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Foundations of Nutrition > Vitamin A > Flashcards

Vitamin A Flashcards

1
Q

What type of vitamin is VA?

A

Fat Soluble

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2
Q

What is the name of the precursor to all types of VA?

A

All-trans-retinol

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3
Q

What are the main types of vitamin A?

A 
Preformed = Retinoids 
Proformed = Carotenoids
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4
Q

Give 3 examples of retinoids?

A

Retinol
Retinal / Retinaldehyde
Retinoic Acid

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5
Q

What is the generic structure of a retinoid?

A

Long carbon chain
One end a saturated cyclic carbon structure/ring
Other end is a functional group relating to the type of vitamin A it is

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6
Q

What conformation is retinol found in food?

A

Trans - never cis

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7
Q

Give 4 examples of carotenoids

A

Alpha,beta, gamma carotenes

Beta-cryptoxanthin

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8
Q

What is the general structure of a carotenoid?

A

Long carbon chain with a mix of double and single bonds with carbon rings either ends normally

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9
Q

What is the biological activity of carotenoids?

A

B-carotene = 2:1 if pure, but in food 6:1

Other carotenoids = 12:1

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10
Q

How does carotenoids become biologically active?

A

The carotenoids undergo a reaction with an enzyme called carotene deoxygenase to become retinal

The retinal can then become either retinol or retinoic acid

Retinal -> Retinol
Retinol dehydrogenase, reversible

Retinal -> Retinoic Acid
Aldehyde Oxidase

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11
Q

What enzyme converts b-carotene to retinal?

A

Carotene deoxygenase

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12
Q

What enzyme converts retinal to retinol?

A

Retinol dehydrogenase

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13
Q

What enzyme converts retinal to retinoic acid?

A

Aldehyde oxidase

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14
Q

What reaction is reversible and which one is non-reversible when thinking about what retinal can convert to?

A

Retinal -> retinol = reversible

Retinal -> Retinoic acid = non-reversible

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15
Q

What form must vitamin A be in to be absorbed into enterocytes from the lumen?

A

Retinol

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16
Q

How does the body absorb retinyl esters?

A

First digestion of them from pancreatic lipases and retinyl ester hydroxylases from both pancreatic secretion and within the brush border

Then the retinol produced from the reaction is absorbed via the same mechanism as lipids -> i.e. micelles etc

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17
Q

Once retinol is absorbed into enterocyes what happens next?

A

The retinol needs to be re-esterfied to form retinyl esters via 2 main enzymes ARAT & LRAT

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18
Q

What are the two main enzymes involved in the resterfication process in the enterocytes?

A 
ARAT = Acyl-CoA:Retinol Acyltransferase 
LRAT = Lecithin:Retinol Acyltransferase
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19
Q

How is vitamin A transported to the liver once leaving the enterocyte

A

Retinyl Esters are packed into chylomicrons, these are secreted into the Lymph and taken to the thoracic duct, pass into the blood and then taken to the liver

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20
Q

What i unique about b-carotene digestion & absorption?

A

50% of BC is oxidised into retinal which can then form retinyl esters which then undergo the same process as mentioned before with lipases & hydroxylases

The other 50% BC passively diffuses across the enterocyte and enters the blood directly which is then take to the liver

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21
Q

What are the absorption rates of pre-vitamin A and pro-vitamin A?

A

70-90% Pro

5-50% Pre

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22
Q

What major factor regulates how much vitamin A is absorbed?

A

Presence of fat in the diet

If less than 10% of food energy is from lipids, absorption is diminished

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23
Q

What happens with vitamin A during the exogenous chylomicron pathway?

A

Retinyl Esters can be released and acted upon by lipoprotein lipases and be released to tissues on their way to the liver

The bulk of REs are however delivered to the liver in the chylomicron remmnants when these are taken up by the liver (B-48 & LDL-r ligand bonding?)

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24
Q

Once retinyl esters are delivered to the liver what can happen?

A

First thing is REs are metabolised into retinol
Retinol then can have two options

1st is to be bound to retinol binding protein for transport to tissues

2nd is stored in stellate cells within liver as REs (so converted back to REs)

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25
Q

What is the purpose of Retinol binding protein?

