1
Q
What are vitamins?
A
organic compounds required in small amounts for normal functioning of the body
- cannot be synthesised in the body
- must be provided by diet
2
Q
What are the general outcomes of vitamin toxicity?
A
- abnormal accumulation in tissues
- overloading of normal metabolic pathways
- possibly irreversible lesions
3
Q
What are some vitamins that are toxic in access?
A
- vitamin A, D, B6
- niacin
(possibly Vitamin C, beta-carotene, vitamin E)
4
Q
What is produced from the reduction of oxygen to water in mitochondria?
A
- produces ATP
- produces free radicals
5
Q
What happens to 1-2% of the O2 used by respiratory chain?
A
ends up as superoxide
6
Q
What are free radicals?
A
- unstable oxygen species
- capable of oxidising PUFA/damaging organs/tissues and DNA (@ cell mem = lipid peroxidation)
- contains one or more unpaired electrons
- capable of independent existence
7
Q
What damage do free radicals do?
A
- nucleic acids
- nucleotides
- thiols
- covalent bonding
- lipids
- membrane structure
8
Q
What diseases can develop from free radicals?
A
- heart disease
- cancers
- parkinsons
- arthritis
- cataracts
- muscular dystrophy
9
Q
Where can we get some nutrients that act as protective antioxidants in conjunction with body enzymes?
A
- fruits, nuts
- leafy greens
- juices
10
Q
What are some metal cofactors that contribute to the integrated antioxidant defence system?
A
- Selenium (GSHPx, X 4)
- Iron (catalase)
- Copper (SOD, ceruloplasmin)
- Zinc (SOD)
- Manganese (SOD)
11
Q
What are some antioxidant compounds integrated into antioxidant defence system?
A
- vitamin E (carotenoids)
- vitamin C (polyphenols)
12
Q
What are fat soluble vitamins?
A
- found in fats and oils of food
- absorbed into lymph and carried in blood with protein transporters (chylomicrons)
- require bile and fats for absorption
- stored in liver/body fat
- can be toxic if large amounts consumed
- normally not excreted in urine
- don’t act as coenzymes
13
Q
What are soluble vitamins?
A
- found in vegetables, fruits, grains, meat
- absorbed into bloodstream
- not stored in body (except B12)
- toxicity is rare, when large amounts consumed
- have threshold for urinary excretion
- act as co-enzymes
14
Q
Name 4 lipid (fat) soluble vitamins:
A
- vitamin A
- vitamin D2
- vitamin E
- vitamin K1
15
Q
What is vitamin A also known as?
A
retinol
16
Q
What are the requirements, biological activity, and sources of vitamin A?
A
- 0.8mg
- eyesight, immune system
- liver, cheese, eggs and oily fish
17
Q
What are the requirements, biological activity, and sources of vitamin D?
A
- 0.01mg
- bones and teeth
- oily fish and eggs
18
Q
What are the requirements, biological activity, and sources of vitamin E?
A
- 10mg
- antioxidant activity
- cereals, vegetable oils, leafy vegetables
19
Q
What are the requirements, biological activity, and sources of vitamin K?
A
- (not stated requirement)
- blood clotting
- leafy vegetables, dairy products, grains
20
Q
what is ß-carotene?
A
- human body converts beta carotene into vitamin A (retinol)
- beta carotene is a precursor of vitamin A.
21
Q
How much retinol is absorbed by the body (%)?
A
70-90%
22
Q
How much ß-carotene is absorbed by the body (%)?
A
20-50%
23
Q
How much ß-carotene is needed for the formation of 1 µg of retinol?
A
6µg
24
Q
Where is ß-carotene stored?
A
liver
25
What can retinyl esters form and what is the use of its product?
- 11-cis-retinal
| - chromophore for rhodopsin
26
What can retinoic acid form and what is the use of its product?
- all-trans and 9-cis-retinoic acid
| - transcriptionally active vit. A species
27
How is free retinol esterified to form retinyl esters?
- via ARAT
or
- bind to CRBP and esterified by LRAT
28
Where are retinyl esters stored until needed?
in liver stellate cells
29
Roughly explain the Hepatic vitamin A metabolism:
1. Retinyl esters taken up into liver cells
2. Free retinol is esterified to retinyl esters
3. CRBP-retinol has a few pathways
- converted to retinoic acid
- released into blood
- form retinyl ß-glucoronide for excretion in bile
4. Retinoic acid has few pathways
- gene expression
- conjugated to glucaronic acid and excreted in bile
- 4-oxoretinoic acid
5. 4-oxoretinoic acid either function like retinoic acid or excretion in bile as glucaronic acid
6. holo-RBP from retinol, released to blood to form trimolecular complex
30
Main functions of vitamin A:
1. Vision
- night vision
- forms visual molecule rhodopsin
2. Antioxidant
- ß-carotene/other carotenoids, reacting with singlet oxygen species
3. Gene expression (differentiation + growth)
4. Immune system function
5. Reproductive process
6. Bone metabolism
31
What are two specific vitamin roles in the eye?
