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NUT2001 > Macronutrients > Flashcards

Macronutrients Flashcards

(89 cards)

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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
Protein digestion in stomach
``` HCL released from parietal cells Denatures protein Pepsinogen made active by low pH Pepsin cleaves non-polar lipophilic chains Phe, Leu, Trp, Tyr ```
26
How is HCL secreted
Cephalic phase Histamine phase gastric phase
27
Cephalic Phase
Sight and smell of food increases enteric neural activity Increasing acetylcholine Causing gastric acid to be secreted
28
Histamine phase
Increased acetylcholine increases histamine release | Histamine acts on H2 receptor causing HCL secretion
29
Gastric phase
Stomach distension and some chemicals in amino acids cause G cell to release hormones causing more gastric acid
30
Parietal cells
Surrounded by vesicle called tubulovesicles Contain H+/K+ ATPase Stimulated causing them to expand and H+ travels across lumen Cl- follows H+
31
Protein digestion in small intestine
Pancreatic enzymes and brush border enzymes break down protein Small peptides use protein transporters for specific amino acids. Na+ and H+ needed
32
Protein pancreatic Enzymes
Trypsinogen Chymotrypsinogen Procarboxypeptidase
33
Brush Border enzymes
Elastase
34
Trypsinogen
Endopeptidase | cleave Lys and Arg of carboxy side
35
Chymotrypsinogen
Endopeptidase | Cleaves Phe, Tyr, Trp on carboxy side
36
Procarboxypeptidase
Exopeptidase A - aromatic and branched amino acids on aliphatic side B - Lys and Arg at COOH terminal
37
Protein Digestion in enterocyte
Degradation of oligopeptides into smaller peptides by brush border enzymes. Then degradation of tri and di peptides by intracellular peptides.
38
Protein uses
``` Structural Hormones Enzymes Immune Energy Muscle ```
39
Transamination
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
Deamination
Amino group removed from amino acid Deaminase Irreversible
41
Urea Cycle
Ammonia into urea – liver and some in the kidneys. 5 steps – first 3 in the mitochondria and last two in the cytoplasm
42
Naming lipids
C no. carbon atoms: No. double bond n- Location of double bond from methyl
43
Palmitic acid
Hexadecenoic acid | C16:0
44
Stearic acid
Octadecanoic acid | C18:0
45
Linoleic acid
Octadecadienoic acid | C18:2 n-9,12
46
alpha-linolenic acid
Octadecatrienoic acid | C18:3 n-9,12,15
47
yonder-linolenic acid
Octadecatrienoic acid | c18:3 n-6,9,12
48
Antioxidant role with lipids
Prevent oxidation of fatty acids on cell membrane
49
Lipid synthesis
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
Linoleic acid uses
Synthesis other fatty acids yonder-linoleic acid dihomo-y-linoleic acid Arachidonic acid
51
Alpha linolenic acid uses
Synthesis EPA DHA
52
Phospholipids
2 fatty acids 1 phosphate 1 glycerol
53
Membrane structure
Phospholipids Fluidity determined by number of unsaturated FA particularly PUFA More PUFA means more liquid and more likely to be oxidised
54
Lipid digestion Stomach
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
Lipid digestion Small intestine
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
Bile
``` Stimulated by CCK Derived from cholesterol Have a store of 2-4g double just to emulsify one meal Recirculated 3012 times a day ```
57
Lipid Absorption
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
Chylomicron
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
Very low density lipoprotein
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
Low density lipoprotein
High level of cholesterol | Main outer protein ApoB-100
61
High density Lipoprotein
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
ApoB-100
Allows for secretion of VLDL from liver Structural protein for VLDL, IDL and HDL Acts as a ligan receptor for LDL
63
ApoB-48
Chylomicrons Secretion of chylomicrons from intestine Core structure protein
64
ApoE
Chylomicrons, VLDL, IDL, HDL | Ligand for binding IDL and remnants to LDLR and LRP
65
ApoC-II
Chylomicrons, VLDL, IDL, HDL Activator of LPL Allows recognition and binding of lipoprotein
66
Cardiovascular disease
``` 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
How to combat cardiovascular disease
Lower LDL cholesterol Increase HDL Eat more unsaturated Do not eat trans fats or saturated
68
Long chain fatty acids make
``` Eicosanoids Endocannabinoids lipoxins Resolvins Lipid rafts ```
69
Eicosanoids
``` Made by COX or lopoxygenase Prostaglandins - Vasodilator Prostacyclin - Vasodilator Thromboxane's - Vasoconstrictor Leukotrienes - Vasoconstrictor ```
70
Conjugated linoleic acid
Milk products Intermediated during biohydrogentation Linoleic acid but two double bonds next to each other Functional food
71
Control of lipid metabolism
PPARs interact with DNA to increase and decrease amount of proteins Leptin - makes you full
72
Maltose
Glucose-Glucose alpha 1-4 glyosidic bond
73
Isomaltase
Glucose-Glucose alpha 1-6 glyosidic bond
74
Lacotse
Galactose and glucose beta 1-4 glyosidic bond
75
Sucrose
Glucose + fructose alpha 1-2
76
Raffinose
Glucose, galactose and fructose
77
Carbohydrate digestion Mouth
Salivary alpha – amylase Requires Ca2+ and Cl- 6.8pH optimum
78
Carbohydrate digestion Small intetine
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
SGLUT1
Apical membrane Glucose and galactose enter enterocyte Na+ enter allowing glucose and galactose to enter cell Na+ leaves via K+/Na+ atpase
80
GLUT5
Fructose
81
GLUT2
Basolateral membrane for sugar to leave
82
GLUT family
single polypeptide chain of 500 amino acid. 12 transmembrane segments
83
GLUT4
Adipose and muscle tissue | Insulin dependent
84
Sugar Alcohol
Lack aldehyde or ketone
85
Sugar acid
Aldehyde of OH and C6 is oxidised to make COOH
86
Amino Sugar
Has an amine group substituted for an OH
87
Glycoproteins
Cell membrane | Serum in blood
88
Proteoglycans
``` 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
Mucoproteins
Key component of mucus | Lubricants

NUT2001 (4 decks)

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