A

Allows for transport of vitamin A to tissues, being able to be transported in an aqueous solution and protects from oxidation

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26
Q

Why is transthyretin protein important in vitamin A delivery?

A

Transthyretin protein binds to the RBP-ROH complex as the complex is tiny and at risk of kidney excretion

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27
Q

How is retinol released into cells?

A

Target tissues will have retinol binding protein receptors which remove arginine from the RBP which reduces its affinity to both the transthyretin and retinol, releasing both

28
Q

How do tissues receive vitamin A?

A

From RBP-ROH-TTR complex

From CM / Lipoproteins

29
Q

How to retinols become metabolically active once taken up by cells?

A

Converted to retinoic acid to interact with RARs & RXRs

RARs = Retinoic acid receptors 
RXRs = Retinoid X receptors

These are steroid hormone receptors that interact with genes. therefore can alter cell function

30
Q

Give 5 metabolic functions of vitamin A

A 
Vision 
Gene expression & cell differentiation 
Reproduction 
Growth 
Integrity of Immune System 
B-carotene is an antioxidant
31
Q

Explain the cycle vitamin A is part of for vision?

A

All-trans-retinol is the starting vitamin A product
This is isomerised to 11-cis-retinol
This is oxidsed to 11-cis-retinal

Opsin the light sensitive protein found in the retina binds with 11-cis-retinal to form rhodospin

Rhodospin found in rods and cones and act as a light absorbing complex

Exposure to light changes composition of complex resulting in 11-cis-retinal converting to the trans form. During which electrical signals released and transmit down the optic nerve

11-trans-retinal released from the complex to be converted to 11-trans-retinol & then 11-cis-retinol which takes you back to the start of the cycle

32
Q

What visual impact do you have with vit A deficiency?

A

Impaired colour vision -> particularly green light
Impairment to the ability to adapt to dim light
Inability to see in dim light (night blindness)

33
Q

What is the opthalmology clinical condition in vitamin A deficiency

A

Xerophthalmia

34
Q

What are the 2 signs of xerophthalmia?

A

Bitot’s spots -> desquamated keratinised conjunctival cells

Keratomalacia ->Liquefaction of the cornea

35
Q

What forms of vitamin A is involved in cell differentiation & turnover?

A

All-trans-retinoic acid

And 9-cis-retinoic acid

36
Q

How does vitamin A regulate cell differentiation and cell turnover? (Go generic)

A

Retinoic acids can bind to nuclear receptors that bind to control regions of DNA and therefore regulate gene transcription

37
Q

What are the mechanisms of vitamin A in gene expression and cell differentiation control?

A

There are two key receptors that form different mechanisms. RARs and RXRs

RARs - Retinoic Acid Receptors
These bind with all-trans-retinoic acid and 9-cis-retinoic acid and act in an inhibitory fashion

RXRs - Retinoid X Receptors
These bind only to 9-cis-retinoic acid and there are many different receptor structures. These usually activate gene expression

38
Q

What retinoic acid activates gene expression?

A

9-cis-retinoic acid (RXR)

39
Q

What retinoic acid inhibits gene expression?

A

all-trans-retinoic acid & 9-cis-retinoic acid (RARs)

40
Q

Why is retinoic acid teratrogenic?

A

Retinoic acid toxicity results in NTDs and limb deformities.

Mechanisms are

The posterior closure of the NT depend on the switch of RARs to change from gamma type to beta type. Retinoic acid exposure prevents this switch so keeps the NT open leading to NTDs and LD

Retinoic acid is also believed to implicate the expression of the HOX genes resulting in limb development issues (one study with chickens resulted in extra limbs)

41
Q

Give 4 functions vitamin A has on the immune system?

A 
Humoural / Adaptive 
Cell Mediate Repsonse 
Mucosal Immunity
NK cell activity 
Phagocytosis 
Key modulator of TGF-beta which suppresses several cytokine
42
Q

Is the pro or pre vitamin A’s more important in immune function?

A

Pro -> beta-carotene is particularly implicated in immune function

43
Q

How will protein malnutrition, fat malabsorption and infection result in vitamin A deficiency?

