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MCBG > Diet And Metabolism > Flashcards

Diet And Metabolism Flashcards

1
Q

What are the essential amino acids?

A 
Phenylalanine
Valine
Threonine
Tryptophan
Isoleucine
Methionine
Histidine
Leucine
Lysine
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2
Q

What are the essential fatty acids?

A

Linoleic

Linolenic

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3
Q

What are the three classes of lipids and some examples?

A

Fatty acid derivatives (Fatty acids, triacyl-glycerol, phospholipids)
Hydroxy-methyl-glutaric acid derivatives (ketone bodies, cholesterol, bile)
Vitamins (A, D, E, K)

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4
Q 
Define:
DRV
LRNI
EAR
RNI
A

DRV: Dietary Reference Values
LRNI: Lower Required Nutritional Intake (Enough energy for 2.5% of the population)
EAR: Estimated Average Requirement (Enough energy for 50% of the population)
RNI: Reference Nutritional Intake (Enough energy for 97.5% of the population)

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5
Q

What is energy spent on in the body?

A

Daily Energy Expenditure (BMR + DIT + PAL)
BMR: Basal Metabolic Rate (Energy required for the resting activities of the body - function of the organs, maintenance of cells and body temperature)
DIT: Diet Induced Thermogenesis (Energy required to process foods)
PAL: Physical Activity Level (Energy required for skeletal, cardiac and respiratory muscles)

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6
Q

Where is energy found and in what order?

A

Immediate: Energy rich molecules (short-term energy)
Quick: Carbohydrates
Long: Adipose tissue (long-term energy)
Reserve: Muscle proteins

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7
Q 
State the equation for BMI and the values for:
Underweight
Desirable weight
Overweight
Obese
Severely obese
A 
BMI = Weight / (Height)^2
Underweight: <18.5
Desirable weight: 18.5 - 24.9
Overweight: 25.0 - 29.9
Obese: 30.0 - 34.9
Severely obese: >35
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8
Q

What is kwashiorkor?

A

Oedema caused by the movement of H2O into the interstitial space
Low serum oncotic pressure (< hydrostatic pressure) from lack of proteins in diet (malnutrition)

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9
Q

What is energy and how do cells use it?

A 
Energy: (Capacity to do work)
Biosynthetic work (Anabolism of cell components)
Transport work (Nutrient uptake, maintenance of ion gradients)
Specialised work (Muscle contraction/Mechanical, Impulse conduction/ Electrical, Water resorption /Osmotic)
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10
Q

What is the difference between catabolism and anabolism?

What is the difference between oxidative and reductive reactions?

A

Catabolism: Break down of molecules
Anabolism: Building of molecules
Oxidative: releases H+ and electrons and energy
Reductive: requires H+ and electrons and energy

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11
Q

Define:
Isothermal
Exergonic
Endergonic

A

Isothermal: Change in the state of a system where temperature is constant
Exergonic: Releases Energy (bonds made)
- Exothermic (-) Gibbs E (Energy of Product < Substrate)
Endergonic: Requires Energy (bonds broken)
- Endothermic (+) Gibbs E (Energy of Substrate < Product)

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12
Q

What are carrier molecules?

A

Molecules that carry H+ and electrons (reducing power) when fuel molecules are oxidised
Nicotinamide Adenine Dinucleotide (NAD+)
Nicotinamide Adenine Dinucleotide Phosphate (NADP+)
Flavin Adenine Dinucleotide (FAD)

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13
Q

What is the reduced form of carrier molecules and what is their main route for passing on their reducing power?

A

NADH + H(+) - ATP Production
NADPH + H(+) - Biosynthesis
FADH2 - ATP Production

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14
Q

How is energy stored in ATP and how is it released?

A

Stored in the terminal phosphate group (concentrated negative charges)
When ATP is hydrolysed to ADP and Pi energy is released

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15
Q

What are the reactions for hydrolysis and phosphorylation of ATP?

