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NUT2001 > Macronutrients > Flashcards

Macronutrients Flashcards

1
Q

What makes nutrients essential

A

Present in all healthy tissues
Concentration consistent between species
Not in diet causes similar withdrawal symptoms between species
Adding into diet prevents issues
Abnormalities produced by deficiencies cause biochemical changes

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2
Q

Ways to assess how much of a nutrient is required

A 
Epidemiology
Amount to rectify deficiency symptoms
Amount excreted in faeces and urine
Factorial
Dose response
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3
Q

Epidemiology

A

if a population is experiencing no deficiency symptoms assume intake is adequate. Average intake of nutrient by population gives estimate
Imprecise and unsure if large overestimate

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4
Q

Factorial

A

Requirement = obligatory loss + retention / availability

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5
Q

Dose response

A

Is the point where the nutrient biomarker value does not vary anymore

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6
Q

What causes deficiency

A 
Intake not meeting requirement
Reduced absorption
Increased requirement due to physical activity
Increased losses
Antagonists
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7
Q

Lower reference intake

A

2 S.D. below mean

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8
Q

Estimated average

A

Mean amount

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9
Q

Reference Nutrient

A

2 S.D. above mean

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10
Q

Joule

A

Energy required to move a mass of 1kg 1 metre with a force of 1 newton

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11
Q

Calorie

A

Amount of energy required raise temperature of 1kg by 1 degree

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12
Q

Joule to calorie conversion

A

1 cal = 4.184

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13
Q

How do you work out how much energy in food

A

Bomb calorimetry - gives total chemical energy

n.b. not all chemicals in food can be digested

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14
Q

Bomb calorimetry

A

Sample is burnt in pure O2 in a sealed container
Has a insulating jacket
Change in temperature of water is then compared to benzoic acid to understand amount of energy in food

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15
Q

Energy in fat

A

9kcal per gram

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16
Q

Energy in protein

A

4kcal per gram

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17
Q

Energy in carbohydrates

A

4kcal per gram

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18
Q

Total energy expenditure

A

Basal metabolism
Physical activity
Thermic effect of food

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19
Q

Basal metabolic rate

A

Keep organs functioning when not digesting or keeping warm. Difficult to measure as participant has to of just woken up so often use Resting Metabolic Rate

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20
Q

What causes slow BMR

A

Aging
Low thyroid
More fat

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21
Q

What increases BMR

A

Height

Muscle

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22
Q

Active energy expenditure

A

Duration, frequency and intensity of exercise

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23
Q

How do you measure energy expenditure

A

Prediction equations
Direct and indirect calorimetry
Isotopic methods

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24
Q

Energy requirements

A

Determined by age, sex and physiological state
Listed in SACN
which uses prediction equations

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25
Q

Protein digestion in stomach

A 
HCL released from parietal cells
Denatures protein
Pepsinogen made active by low pH
Pepsin cleaves non-polar lipophilic chains
Phe, Leu, Trp, Tyr
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26
Q

How is HCL secreted

A

Cephalic phase
Histamine phase
gastric phase

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27
Q

Cephalic Phase

A

Sight and smell of food increases enteric neural activity
Increasing acetylcholine
Causing gastric acid to be secreted

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28
Q

Histamine phase

A

Increased acetylcholine increases histamine release

Histamine acts on H2 receptor causing HCL secretion

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29
Q

Gastric phase

A

Stomach distension and some chemicals in amino acids cause G cell to release hormones causing more gastric acid

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30
Q

Parietal cells

A

Surrounded by vesicle called tubulovesicles
Contain H+/K+ ATPase
Stimulated causing them to expand and H+ travels across lumen
Cl- follows H+

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31
Q

Protein digestion in small intestine

A

Pancreatic enzymes and brush border enzymes break down protein
Small peptides use protein transporters for specific amino acids.
Na+ and H+ needed

