Fat Soluble Vitamins Flashcards

1
Q

What are the 2 Vitamin A classifications?

A

Retinoids = the biologically active form of vitamin A
Exist in 3 forms that can be interconverted:
- Retinol (an alcohol) or retinyl ester
- Retinal (an aldehyde)
- Retinoic acid
Tail of vitamin A molecule can be in cis or trans form: this determines the function of the vitamin

Carotenoids (~700 types found in food) = provitamin A (can be converted to retinol)
Have “non-vitamin A” activity too
Are the yellow-orange pigments in fruit and vegetables
The ones that can be converted to vitamin A are:
1. Alpha-carotene
2. Beta-carotene
3. Beta-cryptoxanthin

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2
Q

Describe the digestion of vitamin A

A

Digestion:
Rentinyl esters and retinol need to be freed from protein in food and retinyl esters must be split into retinol and FA
Provitamin A carotenoids usually bound to a protein molecule in food too
Split via enzymes activity in GIT to be absorbed
Formation of micelles with bile, and other FA

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3
Q

Describe the absorption of vitamin A

A

Absorption:
70-90% of retinol intake absorbed if at least 10g of fat in meal
5-60% of carotenoids intake absorbed (broad range => dependent on fat intake: form of the food – uncooked = less absorption)

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4
Q

Describe the activation of vitamin A

A

Activation:
Carotenoids cleaved to form retinal or retinoic acid. Retinal converted to retinol and retinoic acid
Takes place in the enterocytes and in the liver

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5
Q

Describe the transport of vitamin A

A

Transport:
In enterocytes:
- Retinyl esters are reformed, packaged in chylomicrons, transported via the lymphatic system
- Retinoic acid and carotenoids can enter bloodstream directly, transported to the liver or tissues bound to albumin
From the liver:
- Retinoids bound to retinol binding protein + transthyretin for transport to cells
- Carotenoids that are not transformed are carried out by lipoproteins

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6
Q

Describe the storage and excretion of vitamin A

A

Stores:
>90% of retinoid stores are found in stellate cells of the liver, as retinyl esters (enough to last several months), small amounts in adipose tissue (gives it a yellow tint), kidneys, bone marrow testicles, eyes
Some stores of carotenoids in adipose tissue, cell membrane, in the eye (lutein, zeaxanthin, beta carotene)

Excretion:
Small amount in urine; carotenoid excreted as part of bile

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7
Q

Describe the 2 primary functions of retinoids

A

Cell differentiation: growth and development of foetus
Vitamin A carried by RBP and transtheritin in blood
Enters the target cell and binds to a cellular retinoid binding protein
Is released, enters the nucleus and binds to nuclear retiod receptors (RAR and RXR)
Complex binds to DNA, activating gene transcription
mRNA codes for protein which provides a cellular response

Night vision adaptation:
Rhodopsin (11-cis-retinal + opsin) absorbs light, converting to a11-trans-retinal. A11-trans-retinal separates from opsin. Opsin triggers responses that send a signal to the brain. Enzymes reconvert trans form to cis form and combine with opsin

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8
Q

Describe the requirements for vitamin A

A

RDI for vitamin A as retinol equivalent

UL for retinol only

No UL for beta-carotene

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9
Q

What are international units used?

A

To allow for consistency in dosage information, especially when there is risk of toxicity in large doses, particularly relevant for fat soluble vitamins

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10
Q

What are the signs and symptoms of vitamin A deficiency?

A

Night blindness (cant adapt to change in light levels)
Xerophthalmia
Keratomalacia (involves the cornea, results in blindness)
Follicular hyperkeratosis

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11
Q

What are the signs and symptoms of vitamin A toxicity?

A

Acute = GIT upset/nausea; muscular incoordination, headaches

Chronic = liver damage, haemorrhages, dry skin and mucous membrane, hair loss, bone loss, coma

Teratogenic = if the pregnant woman consumes large amount => foetal malformation, spontaneous abortion risks

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12
Q

What are some food sources of vitamin A?