1. Process of light perception at retina
| 2. Maintenance of healthy cornea
32
What enables the signal that light hits the eyes, to be received by the brain?
rhodopsin in rod cells that are transformed and sends signals
33
How does vitamin A help the immune systems' function?
- synthesis of glycoproteins
| - promotes development of immune cells (NK cells)
34
How does vitamin A help the reproductive process?
- gene transcription in testis
- placental development
- testosterone/oestrogen production
35
What % of vit. A is egested in faeces?
70%
36
What % of vit. A is excreted in urine?
30%
37
Where else apart from faeces and urine, is vit. A excreted?
- CO2 from lungs and - caretenoid metabolites in bile
38
What is the require amounts of vitamin A for men and women?
men = 1000 µg/day women = 800 µg/day
39
What is the minimum vitamin A intake per day?
600µg
40
What are the results of high intake/chronic intake of vitamin A?
- in early pregnancy = birth defects
- anorexia, skin/hair abnormalities, bone/muscle pain
- ß-carotene cause yellow discolouration of skin (fat pads)
41
What are the results of vitamin deficiency?
- skin/mucous membrane dryness + infection + keratin deposits
- anaemia
- impaired immune response
- developmental defects (bones, teeth, immune system, vision)
- eye problems
42
Name 4 specific ways vitamin A deficiency causes eye problems:
1. Squamous metaplasia + keratinisation of conjunctiva
2. Dryness wrinkling + thickening of cornea (xerophthalmia)
3. Ulceration of cornea (blindness)
4. Impaired colour vision
43
What are the toxic effects of vit. C?
- fragile RBC, haemmorage
- bone pain, fractures
- abdominal pain, diarrhea
- blurred vision
- dry skin, hair loss
- liver englargement
- death
44
What are the (animal) sources of retinol?
- egg yolk
- butter
- whole milk
- liver/fish liver oils
45
What are the (plant) sources of ß-carotene?
- dark green leafy vegetables
| - yellow/orange vegetables = carrots
46
What is vitamin D?
- steroid pro hormone
| - made under the skin in UV light presence
47
What is the mean vitamin D intake required?
serum 25(OH)D concentration ≥ 25 nmol/L
48
General outcome of vit. D deficiency?
- rickets (children)
| - osteomalacia (adults)
49
Which vitamin is the most potentially toxic?
vitamin D
50
Explain how we synthesise vitamin D:
1. UV light shines on cholesterol compound in human skin
2. Transformed into vit. D precursor + absorbed to blood
3. Next day, liver and kidneys finish converting precursor to vit. D
51
25(OH)D (vitamin D) compound is needed in 4 areas, what are they?
1. Intestine - increase absorption of Ca2+ and P
2. Bone - increase boe mineralisation
3. Immune cells - induces differentiation
4. Tumour microenvironment
- inhibits proliferation
- induces differentiation
- inhibits angiogenesis
52
What is the final form of vitamin D when synthesised?
calcitroic acid
53
Which form of vit. D doesn't require digestion?
D2 and D3
54
Vit. D is absorbed via a _____ with the aid of ____ by _____ into the intestinal cell.
- micelle
- bile salts
- passive diffusion
55
What is vit. D incorporated into for transport into lymphatic system and blood?
chylomicrons
56
What is the % of dietary vit. D absorbed?
50%
57
How is excessive production of vit. D in skin prevented?
through inactive metabolite generation (lumisterol)
58
In liver, what hydroxylates vitamin D to active form?
cytochrome p450 hydroxylases
59
What is the half life of active vitamin D?
15 days to 3 weeks
60
What are the genomic and non-genomic functions of vitamin D?
1. Serum calcium homeostasis (kidney, bone)
2. Phosphorus homeostasis
3. Cell differentiation, proliferation, growth
4. Calcitriol and muscle
5. Blood pressure regulation
6. Immune function
7. Pancreatic beta-cell production, insulin secretion
61
What does vitamin E refer to?
group of 8 tocopherols
62
Which tocopherol is the biologically active form?