A

If you have protein malnutrition you may not have enough amino acids to form RBP so therefore have a functional vitamin A deficiency

If you have a health problem that results in fat malabsorption you will then get reduced absorption of vitamin A

If you have an infection your liver will produce less RBP, if part of the cause of infection was vitamin A deficiency then this will only worsen vitamin A deficiency status

44
Q

What countries are vitamin A deficient?

A

Africa (Middle region) and E Asia

45
Q

What correlation are there between typical vitamin A deficient countries and other factors?

A

These countries often have low fat diets and have increased rates of night blindness

46
Q

What is considered as vitamin A toxicity? (not consumption!)

A

> 70 micro mol / kg in the liver

47
Q

Why is it possible to become vitamin A toxic?

A

Removal of vitamin A relies on the livers cytochrome P450 system to oxidise retinol via glucuronidation and it becomes saturable once the liver reaches concentrations above 70 micro mol / kg

So once saturates retinol builds up and causes toxicity

48
Q

How much vitamin A consumed for a prolonged period of time is thought to cause toxicity?

A

> 7mg / d

49
Q

Give 4 signs or symptoms of vitamin A toxicity

A

Headache, nausea, ataxia, anorexia
Hepatomegally hyperlipidemia
Joint pains, hypercalcaemia, calcification of soft tissues
Excessive dry skin, scaling, cracking of skin, alopecia

50
Q

Give 3 risks of VA toxicity in pregnancy

A

Spontaneous abortion
Birth defects
Permanent LD

51
Q

What is the toxic effects of b-carotene

A

Hypercarotenosis -> orange-yellow colouring of skin

No other toxic effects (relatively safe)

52
Q

What is vitamin A dietary requirements based on?

A

To maintain a liver concentration of 70 micro moles per kg

53
Q

How long do liver stores last?

A

months

54
Q

What is the average dietary requirements of VA?

A

6.7 micrograms of retinol equivalents / kg

55
Q

What is the tolerable upper limit of vitamin A consumption?

A

3000 micrograms for adults

56
Q

What are retinol equivalents?

A

A way to standardise the impact vitamin A types have on the body in regards to bioavailability and biological action

I.e. 1 RE is equivalent to
1 microgram preformed retinol
6 micrograms b-carotene
12 micrograms other carotenoids

57
Q

What is happening in the UK in reference to dietary intake and plasma vitamin A levels?

A

Dietary intake is dropping in most ages groups (<75’s) towards the cut off for RNI

Plasma vitamin A levels are doing ok tho and remaining above the deficiency cut off

58
Q

Where does retinol come from in the diet? (not examples yet)

A

Animal Foods & Small number of bacteria produce it

59
Q

WHat is the most common form of retinol / pre-formed vitamin A in the diet?

A

Retinyl Palmitate

60
Q

Give 5 food sources of vitamin A

A

Liver, Fatty Fish
Egg Yolk, Milk, Butter
Enriched Margarine

61
Q

Where does carotenoids / beta-carotene come from in the diet?

A

Fruits and veg

62
Q

Give 6 food examples of b-carotene sources?

A

Carrots, peppers, tomatoes, broccoli, sprouts, kale, spinach, mango, watermelon, pink grapefruit

63
Q

In the UK diet what makes up the bulk of vitamin A consumption?

A

Fruits and veg

Remember there are differences across age groups e.g. kids rely on milk for their source more than adults

64
Q

Give 3 methods of assessing vitamin A status in individuals? Comment on each in terms of accuracy, usefullness etc

A

Liver Biopsy -> most accurate however uncomfortable for individuals and not readily determined in living subjects

Plasma / Serum Retinol Concentration -> easy to perform but insensitive indicator (levels are maintained constantly over a wide range of dietary intakes)

Breast milk concentration -> this is thought of as quite a good indicator but obviously restricted to that one group of individuals

65
Q

What are the serum retinol concentrations for cut off of marginal and deficiency?

A

Deficiency:
10 micrograms / 100 ml
0.3 micro moles / litre

Marginal:
20 micrograms / 100ml
0.7 micro moles / litre

Foundations of Nutrition (13 decks)

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