A

Retinoids (preformed vitamin A)

- Beef and cod liver
- Eggs
- Dairy butter, milk/cheese
- Low fat dairy products are commonly fortified with vitamin A (voluntarily)

Carotenoids (provitamin A) - eat with fat to improve absorption

- Sweet potato
- Pumpkin
- Carrot
- Mango
- Spinach

Supplemental form: usually retinyl palmitate and acetate +/- beta carotene

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13
Q

What is the biologically active form of vitamin D?

A

Calcitriol (1,25-dihydroxy-cholecalciferol)

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14
Q

Which fat soluble vitamin can be synthesised endogenously? Describe this production

A

Ultraviolet B (UVB) converts 7-dehydrocholesterol to cholecalciferol (vit.D3)

Cholecalciferol travels to liver to undergo hydroxylation to produce 25-hydroxy-cholecalciferol (calcidiol)

25-hydroxy-cholecalciferol is taken to the kidneys for the second hydroxylation, to produce the bioactive form of vitamin D: 1,25-dihydroxy-cholecalciferol (or calcitriol)

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15
Q

Which vitamin has hormone-like activity

A

Calcitriol

VItamin D from food a pro-hormone = precursor of calcitriol

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16
Q

What is measured to determine vitamin D status in the blood and why?

A

25-hydroxy-cholecalciferol (calcidiol) = the type of vitamin D that is measured in blood tests. But not active form

1,25-dihydroxy-cholecalciferol (1,25-dihydroxy Vit. D3, or calcitriol = active form of vitamin D) is not measured as a marker of vitamin D status because it has a short half-life in the blood (its constantly used up)

17
Q

Describe the absorption, transport, activation and excretion of vitamin D

A

Absorption (dietary and supplemental):
Micelles + enterocytes: dependent on bile and pancreatic lipase
Into chylomicrons, through lymphatic system and into circulation to the liver
Endogenously produced vitamin D3 is transported by vitamin D binding protein (VDBP) = slower

Transport:
Transported after activation through VDBP

Activation:
Conversion to the active form is regulated by the parathyroid hormone, takes place in the liver and kidneys

Excretion:
Small amount in urine, but mainly via bile and faeces

18
Q

Describe the primary function of vitamin D

A

Maintaining blood concentration of calcium (and phosphorus):

Low blood calcium levels cause increased parathyroid hormone (PTH) production

PTH reduces calcium excretion from the kidneys and stimulates calcitriol synthesis

PTH and calcitriol mobilise calcium from the bone

Calcitriol increases dietary calcium absorption from the GIT by: binding to VDRs (vitamin D receptor), going into the nucleus and increasing expression of calcium transporters and calbindin (D28K), and increasing ATP-dependent Ca2+ pump activity

19
Q

Describe the requirements for vitamin D

A

No dose-response data to set an EAR, hence no RDI

Is an AI and UL

20
Q

What are the signs and symptoms of vitamin D deficiency?

A

In children: Ricket’s disease (bowed logs). Rickets linked to vitamin D deficiency since 1918

In adults: osteomalacia = soft bones (calcitriol promotes bone resorption to restore blood calcium levels)

Deficiencies are related to:
- Season
- Location
- Ageing skin, always covered skin
- Chronic liver and kidney disease (why?)
- Dark skin
Intestinal disease (malabsorption issues, e.g. Chron’s disease)

21
Q

What are the signs and symptoms of vitamin D toxicity?

A

Occurs with supplementation overuse

Above UL: can cause over absorption of calcium and thus hypercalcaemia, calcium deposit in kidney, joints, blood vessels, heart

Vitamin D excess can also lead to bone demineralisation (via too much bone resorption), and can be fatal in chronic excess

22
Q

What is a good food source of vitamin D

A

Oily fish, red meat, liver, egg yolks

23
Q

What is vitamin E? Which is its most biologically active form?

