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Physiology 3003 > Lecture 11--Metabolism of vitamins > Flashcards

Lecture 11--Metabolism of vitamins Flashcards

1
Q

What are the lipid soluble vitamins

A

Vitamin A, D, E, K

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2
Q

How are the lipid soluble vitamins ABSORBED?

A

…by DIFFUSING through plasma membranes

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3
Q

How are the lipid soluble vitamins TRANSPORTED?

A

…in LIPOPROTEINS or complexed to SPECIFIC BINDING PROTEINS

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4
Q

How are lipid soluble vitamins stored?

A

Readily stored… predominantly stored in the liver

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5
Q

What are the water soluble vitamins?

A

B Vitamins

Vitamin C

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6
Q

How are the water soluble vitamins ABSORBED?

A

through specific CHANNELS

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7
Q

How are water soluble vitamins TRANSPORTED?

A

Dissolved in blood

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8
Q

What’s special about Vitamin B12?

A

Vitamin B12 does not have a specific channel/carrier protein on the surface of cells.
Needs to be actively transported COMPLEXED TO INTRINSIC FACTOR

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9
Q

How are water soluble vitamins stored?

A

Because they are HYDROPHILIC they are not readily stored .: a DAILY SUPPLY IS REQUIRED (in diet)

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10
Q

What are/is the precursor(s) for Vitamin A?

A

(1) PLANT form: B-CAROTENE

(2) ANIMAL form: RETINOL ESTER

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11
Q

What enzyme deficiency can lead to a vitamin A deficiency? This is specifically an issue for which group in the population?

A

A deficiency in the ENZYME that CONVERTS B-CAROTENE –> RETINOL can lead to a vitamin deficiency

Especially in VEGETARIANS (who aren’t getting Retinol ester (precursor for it A) in their diet.

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12
Q

Outline the processing of B-Carotene and retinol esters…

Gut:
Enterocyte:
Export into blood:

A

–B-CAROTENE:
Gut: B-carotene
Enterocyte: B-carotene–>retinAL –>RetinOL–>Retinol Ester –> CHYLOMICRON

–RETINOL ESTER:
Gut: Retinol ester –> Retinol
Enterocyte: Retinol –> Retinol Ester –> CHYLOMICRON

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13
Q

What are the modifications of vitamin A that occur in the liver? What function do they serve?

A

For EXPORT: Retinol ester==> RETINOL

For STORAGE: RETINOL ESTER

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14
Q

What is the STORAGE FORM of vitamin A? Where is it stored?

A

Retinol Ester

The liver

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15
Q

What is the ACTIVE FORM of vitamin A?

A

RETINOIC ACID

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16
Q

How is vitamin A transported in the blood?

A

Bound to RETINOL BINDING PROTEIN (RBP)

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17
Q

What is the MAIN ROLE of Vitamin A?

A

VISUAL PIGMENT

1) Retinol–converted–> Retinoic Acid (Active form) (in the retina
(2) Retinoid Acid + Opsin –> RHODOPSIN

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18
Q

What is RHODOPSIN? From what is Rhodopsin synthesised?

A

RHODOPSIN = the visual pigment. Used for PHOTO-TRANSDUCTION in the retina. Converts light –> biochemical messages enabling us to perceive light…

Opsin + Retinoid Acid (Active form of it A) = RHODOPSIN

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19
Q

What are the 3 general uses for Vitamin A?

A

(1) VISUAL PIGMENT (Retinoid acid + Opsin = Rhodopsin)
(2) TRANSCRIPTION COFACTOR (essential in embryonic development, excess/deficiency = TERATOGENIC)
(3) Form is used as a CHEMOTHERAPEUTIC (kills highly proliferative cells, causes cells to differentiate, big side effects)

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20
Q

What are the symptoms of a deficiency in vitamin A?

A

(1) Night blindness

(2) Follicular hyperkeratosis

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21
Q

What symptoms are there for toxicity of vitamin A?

A

(1) Vomiting
(2) Headache
(3) Impaired vision
(4) Weight loss
(5) Excessive bone growth (stimulates osteoblast metabolism)

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22
Q

What is the active form of Vitamin D?

A

CALICTRIOL (1,2,5-dihydroxy D3)

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23
Q

How is vitamin D transported in the blood?

A

Bound to VITAMIN D BINDING PROTEIN (VDBP)

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24
Q

Outline the processing/transport of vitamin D

A

SKIN: Cholesterol –> CHOLECALCIFEROL (vit D3)

LIVER: Cholecaliferol –> 2, 5 hydroxy D3

KIDNEY: 2, 5 hydroxy D3 –> CALITRIOL (1, 2, 5 dihydroxy-D3)

BLOOD: Calcitriol is bound to vitamin D binding protein (VDBP)

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25
Q

What is the function of vitamin D?

