium, potassium and calcium

93
Q

What are the concentrations of sodium and potassium inside and outside the cell?

A

Inside: Na 12 mM, K 140 mM
Outside: Na 140 mM, K 5 mM

94
Q

What is the function of magnesium?

A

Cofactor complex (ATP) and enzyme complex

95
Q

Which are the essential ‘trace’ minerals?

A

Mn, Fe, Co, Cu, Zn, Mo

96
Q

Where is iron stored and how is it transported?

A

Stored in ferritin, transported by transferrin

97
Q

How is iron uptaken into cells?

A

receptor mediated endocytosis (DMT1)

98
Q

Which proteins are important for Zn haemostasis?

A

ZIP: zinc import proteins
ZNT: zinc export proteins
MT: methallothioneins (zinc transport)
MTF1: zinc sensor

99
Q

What stimulates and inhibits insulin secretion?

A

Stimulation by: high glucose and aa concentrations, secretin, glucagon
Inhibition by: adrenaline

100
Q

How do increased concentrations of glucose and aa lead to insulin secretion?

A

ATP production –> K+ channels close –> calcium channels open –> insulin is secreted

101
Q

What are the intracellular effects of insulin?

A

Tyrosine receptor activation –> Akt protein kinase activation which leads to:

  1. Expression of GLUT4 receptors
  2. Inactivation of glycogen synthase kinase through phosphorylation –> active glycogen synthase
  3. Activation of phosphodiesterase (cAMP –> AMP) –> PKA is inhibited –> hormone sensitive lipase is inhibited –> TAG is stored
  4. Activation of Ras and MAPK –> gene expression
102
Q

Which compounds act as ketone bodies?

A

Acetoacetate and beta-hydroxybutyrate

103
Q

What is the action of ketone bodies on the pancreas?

A

Stimulates release of insulin –> limits muscle proteolysis and adipose tissue lipolysis –> muscle tissue is preserved

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