A

Hydrolysis: (exergonic)
ATP + H2O —> ADP + Pi + H(+) with Phosphatase

Phosphorylation: (endergonic)
ADP + H(+) + Pi —> ATP + H2O with Kinase

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16
Q

What do Energy signals cause?

A

High-Energy signals: (High [ATP])
Activation of anabolic pathways
Oxidation of carrier molecules (ATP, NADH, NADPH, FADH2)
Low-Energy signals: (Low [ATP])
Activation of catabolic pathways
Reduction of (ADP, NAD+, NADP+, FAD)
Activation of Adenylate Kinase (2ADP —> ATP + AMP)

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17
Q

How can phosphocreatine be used as a source of energy?

A

Energy is released when phosphocreatine is hydrolysed to form creatine (more than ATP hydrolysis)
(ADP Cr
(Kinase ->) Kinase catalyses forward reaction

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18
Q

How are phosphocreatine and creatine broken down?

A

Phosphocreatine —> Creatine (hydrolysis)
Creatine —> Creatinine + H2O (condensation)
Normal, Spontaneous (exergonic) reaction

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19
Q

How can creatinine be used as a clinical marker and what other substance is used as a clinical marker?

A

Excretion of creatinine from the kidneys is proportional to muscle mass
Creatine Kinase isoenzymes can be used a clinical marker in the blood:
CK-MM: raised in muscle injury
CK-MB: raised in cardiac injury
CK-BB: raised in brain injury

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20
Q

What happens during stage 1 of catabolism, where does it take place and is energy created?

A

Breakdown of large foods for absorption (C-N and C-O bonds)
Takes place in the GI tract (digestion)
No energy created

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21
Q

What happens during stage 2 of catabolism, where does it take place and is energy created?

A

Break down to metabolic intermediates (C-C bonds)
Takes place in the cytosol and mitochondria
Some oxidation occurs (ATP produced)

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22
Q

What happens during stage 3 of catabolism, where does it take place and is energy created?

A 
Krebs (Tricarboxylic acid) Cycle - Acetyl CoA is broken down releasing CO2
Takes place in the mitochondria
Oxidation occurs (GTP produced)
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23
Q

What happens during stage 4 of catabolism, where does it take place and is energy created?

A

Oxidative phosphorylation (reducing power is converted to ATP)
Takes place in the mitochondria
The oxidation of NADH/FADH2 (ATP produced)

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24
Q

How are each of the major food groups broken down in stage 1?

A

Proteins -> Amino acids
Carbohydrates -> Monosaccharides
Lipids -> Fatty acids and Glycerol
Alcohol -> Alcohol

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25
Q

What happens to the metabolic intermediates in stage 2?

A 
Amino acids are broken down and form:
- NH4+ —> Urea
- Alpha-Keto Acids (joins Krebs cycle)
- Pyruvate
- Acetyl-CoA
Monosaccharides go through glycolysis and form Pyruvate
Fatty acids help form Acetyl-CoA
Glycerol can form ketone bodies which undergo glycolysis and form Pyruvate
Alcohol helps form Acetyl-CoA
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26
Q

What are the units of sugars?

A

Monosaccharide: single-sugar unit
Disaccharide: 2 units joined by a glycosidic bond
Oligosaccaharide: Dextrin - 10s of units
Polysaccharide: Polymer of sugar (glycogen/starch)

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27
Q

What are the required concentrations of glucose for different body components?

A

Blood serum: 5mM
Erythrocytes, Neutrophils, (inner) cells of the kidneys, lens of the eye: 40g/day
CNS: 140g/day

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28
Q

What are the types of sugars?

A 
Disaccharides:
Maltose: Glu-Glu (alpha-1,4 bonds)
Cellulose: Glu-Glu (beta-1,4 bonds)
Sucrose: Glu-Fru
Maltose: Glu-Gal
Polysaccharides:
Glycogen: Polymer in animals
Starch: Polymer in plants
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29
Q

How are polysaccharides broken down for absorption in stage 1?

