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GI Week 3 > Nutrition: Fat-soluble vitamins > Flashcards

Nutrition: Fat-soluble vitamins Flashcards

1
Q

WHat are the four fat=soluble vitamins?

A

A
D
E
K

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2
Q

What is the biologically active form of vitamin A?

A

all-trans-retinol

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3
Q

What are the three structural elements of all-trans-retinol?

A

beta=ionone ring
branched polyunsaturated acyl chain
alcohol at the end

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4
Q

In the body, the alcohol of trans-retinol can be converted to what three options?

A

aldehydde
carboxylic acid
ester with a fatty acid

the biological function varies depending on the form

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5
Q

What are the main DIETARY forms of vitamin A?

A

retinyl-acyl esters and carotenes (alpha or beta)

they can all be converted to all-trans-retinol

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6
Q

What are some foods that are high in vitamin A?

A

any red, yellow or orange fruit and vegetable

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7
Q

Vitamin A is taken up by gut epithelial cells in micelles (fat soluble), but what are the two forms by which is can enter the blood?

A
  1. retinoic acid carried by albumin

2. retinyl ester form carried in the chylomicron

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8
Q

What cells in the liver will serve as a reservoir for Vitamin A storage? In what space?

A

stellate cells in the space of Disse

they will maintain normal serum vitamin A concentrations

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9
Q

What forms of vitamin A will leave the hepatocyte after processing?

A
  1. retinol goes out to the serum in complex with transthyretin and retinol binding protein
  2. retinoic acid goes out to the serum complexed wtih albumin
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10
Q

What is the main function of retinol?

A

hugely important for vision

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11
Q

Describe how retinol is used in vision?

A
  1. cis-retinal is bound to the protein opsin in the photoreceptor to form rhodopsin
  2. when light hits the photoreceptor the cis form changes to trans-retinal
  3. this makes the opsin and retinal let go of each other
  4. free opsin activates a heterotrimeric G protein
  5. You get closure of a Na+ channels and hyperpolarization of the rod, which signals to the neuron
  6. After a while the trans form will switch back to cis-retinal and it will recombine with opsin and shut off the signal
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12
Q

Retinoic acid will act as a ligand to activate which ligand-activated transcription factors?

A

Retinoic acid receptor
retinoic x receptor
peroxisome proliferator activated receptor

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13
Q

WHat are 5 general results of activation of these transcription factors?

A
  1. differentiation of goblet cells
  2. inhibition of keratinization
  3. apoptosis of cancer cells
  4. maturation of dendritic cells
  5. recruitment of antibody secreting cells to the small itnestine
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14
Q

Carotenes can be cut by a monooxygenase to form two molecules of retinal, but what do they do if they’re not cut?

A

act as antioxidants

their double bonds can neutralize singlet oxygen and free radicals

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15
Q

What are symptoms of vitamin A deficiency

A

Eyes: night blindness, xeropthalmia (keratinization), Bitot’s spots

anorexia, retarded growth, increased susceptibility to infections, alopecia, keratinization of epithelial cells

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16
Q

How do you diagnose vitamin A deficiency?

A

use the relative dose response

  1. measure plasma retinol concentratino
  2. give oral bolus of retinyl-palmitate
  3. measure plasma retinol concentration again after 5 hours

The higher the RDR, the more the body is relyingon short term dietary vitamin K that liver and adipose stores - suggests depletion

RDRs over 20% indicate the liver is not maintaining serum vitamin K

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17
Q

What is the tolerable upper limit for vitamin A?

A

3,000 micrograms RAE?day

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18
Q

What happens in hypervitaminosis A?

A 
nausea, vomiting
blurred vision
headache
desquamation of skin
alopecia
ataxia
liver damage (from excess cstellate cell growth and proliferation)
conjuncitivites and eye pain

can also be a teratogen in very high doses

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19
Q

What are the two dietary forms of vitamin E? How do they differ from each other>

A

tocopherols - completely saturated acyl chain

tocotrienols - polyunsaturated acyl chain

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20
Q

What foods have vitamin E in abundance?

A

palm oil
sunflower oil
canola oil
wheat germ

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21
Q

What is the main function of vitamin E?

A

It functions as an antioxidant in lipid bilayers of intracellular and plasma membrnaes

22
Q

What vitamin is necessary to allow vitamin E to be reused after it’s oxidized?

A

vitamin C is required to reduce it back to the form in which it can work as an antioxidant

23
Q

Absorption and metabolism of what other vitamin is inhibited by vitamin E?

A

K

24
Q

Vitamin E deficiency is rare, but can occur in people with absorption problems. What are the symptoms?

A

myopathy
hemolytic anemia
peripheral neuropathy
ataxia with loss of vibratory sense

25
Q

What is the main form of vitamin K in the diet? What foods is it abundant in?