A-tocopherol
63
What are the functions of Vit. E?
1. Antioxidant
2. Prevent damage to lungs, RBCs, WBCs (immunity), heart
3. Necessary for normal nerve development
64
What is the result of vitamin E deficiency?
- Decreased absorption of fats
- liver disease
- low fat diets
- premature babies - fragile RBCs (haemolysis)
- Loss muscle coordination, vision, immune function
65
What is the exceeding upper intake of vit. E?
1000 mg/day
66
Which vitamin is the least toxic from the fat-soluble vitamin list?
Vitamin E
67
What might extreme doses of vitamin E cause?
- affect blood clotting effects of vit K
- increased haemmorage
- increase effects of anticoagulants (coumadin, warfarin)
68
What can destroy vit. E?
high temperatures
69
What is the daily recommended intake for Vit. E?
15mg
70
What are some sources of vit. E?
- safflower oil
- mayonnaise
- canola oil
- wheat germ
- sunflower seeds
71
What and which part produces vitamin K?
produced by bacteria, in the large intestines
72
What are the functions of vitamin K?
1. Coagulation
2. Promotes synthesis of blood clotting proteins (interfere with anti-coagulants
3. Bone formation
73
What was vitamin K named after?
Danish word, "koagulation"
74
What are the recommended daily intakes of vit. K for men and women?
```
men = 120µg
women = 90µg
```
75
What are good sources of vit. K?
- cauliflower
- cabbage
- canola oil
- spinach (steamed)
- salad greens
- soybeans (dry roasted)
76
Are there any vitamin K deficiencies?
rare, unlikely in healthy adult
77
Which populations are at risk of vitamin K deficiency?
- infants (after prolonged antibiotic therapy)
- patients with decreased bile production
- patients with chronic malabsorptive disorders
78
Why are infants given vit. K injection?
- milk is low in vit K
- low vit K stores at blood
- GI not populated with vit K producing bacteria
79
What is the result of vit. K toxicity?
- ingestion of large amounts doesn't cause toxicity but maybe above >1000mg/d
- haemolytic anaemia (rupture of RBCs)
- liver damage (jaundice)
80
What are the water-soluble vitamins?
non-B complex (vit. C) and B-complex
81
Who cannot synthesise vit. C?
- humans
| - guinea pigs, primates, birds
82
Why can't humans synthesise vit. C?
have congenital absense of gulonolactone oxidase
83
What was used in the experiment to cure scurvy, 250 years ago?
lemons
84
Vitamin C is also known as?
ascorbic acid
85
What are the main food sources of vitamin C?
fruits and vegetables
86
What are the main deficiency symptoms of vit. C?
- scurvy
| - capillary fragility
87
Does vitamin require digestion prior to absorption?
No
88
What assists absorption of ascorbic acid?
- sodium dependent vit. C transporters (SVCT 1 and 2)
89
What is SVCT1?
- main carrier responsible for vit C absorption
- enables intestinal absorption of vitamin in excess of cell needs
- downregulated by ascorbic acid
90
What is SVCT2?
present in most metabolically active tissues except muscle/lungs
91
What is involved in transport of dehydroascorbic uptake into cells?
GLUT transporters
92
What generally happens in interconversion of ascorbic acid and dehydroascorbic acid?
1. Ascorbyl radical formed but has short half-life - doesn't form ROS
2. Oxidation of this radical forms vit. C
3. Dehydroascorbic acid reduced to ascorbin acid with H provided from reduced glutathione (GSH)
93
What is the range of recommended vit. C intake per day?
30-180mg
94
What is the % of absorption?
70-90%
95
What is the relationship of absorption and intake?
Absorption decreases with increased intake
96
At what levels of vit. C is is there 98% absorption?
>20mg
97
What is the normal plasma ascorbic acid concentration range?
0.4-1.7mg/dL
98
Where in the body are is the highest level of vit C plasma concentration and how much?
adrenal and pituitary glands
| 30-50mg/100g
99
But where in the body contains the most vitamin C?
liver
100
What is the maximum vitamin C pool taken per day?
2g
101
What can result from taking more than 2g vit. C a day?
- alteration of insulin response to carbohydrate
- interference with blood clotting medications
- kidney stones
- gout
- digestive upsets
102
How is vit C excreted?
in urine after chemical reactions as various metabolites, 25% in form of oxalic acid
103
What can high doses of vit. C result in?
- formation of kidney stones, from overproduction of oxalate
| - DNA damage (500mg/d)
104
In terms of its function as antioxidant, what roles do vit. C play?