A

Starch/Glycogen —> Dextrins (amylase in the saliva and mastication)
Dextrins —> Monosaccharides (amylase from the pancreas)
Disaccharides —> Monosaccharides (Brush-border enzymes secreted by brush-border epithelial cells which trap disaccharides)

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30
Q

What are the types of brush border enzymes?

A

Lactase: Lactose
Sucrase: Sucrose
Isomaltase: Maltose (alpha-1,4 bonds)
Pancreatic amylase: alpha-1,6 bonds

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31
Q

Why can’t we digest cellulose?

A

Cellulose is made up of Glucose’s attaches via a beta-1,4 bond
Beta-1,4 bonds require a beta-amylase which we do not possess
Therefore, we cannot digest cellulose and we have a source of dietary fibre

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32
Q

What are the types of lactose intolerance?

A

Primary: Absence of lactase persistence allele (diagnosed after diet becomes less reliant of dairy and lactase concentration drop)
Secondary: Injury/damage to the small intestine
Congenital lactase deficiency: Abnormal/Absent lactase gene (no dairy ever been metabolised)

33
Q

How are Monosaccharides absorbed?

A

Jejunum of small intestine:
Co-transported through SGLT1 (Sodium-Glucose Transporter) with 2 Na+ into an enterocyte
Passively diffuse through GLUT2 (Glucose Transporter) into the lumen of capillaries

34
Q

What is phase 1 of glycolysis?

A 
Investment phase
1) Glucose —> Glu-6-P (Hexokinase)
(ATP —> ADP)
2) Glu-6-P —> Fru-6-P
3) Fru-6-P —> Fru-1,6-Bis-P (Phosphofructokinase)
(ATP —> ADP)
35
Q

Why is Glucose converted to Glucose-6-P in step 1?

A

Forms an anionic glucose which cannot cross membrane or leave the cell (increases the reactivity)

36
Q

What is phase 2a of glycolysis?

A

Cleavage of 6 Carbon into two 3 Carbon molecules

4) Fru-1,6-Bis-P —> DHAP (Dihydroxy acetone phosphate) + Glyceraldehyde-3-P (aldolase)
5) DHAP —> Glyceraldehyde-3-P (Interconversion)

37
Q

What is phase 2b of glycolysis?

A

Payback phase
6) Glyceraldehyde-3-P —> 1,3-Bis Phosphoglycerate
(NAD+ —> NADH)
7-9) 1,3-Bis Phosphoglycerate —> PEP (Phosphoenol Pyruvate)
(ADP —> ATP) - Substrate level phosphorylation
10) PEP —> Pyruvate (Pyruvate Kinase)
(ADP —> ATP)

38
Q

What is glucogenesis and why is it rare?

A

Reverse of glycolysis (reverting Pyruvate to glucose)

Must overcome all the irreversible steps (1, 3, 10) with large (-) Gibbs Energy values

39
Q

What is the committing step in glycolysis and how is it controlled?

A

Step 3: first irreversible step that occurs primarily in glycolysis
Fru-6-P —> Fru-1,6-Bis-P (Phosphofructokinase)
Concentrations of ATP (inhibits) and ADP (stimulates)
Concentrations of glucagon (inhibits) and insulin (stimulates)

40
Q

What is the overall equation of glycolysis?

A

Glucose + 2ATP + 2NAD+ —> 2Pyruvate + 4ATP + 2NADH

41
Q

Why is glycolysis a multiple-step mechanism?

A 
Easier chemistry (small changes to molecules)
Energy conservation (no loss/waste)
Versatility (interconnects with other pathways, production of intermediates)
Allows for finer control of products
42
Q

What are the intermediates made during glycolysis and what are they used for?

A

Lipid synthesis (production of glycerol phosphate):
DHAP —> Glycerol Phosphate (Glycerol-3-P dehydrogenase)
(NADH —> NAD+)
Decreasing O2 affinity in Haemoglobin (production of 2,3-Bis-Phosphoglycerate):
1,3-Bis-Phosphoglycerate —> 2,3-Bis-Phosphoglycerate (Bis-phophoglycerate mutase)

43
Q

How is glycolysis regulated?