A

A family of compounds:
• 4 tocopherols (alpha, beta, gamma, delta)
• 4 tocotrienols (alpha, beta, gamma, delta)

Body “prefers” alpha tocopherol = most biologically active

Natural form more potent than synthetic form

24
Q

Describe the absorption, transport, storage and excretion of vitamin E

A

Absorption:
Depends on presence of dietary fat and amount consumed
20-70% of DI is usually absorbed

Transport:
Micelles to enterocytes: dependent on bile and pancreatic lipase
Chylomicrons, through lymphatic system and to the liver (with some tissue delivery) transported from liver via lipoproteins (VLDL, LDL, HDL) to tissues

Storage:
Stored in adipose tissue (90%) not in the liver

Excretion:
Bile, urine, skin

25
Q

Describe the primary function of vitamin E

A

Main function is as an antioxidant: as a peroxyl radical scavenger (in membrane phospholipids and plasma lipoproteins)

Free radicals have 1000x greater reactivity with vitamin E than PUFA

Tocopherol reacts with a peroxyl radical to form a hydroperoxide and the tocopheroxyl radical

The tocopheroxyl radical must be reduced by other antioxidants to tocopherol, or reacts with another tocopheroxyl radical to form non-reactive products (tocopherol dimers), or undergoes further oxidation to tocopheryl quinone (an anti-coagulant), or can act as a prooxidant and oxidise other lipids

26
Q

Describe the requirements of vitamin E

A

No EAR and RDI

AI and UL based a-tocopherol

27
Q

What are the signs and symptoms of vitamin E deficiency?

A

Haemolytic anaemia: premature haemolysis of RBCs
Impaired immune function
Oxidative stress

Reasons: malabsorption disease, genetic defects of transporters, and smoking increase requirements of alpha tocopherol

28
Q

What are the signs and symptoms of vitamin E toxicity?

A

High-dose vitamin E (supplement) interferes with vitamin K activity in blood clotting, increasing risk of haemorrhaging

High-does vitamin E (supplement) enhance blood thinning medication activity with the same outcome

29
Q

What are some good food sources of vitamin E?

A

Sunflower oil and seeds, almonds

30
Q

What are the forms of vitamin K?

A

Phylloquinone found in plants = most biologically active

Menaquinone produced by gut bacteria

31
Q

Describe the digestion, transport, storage and excretion of vitamin K

A

Absorption and transport:
Best in presence of fat (since K1 is mainly found in green leafy vegetables), or consumed as vegetable oils (soybean, canola); impaired by plant tissue (whole food matirx), unless in presence of fat
80% of absorbed in SI, via micelles (lipase and bile activity required)
Taken in chylomicrons through the lymphatic system to the liver
Colonic bacteria produced menaquinones: absorbed in the colon by passive diffusion
Transported via lipoproteins (VLDL and LDL) to peripheral tissue

Storage:
Minimal , some in the liver. Recycled rapidly by the K-epoxide cycle for optimal re-use

Excretion:
Primarily via bile in faeces, small amount in urine

32
Q

Describe the primary functions of vitamin K

A

Involved in the blood clotting cascade as a cofactor of the carboxylase enzyme in the conversion of preprothrombin to prothrombin. Reduced vit K becomes oxidised

In bone health: vitamin K is a co-factor in carboxylation of the glutamic amino acid in extra-hepatic vitamin K dependent proteins involved in bone structure (e.g. osteocalcin)

33
Q

How does Warfarin influence the blood clotting cascade?

A

The medication Warfarin inhibits the enzyme epoxide reductase which reduces oxidised vitamin K. People prescribes a dose dependent on their vitamin K consumption. Important that they don’t increase of decrease their consumption. Keeps blood thin

34
Q

Describe the requirments for vitamin K

A

No EAR and RDI

AI, but no UL

35
Q

What are the signs and symptoms of vitamin K deficiency?

A

Increased risk of osteoporosis/fracture
Risk of hemorrhaging
Newborn babies injected at birth to prevent bleeding
Can be due to long term antibiotic use, or fat malabsorption disease

36
Q

What are the signs and symptoms of vitamin K toxicity?

A

No UL as no known toxxicity

37
Q

How do other nutrients impact vitamin K?

A

High dose (suppplemental) vitamin A interferes with vitamin K absorption from GIT

High dose (supplemental) vitamin E interferes with vitamin K activity on clotting factors

38
Q

What are some good food sources of vitamin K

A

green leafy veggies, broccoli