1. React with many reactive free radicals
2. Powerful, non-specific reducing agent, H donator
3. Protects water soluble compartments
4. Neutralises free radicals
5. Regenerates Vit. E (H donor)
105
How can the vit E radical be converted back to vit E?
reaction with vit C
106
Explain the amidation of peptides with c-terminal glycine (involves vit. C):
1. Vit. C = reducing agent, converts copper to reduced form
2. enzyme cleaves carboxyl-terminal residue, residue released as glyoxylate
3. Amidated peptides are active hormones/hormone-releasing factors/neurotransmitters
107
What are other functions of vit. C?
1. Collagen/carnitine synthesis
2. Facilitates Fe (non haem) absorption
3. Co-factor in mono-oxidase reactions - neurotransmitter synthesis
4. Activation of peptide hormones
5. Tyrosine synthesis (liver and kidney - from phenylalanine)
6. Cholesterol catabolism
7. Bile acid formation
108
What is the function of ascorbate?
hydroxylation of peptide-bound proline and lysine in the synthesis of collagen
109
What are the 3 interwoven chains of collagen?
glycine, proline and hydroxyproline
110
What is the use of carnitine?
transfer long chain FAs to inner mitochondria mem. for energy production
111
Tyrosine is synthesised from?
amino acid phenylalanine
112
What are the symptoms of vit. C deficiency?
- bleeding gums
- small skin discolouration (ruptured blood vessels)
- sub-lingual haemmorages
- easy bruising
- impaired wound and fracture healing
- joint pain
- loose/decaying teeth
113
How many b-complex vitamins do we know of?
8
114
What are the b-complex vitamins?
water-soluble, chemically distinct vitamins that coexist in same foods
115
What is the function of the b-vitamins?
- coenzymes
| - important for cells to generate energy, make protein/new cells, metabolise carbs/fats/proteins
116
What is a coenzyme?
molecule that combines with enzyme to make it active
117
What is vitamin B1 known as?
Thiamine
118
What does the deficiency of thiamine cause?
- beri-beri
- possible edema
- muscle wasting, weakness
- pain, apathy
etc (so much)
119
What is beri-beri?
disease that was widespread in Asia, leg paralysis (polyneuritis)
- primary symptom = anorexia
- progresses to cardiovascular/neurological problems
120
What is the recommended intake for vit. B1 (thiamine)?
0.5mg/1000kcal
121
What is the dose at which vit. B1 is toxic?
300mg
122
What are the sources of vit. B1?
- meats (pork, beef)
- salmon
- legumes, grain products
- cereals, breads
- yeast, wheat germ, soy milk
123
What are the 3 functions of thiamine (vit. B1)?
1. Energy transformation
2. Synthesis of pentoses and NADPH
3. Membrane/nerve conduction
124
How many metabolites does degradation break thiamine to?
20 or more
125
What does wet beri-beri cause (reversible)?
- cardiomegaly
- edema
- waxy skin
126
What does dry beri-beri cause (reversible)?
- peripheral neuropathy
| - weakness
127
What is the results of irreversible beri-beri?
- cerebral beri-beri like:
- Wernicke-Kosakoff syndrome
- brain tissue damage
128
How does alcoholism affect thiamine?
- thiamine deficiency related to alcohol consumption
- alcohol inhibits absorption of thiamine in mucosal cells + conversion to TPP
- symptoms: mental confusion, loss recent memory, ataxia
129
What is vitamin B2 known as?
Riboflavin
130
Explain vit. B2 absorption:
- digested from protein prior to absorp.
- via saturable, energy-dependent Na+-independent carrier (9RTF2)
- in large amounts, absorbed via diffusion
- bile facilitates absorp.
- alcohol impairs digestion + absorp.
- 95% absorp.
131
What is the maximum in g of vit. B2 absorbed per day?
25g
132
What are the functions of vit. B2?
- energy metabolism
| - flavoproteins (fatty acid beta-oxidation)
133
Is B2 affected by B1?
Yes, it is low when B1 is low.
134
What are the daily recommendations of vit. B2 for men and women?
```
men = 1.2mg/d
women = 1.1mg.d
```
135
What are the results of vit. B2 deficiency?
- cracks/redness at mouth corners
- sore throat
- inflamed eyes/eyelids
- sensitivity to light/skin rashes
136
What is Vitamin B3 known as?
Niacin
137
How was niacin discovered?
through its deficiency - pellagra
138
Niacin is a generic term for?
nicotinin acid and nicotinamide
139
Niacin absorption is dependent on...?