A 
Reversible steps come to equilibrium
Irreversible steps:
Allosteric regulation of enzymes
Concentrations of substrate : product
Concentrations of ATP/NADH : ADP/NAD+
44
Q

How is NAD+ regenerated for the formation of 1,3-Bis Phosphoglycerate from Glyceraldehyde-3-P (Step 6)?

A

NADH is returned to NAD+ during oxidative phosphorylation (stage 4) but it requires O2
NAD+ can also be produced anaerobically
Lactic acid fermentation in erythrocytes and skeletal muscle (low O2):
NADH + H(+) + Pyruvate Lactate + NAD(+) (Lactate Dehydrogenase)
The Lactate and NAD+ then travel to the heart and liver (high O2) where it is reconverted to Pyruvate and NADH via LDH
Heart: Pyruvate —> Krebs cycle
Liver: Pyruvate —> Glucogenesis

45
Q

State how Lactate is eliminated from the body and the values for the concentrations of Lactate in blood (Normal, Hyperlactaemia, Lactic acidosis)
Decscribe what happens in the blood during lactic acidosis?

A

Lactate is disposed of via the kidneys above the renal threshold
Normal: 1mM
Hyperlactaemia: 2 - 5mM (< renal threshold)
Lactic acidosis: 5 - 10mM (> renal threshold)
During lactic acidosis; buffering fails in the blood and so the pH of the blood drops dangerously low

46
Q

How and where are alternative sugars metabolised?

A

Metabolised in the liver to glucose (cannot leave the liver unless glucose) and then join glycolysis

47
Q

How is fructose metabolised in the liver?

A

Fructose —> Fru-1-P (Fructokinase)
(ATP —> ADP)
Fru-1-P —> Glyceraldehyde-3-P + DHAP (aldolase)

48
Q

What is fructosuria?

What is fructose intolerance?

A

Essential fructosuria: missing Fructokinase

Fructose Intolerance: missing aldolase

49
Q

How is galactose metabolised in the liver?

A

Galactose —> Gal-1-P (galactokinase - GALK)
(ATP —> ADP)

Depending on the concentration of ATP
Low ATP:
Gal-1-P —> Glu-1-P (Uridyl Transferase - GALT)
Glu-1-P —> Glu-6-P (join glycolysis)
High ATP:
Gal-1-P —> UDP-Gal (UDP-Gal Epimerase - GALE)
UDP-Gal —> UDP-Glu (stored as glycogen in the liver)

50
Q

What is galactosaemia?

A

Genetic defect resulting in impaired enzyme function and excess galactose which enters new pathways:
Galactose —> Galactitol (Aldose reductase)
(NADPH —> NADP+)
Aldose reductase has a high Km for reducing sugars and will deplete NADPH while reducing them

51
Q

What does excess reducing sugar and Aldose reductase result in?

A

Aldose reductase has a high Km for reducing sugars and will deplete NADPH while reducing them
NADPH helps maintain free SH (cysteine) groups resulting in S-S (cystine) bond formation and the loss of structure of proteins

52
Q

How are pentose sugars formed and what are the features of the reaction?

A

Oxidative Decarboxylation:
Glu-6-P —> Ribulose-5-P (Glu-6-P Dehydrogenase)
(2NADP+ —> 2NADPH + CO2)
Irreversible loss of CO2
Produces NADPH which prevents the oxidation of SH groups

53
Q

What does a deficiency in Glu-6-P Dehydrogenase result in?

A

Lack of NADPH and oxidation of free SH groups

Loss of structure of proteins (especially GSH found in all cells)

54
Q

How is Ribulose-5-P used?

A

Glycolysis intermediate:
3 Ribulose-5-P —> 2 Fructose-6-P + Glceraldehyde-3-P

Formation of ribose for nucleotides:
Ribulose-5-P —> Ribose-5-P

55
Q

What happens to Pyruvate after stage 2?

A

Pyruvate is transported into the mitochondrial matrix, converted into Acetyl-CoA and enters stage 3 (the Krebs cycle)

56
Q

How is Pyruvate converted into Acetyl-CoA?

