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NUTR*3210 > UNIT 9: MICRONUTRIENTS I: Iodide, Vitamin A > Flashcards

UNIT 9: MICRONUTRIENTS I: Iodide, Vitamin A Flashcards

1
Q

What is a SHR and what is it’s function?

A

Steroid hormone receptor

- binds hormone ligands –> transcription factors (bound complex) regulate gene expression

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2
Q

What is the difference between the 2 types of SHR?

A

Type 1: cytosol
- bind steroids only
Types 2: nucleus
- bind steroids and non steroids

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3
Q

All ligands that bind to SHR are steroid hormones.

True/False

A

False
Type II bind both
(only vitD is steroid hormone from cholesterol)

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4
Q

Iodide, Vitamin A, Vitamin D bind ____

A

SHR Type II

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5
Q

I2 is ___

I- is ___

A

Iodine (elemental) I2

IodiDe = anion I-

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6
Q

Which form is found in diet iodine/iodide.

A

IodiDe (I-)

absorbed well in GIT

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7
Q

What is a good source of iodide?

A

Seafood - higher iodide intakes in costal populations

- fortification of iodide in salt

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8
Q

What is the main role of iodide in the body?

A

Synthesis of thyroid hormones

Iodide is converted to T3 and T4

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9
Q

What is the bioactive form of thyroid? What does the other form act as?

A

T3 is bioactive form
made from T4 (thyroxin)
T4:T3 ratio is 20:1 since T4 is a reserve pool

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10
Q

The thyroid bioactive form binds to the SHRII domain called ___

A

Thyroid Hormone Receptor (THR)

T3 binds THR

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11
Q

Which enzyme converts T4 –> T3

A

5’deiodinase enzyme

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12
Q

What mineral is required in order for T4 –> T3?

A

Selenium required for 5’deiodinase enzyme

Deficiency and dysregulate metabolic rate

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13
Q

What happens if metabolism rate is dysregulated?

A

Dysregulation by selenium deficiency

  • Hypothalamus senses this change in metabolic rate
  • Thyroid stimulating hormone (TSH) secreted to blood stream –> increase metabolic rate
  • TSH arrives to thyroid cell and up regulates iodide transport and increase in T3 and T4 production
  • Increase T3 and T4 synthesis
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14
Q

Iodide deficiency leads to:

A
  • chronic secretion of TSH fro hypothalamus
  • enlargement of thyroid
  • increase T3 and T4 production (but depends on deficiency)
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15
Q

A radical is formed in the thyroid via:

A

iodide + hydrogen peroxide

= reactive IODIDE species

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16
Q

What does the hydrogen peroxide radical in the thyroid attack?

A

thyroglobulin - tyrosine rich protein in thyroid gland

  • iodine added to tyrosine ring
  • iodized thyroglobulin cross linked together
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17
Q

T3 is ____ and can cross biological mebranes

A

lipophillic

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18
Q

T3 binds ___ in the ____

A

T3 binds THR (thyroid hormone receptor) in the nucleus
complex
- incr. transcription

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19
Q

Free THR in the nucleus leads to

A

decrease in transcription

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20
Q

T3 signalling occurs with good nutritional status and signals ___

A

growth hormone synthesis

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21
Q

Iodide deficiency is called ____

A

goiters

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22
Q

Low dietary and blood iodide, thyroid cannot produce T3 and T4. What happens?

A
  • Pituitary increases blood TSH secretion
  • excessive stimulation
  • hyperplasia
  • hypertrophy
    = goiters
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23
Q

Iodine deficiency during pregnancy can lead to ___

A

Cretinism/ cognitive impairment

  • deficiency in maternal iodide
  • stunts mental and physical growth
  • inability to walk or talk
24
Q

Vitamin A is a _____ vitamin.

A

fat-soluble vitamin

25
Q

These are the 5 forms of vitamin A. Distinguish them.

  1. Retinol
  2. Retinal
  3. Retinyl palmitate
  4. Retinoic acid
  5. Carotenoids
A
  1. alcohol form
  2. aldehyde form
  3. ester form (retinol + palmityl CoA)
  4. carboxylic acid form (binds SHRII)
  5. i.e. beta carotene (greatest vitamin A activity)
26
Q

Vitamin A is obtained from:

A

Plants: carotenoids
Animals: retinyl esters
(metabolized to retinol, retinal, retinol palmitate, retinoid acid)

27
Q

What is the main source of vitamin A from plants?

A 
beta carotene (carotenoids)
also metabolized to (1-->4)
28
Q

The digestion of vitamin A compounds like retinyl ester and beta carotenes is from a _____

A

fat droplet from the stomach
- goes through lipid digestion
(triglycerides, phospholipids + vitamin A compounds)

29
Q

Retinyl ester is broken down by what enzyme?

