UNIT 9: MICRONUTRIENTS I: Iodide, Vitamin A Flashcards

(56 cards)

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
These are the 5 forms of vitamin A. Distinguish them. 1. Retinol 2. Retinal 3. Retinyl palmitate 4. Retinoic acid 5. Carotenoids
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
Vitamin A is obtained from:
Plants: carotenoids Animals: retinyl esters (metabolized to retinol, retinal, retinol palmitate, retinoid acid)
27
What is the main source of vitamin A from plants?
``` beta carotene (carotenoids) also metabolized to (1-->4) ```
28
The digestion of vitamin A compounds like retinyl ester and beta carotenes is from a _____
fat droplet from the stomach - goes through lipid digestion (triglycerides, phospholipids + vitamin A compounds)
29
Retinyl ester is broken down by what enzyme?
Pancreatic retinyl esterase | retinyl ester --> palmitate + free retinol
30
Beta carotene from the fat droplets goes to ___
passive diffusion via the brush border | does not require digestion
31
What are the two metabolic fates of beta-carotene?
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
15,15'dioxygenase catalyzes retinal --> retinol | - what regulates this enzyme?
vitamin A status | - high levels inhibit this
33
Chylomicrons, once in circulation, is taken up by what regulatory organ?
The liver - as a chylmomicron remnant - releases beta carotene and retinyl palmitate in liver (none is released in tissues)
34
What happens to beta carotene once it arrives in the liver?
incorporated into VLDL | - stored in adipose tissues (uncontrolled)
35
What happens to retinyl palmitate once it arrives in the liver?
retinyl palmitate --> retinol retinol + RBP (retinol binding protein) = retinol-RBP binding complex retinol-RBP released to blood
36
In the blood, what form of vitamin A is present? (after the liver)
retinol-RBP
37
Once it reaches the target tissue destination, what happens retinol-RBP?
retinol-RBP is converted to it's active forms at the tissues 1. 11-cis retinal (retina) 2. Retinoic acid
38
Retinol-RBP acts as a ____ to vitamin A
The inactive precursor acts as a homeostatic setpoints. *active hormones are NOT setpoints
39
Which form of vitamin A regulates night vision?
11-cis retinal
40
What are other biological roles of vitamin A?
- cell differentiation - growth - synthesis of glycoproteins - reproduction - bone metabolism - immune function
41
What form of vitamin A regulates its biological roles?
retinoic acid (regulated by binding to type II SHR)
42
What is rhodopsin?
= 11-cis retinal + opsin - Retinol-RBP (Blood) --> retinol (rod cells) --> all-trans retinal -->11-cis retinal + opsin
43
What happens when light hits the cis bond in rhodopsin?
- molecule bounces back to all-trans-retinal form to release opsin - transmit nerve impulse (dim purple light)
44
Retinoic acid binds to: | Where?
- retinoic acid receptors (RAR) - retinoid X receptors (RXR) in the nucleus - lipid soluble
45
What happens to the retinoic acid/receptor complex?
dimerizes and binds to promotor region of DNA --> transcription of mRNA --> ribosome assembly --> proteins
46
Proteins regulated by vitamin A including ___growth hormones; ____ collagenase
- increase growth hormones | - decreased collagenase
47
Vitamin A is really important to ______ differentiation
All epithelial cell differentiation (lungs, trachea, cornea, sclera, GIT, esophagus, mammary, skin) Retinoic acid signals differentiation
48
What happens in terms of epithelial differentiation if there is a deficiency in vitamin A?
Deficiency --> impaired gene control and secretes hard keratin instead of mucous
49
Deficiency in ____ leads to night blindness.
11 - cis retinal
50
Impaired epithelial differentiation is a deficiency in _____
Retinoic Acid binding to type II SHR - keratinization - impaired growth of bones/teeth - impaired fertility (sperm formation) - birth defects
51
Vitamin A deficiency causes _____ blindness.
Reversible/preventable | keritinization of cornea - severe blindness
52
What are Bitot's spots?
reversible buildup of keratin outside the cornea (impaired mucosal cell differentiation)
53
What is hypervitaminosis A?
Vitamin A toxicity
54
What does vitamin A toxicity cause?
liver damage - excess retinyl palmitate in the stellate cells of the liver - stellate cells proliferate - scar tissue - liver failure
55
Therapeutic index of vitamin A is ______
narrow | TI = 3
56
Are carotenoids toxic?
no | - they do not stress excess retinol in the liver (goes straight to VLDL to adipose)