A

Pyruvate + CoA + NAD+ —> Acetyl-CoA + CO2 + NADH + H+
(Pyruvate Dehydrogenase)
Loss of CO2 (therefore irreversible)

57
Q

What happens if there is a deficiency in PDH?

How is PDH regulated?

A

A deficiency in PDH will cause a build-up of Pyruvate
Excess Pyruvate will be converted to Lactate causing lactic acidosis
PDH is controlled by:
Concentrations of substrate : product
Insulin (stimulates)
Phosphorylation (Inhibits)

58
Q

What happens during stage 3 of catabolism?

A

Acetyl-CoA (C2) + Oxaloacetate (C4) + H2O —> Citrate (C6) + CoA (citrate synthase)
Citrate —> Isocitrate
Isocitrate (C6) —> alpha-ketoglutarate (C5) +CO2 (Isocitrate DH) - oxidation of a C
(NAD+ —> NADH + H+)
Alpha-ketoglutarate (C5) + CoA —> Succinyl-CoA (C4) + CO2 (alpha-ketoglutarate DH) - oxidation of a C
(NAD+ —> NADH + H+)
Succinyl-CoA —> Succinate (succinyl-CoA synthase)
(GDP + Pi —> GTP)
Succinate —> Fumerate (succinate DH)
(FAD —> FADH2)
Fumerate + H2O —> Malate (Fumerase)
Malate —> Oxaloacetate (Malate DH)
(NAD+ —> NADH + H+)

59
Q

What is the result of the Krebs cycle?

A

Breaking of C-C bonds and oxidation of Carbons
Reducing power produced (NADH, FADH2)
GTP produced

60
Q

What are some of the intermediates of stage 3?

A

Fatty acids formed from citrate
Haemoglobin formed from Succinate
Amino acids formed from and form Succinate, Malate, Oxaloacetate
Glucose formed from Oxaloacetate

61
Q

What happens during stage 4 of catabolism?

A

Reduction carriers produced in stage 3 (NADH, FADH2) are oxidised (Oxygen is reduced to form H2O)
Energy produced move H+ ions out of the matrix and into the intermembrane space through proton translocating complexes (PTC’s)
Movement of H+ ions creates an electrochemical gradient across mitochondria inner membrane (proton motive force: pmf)
H+ ions move back across membrane through F0-F1-ATPase
F0-F1-ATPase uses the pmf created to drive phosphorylation of ADP -> ATP (oxidative phosphorylation)

62
Q

How is stage 4 regulated?

A

Concentration of ADP in matrix
[ADP] too low: Lack of substrate for ATPase
No dissipation of H+ in intermembrane space
Electron transport stops

63
Q

What are Membrane uncouplers?

A

Proteins that increase the permeability (conductance) of certain ions across a membrane

64
Q

What is the mechanism of action of UCP1 and where is it found?

A

(Contained within brown adipose tissue)
Cold causes the release of Nor-A activating lipase
Lipase splits lipids into fatty acids and glycerol
Fatty acids activate UCP1 (increases the permeability of the cristae to H+)
Flow of H+ cause release of thermal energy

65
Q

What are Inhibitors of stage 4 and what are their effects?

A

Lethal

Molecules like Cyanide with higher affinity for electrons than Oxygen prevent electron transport

66
Q

How are lipids broken down for absorption in stage 1?

A

Pancreatic lipases hydrolysed lipids into fatty acids and glycerol in the duodenum
Fatty acids and glycerol are absorbed by enterocytes in the ileum and are recombined to form chylomicrons which leave via lacteals (of the lymphatic vessels) bypassing the hepatic portal system

67
Q

Describe the Fatty acid cycle in adipose tissue

A

Glucose enters adipose cell and forms Pyruvate and glycerol-1-P
Glycerol-1-P and fatty acyl-CoA combine to form a triacylglycerol
(Triacylglycerol cannot leave the adipocyte)
When there is a lack of glucose, the triacylglycerol is lysed to form glycerol (helps in the formation of Pyruvate) and fatty acids (alternative fuel) - both go onto stage 2 of catabolism

68
Q

What happens during stage 2 of catabolism of lipids?