A

Primarily by role in Ca2+ METABOLISM
–maintain Ca2+ Balance

  • -> ++ Ca2+ absorption (small intestine)
  • -> ++ Ca2+ reabsorption (kidney)
  • -> ++ bone mineralisation
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26
Q

What is the effect of vitamin D on Ca2+ metabolism in the body?

A
  • -> ++ Ca2+ absorption (small intestine)
  • -> ++ Ca2+ reabsorption (kidney)
  • -> ++ bone mineralisation
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27
Q

Deficiency in vitamin D

A

= problems with bone metabolism

=> RICKETS (soft pliable bones, impaired ossification of osteoid)

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28
Q

How is Ca2+ absorbed?

A

TRANSCELLULAR ROUTE

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29
Q

What is the function of CALBINDIN?

A

> Found In the cytosol
Binds to Ca2+
LOWERS THE ACTIVE CONCENTRATION OF Ca2+ within the cell .: maintaining the [gradient] required for passive diffusion
Also stops it from being biologically active

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30
Q

How does vitamin D regulate Ca2+ absorption?

A

Transcellular absorption of Ca2+ is vitamin D DEPENDENT…

….Vitamin D activates the transcription of CAT 1 and Calbindin

31
Q

In which family of vitamins does vitamin E belong?

Which is the most biologically active form in this family?

A

TOCHOPHEROLS
4 members: alpha (a), beta (b), gamma (y), delta (d)

a-TOCHOPHEROLS = most biologically active form

32
Q

How is vitamin E transported from the;

(1) GUT –> LIVER?
(2) LIVER–>TARGET ORGANS?

A

(1) In CHYLOMICRONS

2) bound to a-TOCHOPHEROL TRANSPORTER PROTEIN (a-TTP

33
Q

What are the 2 main functions of vitamin E?

A

(1) ANTIOXIDANT (prevents free radical damage to PLASMA MEMBRANES by picking FRs and being Oxidised==can be RECHARGED by vitamin V and converted from OXIDISED form –> REDUCED form)
(2) COFACTOR (synthesis of unsaturated FAs in mitochondria)

34
Q

What is the result of vitamin E deficiencies?

A

(1) reduced fertility (in men)
(2) Peripheral neuropathy
(3) Anaemia

35
Q

What mutation/metabolic issue might lead to a vitamin E deficiency?

A

(1) a-TPP MUTATION

2) Fat absorption problem (Vit E= lipid soluble vitamin

36
Q

Toxicity in vitamin E

A

RARE

causes ++ bleeding

37
Q

Compare and contrast lipid and water soluble antioxidants

A

Vitamin E = lipid soluble antioxidant
Vitamin C = Water soluble antioxidant

They differ in that …
>Vitamin C typically prevents free radical damage (FRD) in the CYTOSOL of cells
WHEREAS
>Vitamin E typically prevents FRD to the outside of cells (plasma membranes, FFA etc.)

These differences are due to their different solubilities

38
Q

What is/are the precursor(s) for vitamin K?

A

1) PLANT form: K1 (PHYLLOQUINON)

2) Animal form: K2 (MENAQUINON)

39
Q

What is the FUNCTION of vitamin K

A

(1) Dominant role as COFACTOR IN BLOOD CLOTTING REACTIONS (=’koagulations vitamin’)
(2) Bone metabolism
(3) Cell growth
(4) Bone mineralisation

40
Q

Vitamin K plays a ‘secondary role’ in blood clotting reactions/bone metabolism. What does this mean?

A

Vitamin K is an important cofactor in BCR & bone metabolism because it CONVERTS PROTEINS involved in these processions from INACTIVE –> ACTIVE forms through POST-TRANSLATIONAL MODIFICATION.

41
Q

What post-translational modifications to proteins are initiated by vitamin K?

A

Converting proteins involved in blood clotting reactions/bone metabolism from inactive–>active forms by CARBOXYLATION OF GLUTAMATE RESIDUES ON THE GLA DOMAINS OF PROTEINS

42
Q

What is the toxicity to vitamin K?

A

No known toxicity

43
Q

How is vitamin K used in a clinical setting?

A

Clinical application in newborns
Babies are not good fat absorbers .: often vitamin K deficient (initially) which means they are prone to excessive bleeding if they ‘spring a leak’ .: injecting newborns with vitamin K promotes blood clotting when/if neccessary

44
Q

What are the consequences of a DEFICIENCY in vitamin K?