Na+-dependent, carrier mediated diffusion
140
At what g is there complete absorption of B3 (niacin)?
3-4g
141
What are the functions of niacin?
1. Coenzyme
- b-oxidation of fatty acids
- fatty acid/cholesterol/hormone synthesis
2. Non-redox roles (donor of ADP)
3. Energy metabolism
4. Cell respiration
5. DNA repair/synthesis
6. Act as secondary messenger
7. Stimulate increased Ca2+
142
What are the symptoms of pellagra (hint: 4Ds)?
- Dermatitis (sunburn-like skin)
- Dementia (neurological, headache, memory loss)
- Diarrhoea (+ vomiting)
- Death
143
What re the recommended daily intakes of vit. B3 (niacin) for men and women?
```
men = 16mg
women = 14mg
```
144
What is the tolerable upper intake level of B3?
35mg/day
145
What is pantothenic acid bound as?
coenzyme A (CoA)
146
What reactions do CoA participate in?
- nutrient metabolism
- energy production (TCA cycle)
- Acyl-carrier protein (ACP)
147
What results from pantothenic acid deficiency?
Burning feet syndrome
148
What was biotin usually called?
Vitamin H or B7
149
Although rare, when the biotin deficiency occur?
in patients treated with anticonvulsnts/antibiotics
150
What synthesises significant quantities of biotin?
- intestinal flora
151
What does avidin do?
- irreversibly binds to biotin
| - prevents biotin absorption (not heat resistant)
152
What is the tightest non-covalent bond found in nature?
avidin binding with biotin
153
What are the coenzyme forms of folate?
DHF and THF
154
What is folate known as?
Vitamin B9
155
What are the functions of folate?
1. Amino acid metabolism
| 2. Purine and pyrimidine synthesis/nucleotide metabolism
156
What is the recommended daily intake of folate (vit. B9) for adults?
400μg/d
157
When would there be requirement of additional dietary intakes of folate?
during pregnancy and lactation
158
What are the sources of folate?
- leafy green vegetables
- liver, kidney beans, lima beans
- leaf beef, potatoes, whole grain bread
- excludes oranges and root vegetables
159
What destroys half of folate in foods?
heat and oxidation during cooking/storage
160
What is the % of dietary folate that is nutritionally available?
25-50%
161
What are the results of folate (B9) deficiency?
- anaemia, mental confusion
- increase of neural tube defects, anencephaly, absence of cerebral hemisphere
- alterations in DNA metabolism
- changes in cellular nuclear morphology
- poor growth, GI tract disturbances
162
How does a women achieve maximum benefit from folate supplementation?
enhance her folic acid intake before she becomes pregnant
163
Why is vitamin B12 unique?
contains metal ion, cobalt
164
What is required for B12 absorption?
intrinsic factor
165
What are the functions of B12?
1. Methyl transfer reactions (with folate)
2. Homocysteine to methionine
3. DNA/RNA
4. L-methylmalonyl-coA to succinyl-coA
5. Fat and protein metabolism
6. Haemoglobin metabolism
166
What are sources of B12?
- food from animals
- liver and kidney
- milk, egg, fish, cheese, meat
167
When how much B12 is lost % when milk is pasteurised or evaporated?
40-90%
168
What is the recommended intake of B12 in adults?
2.4μg/d
169
What are the results of vitamin B12 deficiency?
- reflects inadequate absorption and not poor intake
- lack of HCL (development of atrophic gastritis esp. in elderly)
- Lack intrinsic factor (defective gene of IF)
- impaired DNA synthesis
- defective proliferation of rapidly dividing cells (megalobasltic anaemia, glossitis, hypospermia.. etc)
Malnourishment and Obesity
flashcards
Decks in class (21)
# Cards
-
Undernutrition and Overnutrition0
-
Starvation0
-
Adipose Tissue, Inflammation and Obesity60
-
Immunological Response to Injury Sepsis72
-
Metabolic response to injury and infection19
-
Minerals118
-
Vitamins169
-
Practical Nutrition Assessment15
-
Alcohol and Nutrition38
-
Fluid and Electrolyte Requirements in Disease52
-
Eating Disorders43
-
Cardiovascular Disease56
-
Diabetes and Metabolic Syndrome0
-
Obesity17
-
Restricted diets and Nutritional Deficiencies32
-
Physical Inactivity0
-
Non-communicable disease and Prevention8
-
Dietary assessment21
-
Consumer Eating Habits (Part 1 and 2)5
-
Problems in Human Nutrition11
-
Behavioural Change and Dietary Interventions2