A

Pancreatic retinyl esterase

retinyl ester –> palmitate + free retinol

30
Q

Beta carotene from the fat droplets goes to ___

A

passive diffusion via the brush border

does not require digestion

31
Q

What are the two metabolic fates of beta-carotene?

A
  1. incorporated into chylomicron WITHOUT modification
  2. clipped to retinal, reduced to retinol
    - via enzyme 15,15’dioxygenase
    retinol –> retinyl palmitate –> incorporated chylomicron

(both incorporated into chylomicron: one as beta carotene, one as retinyl palmitate)

32
Q

15,15’dioxygenase catalyzes retinal –> retinol

- what regulates this enzyme?

A

vitamin A status

- high levels inhibit this

33
Q

Chylomicrons, once in circulation, is taken up by what regulatory organ?

A

The liver

  • as a chylmomicron remnant
  • releases beta carotene and retinyl palmitate in liver (none is released in tissues)
34
Q

What happens to beta carotene once it arrives in the liver?

A

incorporated into VLDL

- stored in adipose tissues (uncontrolled)

35
Q

What happens to retinyl palmitate once it arrives in the liver?

A

retinyl palmitate –> retinol
retinol + RBP (retinol binding protein)
= retinol-RBP binding complex

retinol-RBP released to blood

36
Q

In the blood, what form of vitamin A is present? (after the liver)

A

retinol-RBP

37
Q

Once it reaches the target tissue destination, what happens retinol-RBP?

A

retinol-RBP is converted to it’s active forms at the tissues

  1. 11-cis retinal (retina)
  2. Retinoic acid
38
Q

Retinol-RBP acts as a ____ to vitamin A

A

The inactive precursor acts as a homeostatic setpoints.

*active hormones are NOT setpoints

39
Q

Which form of vitamin A regulates night vision?

A

11-cis retinal

40
Q

What are other biological roles of vitamin A?

A
  • cell differentiation
  • growth
  • synthesis of glycoproteins
  • reproduction
  • bone metabolism
  • immune function
41
Q

What form of vitamin A regulates its biological roles?

A

retinoic acid (regulated by binding to type II SHR)

42
Q

What is rhodopsin?

A

= 11-cis retinal + opsin

  • Retinol-RBP (Blood) –> retinol (rod cells) –> all-trans retinal –>11-cis retinal
    + opsin
43
Q

What happens when light hits the cis bond in rhodopsin?

A
  • molecule bounces back to all-trans-retinal form to release opsin
  • transmit nerve impulse (dim purple light)
44
Q

Retinoic acid binds to:

Where?

A
  • retinoic acid receptors (RAR)
  • retinoid X receptors (RXR)

in the nucleus - lipid soluble

45
Q

What happens to the retinoic acid/receptor complex?

A

dimerizes and binds to promotor region of DNA –> transcription of mRNA –> ribosome assembly –> proteins

46
Q

Proteins regulated by vitamin A including ___growth hormones; ____ collagenase

A
  • increase growth hormones

- decreased collagenase

47
Q

Vitamin A is really important to ______ differentiation

A

All epithelial cell differentiation
(lungs, trachea, cornea, sclera, GIT, esophagus, mammary, skin)

Retinoic acid signals differentiation

48
Q

What happens in terms of epithelial differentiation if there is a deficiency in vitamin A?

A

Deficiency –> impaired gene control and secretes hard keratin instead of mucous

49
Q

Deficiency in ____ leads to night blindness.

A

11 - cis retinal

50
Q

Impaired epithelial differentiation is a deficiency in _____

A

Retinoic Acid binding to type II SHR

  • keratinization
  • impaired growth of bones/teeth
  • impaired fertility (sperm formation)
  • birth defects
51
Q

Vitamin A deficiency causes _____ blindness.

A

Reversible/preventable

keritinization of cornea - severe blindness

52
Q

What are Bitot’s spots?

A

reversible buildup of keratin outside the cornea (impaired mucosal cell differentiation)

53
Q

What is hypervitaminosis A?

A

Vitamin A toxicity

54
Q

What does vitamin A toxicity cause?

A

liver damage

  • excess retinyl palmitate in the stellate cells of the liver
  • stellate cells proliferate
  • scar tissue
  • liver failure
55
Q

Therapeutic index of vitamin A is ______

A

narrow

TI = 3

56
Q

Are carotenoids toxic?

A

no

- they do not stress excess retinol in the liver (goes straight to VLDL to adipose)

NUTR*3210 (15 decks)

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