A

(1) Blood clotting disorders

2) Can lead to OSTEOPOROSIS (due to role in bone metabolism

45
Q

What could cause a vitamin K deficiency?

A

RARE

Liver failure –> absence of bile secretion –> not absorbing fats

46
Q

What are the general functions of the B vitamins?

A

(1) COFACTORS IN METABOLIC PROCESSES (protein, CHO & fat metabolism) .: essential in producing energy
(2) COENZYMES are derived from Vitamin B

47
Q

Name: Vitamin B1

A

B1= THIAMINE

48
Q

Name: Vitamin B2

A

B2= RIBOFLAVIN

49
Q

Name: Vitamin B3

A

B3= NIACIN

50
Q

Name: Vitamin B5

A

B5= PANTOTHENIC ACID

51
Q

Name: Vitamin B6

A

B6= PYRIDOXINE & PYRIDOXAMINE

52
Q

Name: Vitamin B7

A

B7= BIOTIN

53
Q

Name: Vitamin B9

A

B9= FOLIC ACID

54
Q

Name: Vitamin B12

A

B12= COBALAMIN

55
Q

Recite all the water soluble vitamins (with proper names) to the tune of twinkle twinkle

A 
1 is thiamine 
Riboflavin's 2
3 is niacin 
...Hey B4 where are you?
5 is pantothenate 
Pyridoxine's 6
7 is biotin
and 12's cobalamin 
Those are the B's then comes C and FOLATE (B9) 
ANDDD THOSE WERE ALL THE WATER SOLUBLE VITAMINS I ATE
56
Q

What is the active coenzyme of B1

A

TPP (Thiamin pyrophosphate)

57
Q

What is the active coenzyme of B2

A

FAD/FADH

58
Q

What is the active coenzyme of B3

A

NADH/NADH & NADP

59
Q

What is the active coenzyme of B5

A

Acetyl CoA

60
Q

What is the active coenzyme of B6

A

PLP

61
Q

What is the active coenzyme of B7

A

Biotin

62
Q

What is the active coenzyme of B9

A

THF

63
Q

What is the active coenzyme of B12

A

B12 (cobalamin)

64
Q

What causes BERI-BERI? Symptoms?

A

Beri Beri is caused by severe THIAMINE (B1) deficiency

  • -severe muscle weakness
  • -Muscle wasting
  • -Delerium & memory loss
65
Q

What causes Pellagra? Symptoms? Who is at an increased risk?

A

Severe NIACIN (B3) deficiency

x4 D’s:

(1) Diarrhoea
(2) Dermatitis (loss of rapidly proliferating cells)
(3) Dementia (Neuronal activity requires a lot of energy)
(4) Death

Increased risk in

(1) longterm ALCOHOLICS (due to reduced vitamin absorption, esp niacin)
(2) POOR DIET (e.g. corn based diets are low in tryptophan)

66
Q

B3 (niacin) is synthesised from _______ in the ______.

It’s rate of synthesis is ____ and requires vitamin _______.

A

from TRYPTOPHAN (essential AA)

in the LIVER

rate of synthesis is SLOW

requires vitamin B6 (pyridoxine)

67
Q

Which vitamin is involved in nucleotide/nucleic acid synthesis?

A 
Vitamin B9 (Folate) 
The backbone of folate is used to synthesise purines & pyrimidines (essential for NT/NA synthesis)
68
Q

What is the biologically active form of vitamin C?

A

L-enantiomer = biologically active form

69
Q

What are the functions of vitamin C?

A

(1) ANTIOXIDANT (preventing FRD in cytosol)
(2) COFACTOR in some metabolic processes (synthesis of adrenaline/dopamine)
(3) COLLAGEN SYNTHESIS (effects of vit C deficiency = symptomatic scurvy due to this function)

70
Q

What function of vitamin C leads to symptomatic scurvy in Vit. C deficiency?

A

The role of vit. C in COLLAGEN SYNTHESIS

71
Q

What lifestyle factors can increase risk for developing a vitamin B7 (biotin) deficiency?

A

eating a lot of raw egg whites over long period drags out B7!

72
Q

What are the results of a moderate vitamin C deficiency?

A
  1. fatigue
  2. personality change
  3. decline in psychomotor performance & motivation
73
Q

What are the results of severe vitamin C deficiency?

A

SYMPTOMATIC SCURVY

  • spongy gums
  • liver spots on skin
  • bleeding from mucous membranes
74
Q

What are the two states in which vitamin C exists? Why does it exist in multiple states?

A

(1) ASCORBATE (vit C) (reduced)
(2) DEHYDROASCORBATE (oxidised form vit C)

Exists in two states due to it’s role as an antioxidant

Physiology 3003 (15 decks)

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