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32
Q

Protein pancreatic Enzymes

A

Trypsinogen
Chymotrypsinogen
Procarboxypeptidase

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33
Q

Brush Border enzymes

A

Elastase

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34
Q

Trypsinogen

A

Endopeptidase

cleave Lys and Arg of carboxy side

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35
Q

Chymotrypsinogen

A

Endopeptidase

Cleaves Phe, Tyr, Trp on carboxy side

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36
Q

Procarboxypeptidase

A

Exopeptidase
A - aromatic and branched amino acids on aliphatic side
B - Lys and Arg at COOH terminal

37
Q

Protein Digestion in enterocyte

A

Degradation of oligopeptides into smaller peptides by brush border enzymes. Then degradation of tri and di peptides by intracellular peptides.

38
Q

Protein uses

A 
Structural
Hormones
Enzymes
Immune 
Energy
Muscle
39
Q

Transamination

A

Transfer amine group to keto acid to create new keto acid and a new amino acid
Transaminase
Aminotransferase
Only in non-essential and conditionaly essential AA
Reversible

40
Q

Deamination

A

Amino group removed from amino acid
Deaminase
Irreversible

41
Q

Urea Cycle

A

Ammonia into urea – liver and some in the kidneys. 5 steps – first 3 in the mitochondria and last two in the cytoplasm

42
Q

Naming lipids

A

C no. carbon atoms: No. double bond n- Location of double bond from methyl

43
Q

Palmitic acid

A

Hexadecenoic acid

C16:0

44
Q

Stearic acid

A

Octadecanoic acid

C18:0

45
Q

Linoleic acid

A

Octadecadienoic acid

C18:2 n-9,12

46
Q

alpha-linolenic acid

A

Octadecatrienoic acid

C18:3 n-9,12,15

47
Q

yonder-linolenic acid

A

Octadecatrienoic acid

c18:3 n-6,9,12

48
Q

Antioxidant role with lipids

A

Prevent oxidation of fatty acids on cell membrane

49
Q

Lipid synthesis

A

Acetyl CoA + ATP + HCO3 -> Malonyl CoA
Add acetyl CoA to malonyl
Repeat adding acetyl (adds 2 extra carbond)
To de saturate need vitamins as coenzymes
Only add double bonds to n-9

50
Q

Linoleic acid uses

A

Synthesis other fatty acids
yonder-linoleic acid
dihomo-y-linoleic acid
Arachidonic acid

51
Q

Alpha linolenic acid uses

A

Synthesis
EPA
DHA

52
Q

Phospholipids

A

2 fatty acids
1 phosphate
1 glycerol

53
Q

Membrane structure

A

Phospholipids
Fluidity determined by number of unsaturated FA particularly PUFA
More PUFA means more liquid and more likely to be oxidised

54
Q

Lipid digestion Stomach

A

Lingual lipase released in saliva becomes active in the stomach
Gastric lipase secreted by chief cells remove on FA leaving a free fatty acid and diglyceride
Stomach emulsify through mechanical mixing

55
Q

Lipid digestion Small intestine

A

Mechanical mixing
When fat enters duodenum it causes CCK to be released in blood
Causes biled to be secreted into small intestine
CCK also stimulate pancreatic enzymes
Pancreatic lipase make MAG and anothe free fatty acid

56
Q

Bile

A 
Stimulated by CCK
Derived from cholesterol
Have a store of 2-4g
double just to emulsify one meal
Recirculated 3012 times a day
57
Q

Lipid Absorption

A

Micelle pass through water layer and become adjacent to enterocyte
Passive absorption of the fatty acids and facilitated absorption by FABP and FAT transporter
In cell realign as TAG
Incorporated into a VLDL

58
Q

Chylomicron

A

Lower the density of fat the higher the lipid:protein ratio

Inside chylomicron have lipase to hydrolyse TAG to free fatty acids to pass through capillary walls

59
Q

Very low density lipoprotein

A

Main function transport TAG from liver to tissue
High TAG
Once at tissue and TAG removed becomes a LDL
Main outer protein is ApoB-100