A

Fatty acids undergo beta-oxidation until Acetyl-CoA and join the Krebs cycle
Glycerol is converted to Dihydroxyacetone Phosphate which completes glycolysis

69
Q

What happens to fatty acids in stage 2 of catabolism?

A

Fatty acids are activated by linking to CoA in the cytoplasm:
Fatty acid + CoA + ATP —> Fatty acyl-CoA + AMP + PPi
(Fatty Acyl-CoA synthase)
Fatty acyl-CoA is transported into the matrix and undergoes beta-oxidation

71
Q

How is Fatty acyl-CoA transported into the matrix?

A

Carnitine Transporter: (CAT1, Shuttle, CAT2)
Fatty acyl-CoA binds with Carnitine-acyl Transferase 1, releasing CoA + forming Carnitine-acyl complex
Shuttle switches carnitine-acyl complex outside with carnitine from inside the matrix
Carnitine-acyl complex and CoA binds with Carnitine-acyl Transferase 2, releasing Fatty acyl-CoA

72
Q

What is beta-oxidation?

A

Reaction breaking the C-C bonds to produce reducing power which can be used in oxidative phosphorylation
Fatty acyl-CoA + H2O + CoA + NAD+ + FAD —> FADH2 + NADH + Acetyl-CoA

73
Q

Why is acetyl-CoA used as the convergence point for all food groups?

A

Can be formed from all food groups
Used in catabloic and anabolic pathways
Releases a lot of energy when the Acetyl-S-CoA bond is hydrolysed

74
Q

What are the normal, starved, untreated type I diabetes concentrations of ketone bodies in the blood?

A

Normal: 1mM
Starved: 2 - 10mM (physiological ketosis)
Untreated type I diabetes: > 10mM (pathological ketosis)

75
Q

What is ketonuria?

What ketone bodies contribute to ketoacidosis?

A

Ketone bodies > renal threshold

Acetoacetate and beta-hydroxy butyrate
Acetone leaves via blood, volatile from the lungs

76
Q

What happens to glycerol in stage 2 catabolism?

A 
Glycerol is transported via the blood to the liver
Glycerol —> Glycerol-P (Glycerol Kinase)
(ATP —> ADP)
Glycerol-P —> DHAP
(NAD+ —> NADH)
77
Q

How and where are ketone bodies synthesised?

A

Synthesised by liver mitochondria:
Acetyl-CoA —> Hydroxymethyl glutaryl-CoA (HMG-CoA synthase)
Fed: (High [Insulin])
HMG-CoA —> Mevalonate (HMG-CoA reductase) (Mevalonate eventually forms cholesterol - statin drugs inhibit HMG-CoA reductase)
Starved: (High [Glucagon])
HMG-CoA —> Acetoacetate (HMG-CoA lyase)
Acetoacetate —> Acetone + CO2 (non-enzymatic decarboxylation)
Acetoacetate —> beta-hydroxy butyrate (beta-hydroxy butyrate DH)

78
Q

How are ketone bodies catabolised?

A

Liver: (high O2)
Beta-hydroxy butyrate produced in the liver
Transported via blood to the muscle cells
Muscle: (low O2)
Beta-hydroxy butyrate reforms acetoacetate (beta-hydroxy butyrate DH)
Acetoacetate reforms Acetyl-CoA which enters Krebs cycle
(Succinylcholine-CoA —> Succinate)

79
Q

How is ketone body synthesis regulated?

A

Depends on the activity of the Krebs cycle

Diverts Acetyl-CoA from the Krebs cycle if there’s low NAD+ or high levels of glucose (diabetes)

80
Q

How can ketone bodies spare glucose in diabetes?

A

Short-term:
Ketone bodies used for muscle cells
Glucose used for important cells

Long-term:
Amino-acids form pyruvate to resupply glucose stores

MCBG (9 decks)

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