A

Phylloquinone in leafy green vegetables

26
Q

What’s the synthetic vitamin K used in animal feed?

A

menadione

27
Q

What happens to the phylloquinone in our gut? What is the new name for it?

A

the gut bacteria ferment is and put desaturations into the 5-carbon repeating acyl chain (that was completely saturated in the phylloquinone form)

now called menaquinone

28
Q

Where is excess vitamin K stored?

A

cellular membranes throughout the body, but especially in the lung, kidney, bone marrow and adrenal glands

29
Q

What is VItamin K necessary for?

A

It’s a cofactor required for gamma-glutamyl carboxylase of coagulation factors II, VII, IX and X.

30
Q

What anticoagulating drug works via the vitamin K-dependent gamma-carboxylation of coagulation factors? How?

A

Warfarin

It inhibits Vitamin K epoxide reductase, which is necessary to reduce the vitamin K back into the form required as the cofactor

31
Q

Vitamin K deficiency really only occurs in infants and people with absorption disorders, but what are the symptoms?

A

severe deficiency manifests as a coagulatoin disorder with increased prothrombin time and increased bleeding

32
Q

What happens in vitamin K toxicity?

A

It’s not described - there’s no TUL for vitamin K

Menadione can cause liver toxicity at high doses

33
Q

What foods have vitamin D?

A

primarily in foods of animal origin such as liver, eggs, fatty fish

also shitake muschrooms and fortified in many dairy products

34
Q

How can we get vitamin D if we don’t eat it?

A

It can be synthesized de novo from cholesterol

35
Q

What organs are required to make active vitamin D from cholesterol?

A

skin, liver and kidneys

36
Q

What happens in the skin to cholesterol?

A

UV light breaks one of the rings on the cholesterol open to yiel cholecalciferol

37
Q

What form is most dietary vitamin D in?

A

cholecalciferol

38
Q

What happens to cholecalciferol in the liver?

A

It gets hydroxylated at the 25 carbon to 25-hydroxycholecalciferol

39
Q

Why is 25-hydroxycholecalciferol the form we look for to see if someone is deficient?

A

It’s the predominant form circulating in the blood

40
Q

What happens to the 25-hydroxycholecalciferol in the kidney?

A

It’s acted on by 1-alpha-hydroxylase to add an additional hydroxyl to the 1 carbon

yields active vitamin D = 1,25-Dihydroxycholecalciferol

41
Q

Which hydroxylation step is regulated? How?

A

the 1-alpha hydroxylase in the kidney is upregulated by parathyroid hormone

42
Q

When is parathyroid hormone released?

A

produced by the parathyroid in response to low calcium concentrations

43
Q

Thus, what is the main purpose of vitamin D in the body?

A

It regulates calcium homeostasis by increasing Ca uptake from the gut and increasing mobilization of bone Ca

44
Q

Vitamin D promotes calcium uptake and mobilization through what mechanism?

A

It binds to the vitamin D receptor, which is will then dimerize and act as a transcription factor to promote expression of calcium transport proteins like calbindin, TRPV6, and calcium ATPase bumps

45
Q

What does TRPV6 do?calbindin?

A

TRPV6 is the luminal calcium transporter on the gut epithelial cells

calbindin is the molecule that carries Ca intracellularly until it reaches the Ca ATPase on the basolateral side

46
Q

What does vitamin D do to claudin to affect calcium uptake?

A

it messes with is such that the tight junctions become a little less tight, allowing Ca2+ to move paracellularly as well

47
Q

What happens in vitamin D deficiency?

A

Rickets, characterized by seizures, growth retardation, failure of bone mineralization and alopecia

48
Q

What happens in vitamin D toxicity?

A

It’s the most likely vitamin to have toxic effects!!!!!!

calcification of soft tissues like kidneys, heart, lungs and blood vessels (too mch Ca2+ mobilization), hyperpphosphatemia from bone breakdown and HTN

49
Q

At what serum levels do the toic effects begin?

A

when serum 25-OHD3 is over 500 ng/ml

50
Q

Describe how the wnt/catenin signalling works in the colon under normal conditions..

A

In the absence of Wnt, beta catenin is phosphorylated by the APC complex, resulting in ubiquitination and degradation in the proteasome

stems cells secrete Wnt, which inhibit APC. Thus, beta catenin isn’t phosphorylated or broken down and it can build up and go to th enucleus where it binds Lef1/TCF and activates transcription of target genes like cyclin D1 and myc - helps them stay de-differentiated

51
Q

What are the proposed effects of vitamin D on this pathway in terms of colon cancer?

A

it seems to physically bind beta-catenin such that it can’t promote uncontrolled cell proliferation and thus helps protect against colon cancer

52
Q

Min+ mice (with tumors) that lack any VDR will have more or less cyclin D expression?

A

More - no VDR, more free beta catenin to go turn on expression of cyclin D

GI Week 3 (15 decks)

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