60
Q

Low density lipoprotein

A

High level of cholesterol

Main outer protein ApoB-100

61
Q

High density Lipoprotein

A

Excess cholesterol in cell membrane taken up
In HDL free cholesterol is converted to cholesterol ester
ApoE on outer membrane allows liver to recognise and uptake

62
Q

ApoB-100

A

Allows for secretion of VLDL from liver
Structural protein for VLDL, IDL and HDL
Acts as a ligan receptor for LDL

63
Q

ApoB-48

A

Chylomicrons
Secretion of chylomicrons from intestine
Core structure protein

64
Q

ApoE

A

Chylomicrons, VLDL, IDL, HDL

Ligand for binding IDL and remnants to LDLR and LRP

65
Q

ApoC-II

A

Chylomicrons, VLDL, IDL, HDL
Activator of LPL
Allows recognition and binding of lipoprotein

66
Q

Cardiovascular disease

A 
High LDL and TAG in plasma and low HDL
Oxidated LDL accumulate beneath leaky endothelial arteries
Removed by white blood cells
High concentration of cholesterol in macrophages causes fatty streaks
Fatty streaks produce collage
Causing fibrous plaque
Narrowing lumen
Reducing blood flow
Encouraging blood to clot
67
Q

How to combat cardiovascular disease

A

Lower LDL cholesterol
Increase HDL
Eat more unsaturated
Do not eat trans fats or saturated

68
Q

Long chain fatty acids make

A 
Eicosanoids
Endocannabinoids
lipoxins
Resolvins
Lipid rafts
69
Q

Eicosanoids

A 
Made by COX or lopoxygenase
Prostaglandins - Vasodilator
Prostacyclin - Vasodilator
Thromboxane's - Vasoconstrictor
Leukotrienes - Vasoconstrictor
70
Q

Conjugated linoleic acid

A

Milk products
Intermediated during biohydrogentation
Linoleic acid but two double bonds next to each other
Functional food

71
Q

Control of lipid metabolism

A

PPARs interact with DNA to increase and decrease amount of proteins
Leptin - makes you full

72
Q

Maltose

A

Glucose-Glucose alpha 1-4 glyosidic bond

73
Q

Isomaltase

A

Glucose-Glucose alpha 1-6 glyosidic bond

74
Q

Lacotse

A

Galactose and glucose beta 1-4 glyosidic bond

75
Q

Sucrose

A

Glucose + fructose alpha 1-2

76
Q

Raffinose

A

Glucose, galactose and fructose

77
Q

Carbohydrate digestion Mouth

A

Salivary alpha – amylase
Requires Ca2+ and Cl-
6.8pH optimum

78
Q

Carbohydrate digestion Small intetine

A

Pancreatic alpha-amylase – releases maltotriose, maltose, isomaltose and some glucose
Requires Ca2+ and Cl-
6.8pH optimum
Brush boarder enzymes – maltase, isomaltase, sucrase and Lactase

79
Q

SGLUT1

A

Apical membrane
Glucose and galactose enter enterocyte
Na+ enter allowing glucose and galactose to enter cell
Na+ leaves via K+/Na+ atpase

80
Q

GLUT5

A

Fructose

81
Q

GLUT2

A

Basolateral membrane for sugar to leave

82
Q

GLUT family

A

single polypeptide chain of 500 amino acid. 12 transmembrane segments

83
Q

GLUT4

A

Adipose and muscle tissue

Insulin dependent

84
Q

Sugar Alcohol

A

Lack aldehyde or ketone

85
Q

Sugar acid

A

Aldehyde of OH and C6 is oxidised to make COOH

86
Q

Amino Sugar

A

Has an amine group substituted for an OH

87
Q

Glycoproteins

A

Cell membrane

Serum in blood

88
Q

Proteoglycans

A 
Protein conjugate to glycosaminoglycan
Structural components of lubricants
Feature GAGs and link to serine
Structure of GAG allows to interact with many proteins
Growth factors, extracellular matric
Role in molecular signalling
89
Q

Mucoproteins

A

Key component of mucus

Lubricants

NUT2001 (4 decks)

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