Chapter 7: Vitamins and New Nutrients

Vitamins

= organic compounds that

• are not insufficiently produced in the body

• are naturally present in foods

• are necessary in small amounts to maintain normal functioning

• lead to specific deficiency symptoms when absent from the diet

Vitamins: Remarks

• Are essential FA and AA vitamins?

• Endogenous synthesis by microbial flora

• Synthesis capacity differs

  • according to animal species

  • according to conditions

• Relation trace element - vitamin

• Deficiency: difficult to detect and variable

Vitamins: General characteristics

= co-enzymes

Bonding to enzyme

• covalently bound as substrate

• strongly but non-covalently bound as substrate

  • Holo (with cofactor) vs apo (without cofactor)

• weakly bound as substrate

  • Holo (with cofactor) vs apo (without cofactor)

Utilisation

• vitamins need to be converted into active form so that they can be absorbed

Groups

group	vitamins
vitaminers	E
pro-vitamins	carotenoids and A
water soluble	B,C
fat soluble	A, D, E, K

Vitamins: General characteristics: Groups according to function

group	vitamins
involved in mono carbon transfer reactions	folate (M), B12, K and biotin
hormones	A and D
energy metabolism	B1, B2, B3, B5
anti-oxidants	C and E

Vitamins: General characteristics: Deficiencies

Vitamin	Deficiency
A	xerophtalmia
B1	beri-beri (dry and wet) → can be destructed by technology
B12 and folate	megaloblastic anemia → inhibited DNA and RNA synthesis
B3	pellagra → in parts of body that are exposed to the sun
C	scurvy
K	flora or fat disturbance, infants

Vitamin A (!)

Source

Animal	Plant
retinyl palmitate in liver and fatty fish	carotenoids in green and yellow-red vegetables
high bioavailability	Low bioavailability Conversion beta-carotene into retinol beta-carotene → retinal → retinol

Absorbation form

= retinol

Transport and storage of retinol

1) retinol is bound to cellular retinol binding protein (c-RBP) and esterified

2) Esterified form is transported in chylomicrons (CM) to the liver (stellate cells in liver)

3) Retinol is mobilised from the liver after release by a retinyl ester hydrolase (low during protein malnutrition and inhibited by vitamin E and vitamin K)

4) Retinol binds as trans isomer to the plasma retinol binding protein (p-RBP) → secreted by the liver with regulation by estrogens and Zn

5) Retinol binds in target organ (eye, testes, uterus) to specific c-RBP

Metabolism of retinol

What	From … to …	Function + (location)
Binding to a protein	retinol < - > holo-RBP	transport vitamin A (blood)
Esterification	retinol < - > retinyl esters	storage vitamin A (liver)
Conjugation	retinol < - > retinyl b-glucuronide	detoxification = only way to remove vitamin A when overdosis (bile / urine)
Fosforylation	retinol < - > retinyl phosphate	lipid-carrier for sugar rests
Glycosylation	retinyl phosphate < - > retinyl phosphomannose	glycoprotein synthesis (ephithelium)
Reversible oxidation	retinol < - > retinal	sight (eye)
Irreversible Isomerisation	retinal → retinoic acid	light sensitivity of eye

Functions of vitamin A

1. Vision

2. Immune function

3. Cell growth and differentiation

4. Skin and epithelial health

5. Anti-oxidant (beta-carotene)

Toxicity vitamin A

Too much →

• pregnancy dangers

• eye dangers

• neurological dangers

Vitamin D (source, metabolism, role in body, target groups, toxicity)

Source

• vitamin D’s are not abundant in nature, but their pro-vitamins ergosterol and 7-dehydrocholesterol are present in vegetable and animal food

Metabolism

• UV-light needed to form vitamins out of provitamins !!

• 1,25-diOH - cholecalciferol binds to vitamin D receptor protein in nucleus

Role in body

• in Ca-P homeokinesis

plasma concentration of Ca	pathway
Hypocalcaemia = low Ca-levels	PTH↑ → P diuresis + 25-OH-D hydroxylase ↑ → absorption Ca ↑ → bone mobilization Ca and P ↑
Hypercalcaemia = high Ca-levels	calcitonine in thyroid gland ↑ → Ca diuresis + 25-OH-D hydroxylase ↓ → absorption Ca ↓ → bone mobilisation Ca and P ↓

Target groups

• Breastfed > bottlefed infants

Toxicity

• excessive vitamin D → high 25-OH-D concentrations → bone weakening

Vitamin B9 (source, metabolism, risk-benefit)

= folic acid = folate

= M

Source

• in plants and animals as polyglutamyl derivates of tetrahydrofolic acid (FH4)

• Bioavailability dependent of vitamin C, Fe, conjugase inhibitors

Metabolism

1. Further oxidation to 5-methyl-FH4 (methionine)

2. B12 brings 5-methyl-FH4 back to FH4 so that FH4 is not stuck in 5-methyl-FH4

Risk-benefit

High intake of synthetic folic acid (>400 µg) can lead to accumulation of unmetabolized folic acid in the blood, competition with natural folates, and masking of vitamin B12 deficiency.

Toxicity

• masking of vitamin B12 shortage

  • Normally shortage of B12

    • Anemia (shortage of B9) + nerve complaints

  • Shortage of B12 + high B9

    • No anemia + nerve complaints → more difficult to see that this is a problem of B12

interactions B9 and B12

= from 5-methyl-FH4 to tetrahydrolate (FH4)

= donates methylgroup

Vitamin B12 (source, metabolism, role in body, target groups, toxicity)

= cyanocobalamin

Co+ in center !!

Source

• only by microbial synthesis

Metabolism

• uptake via active transport in ileum with IF (requires calcium)

• transport of adenosyl-B12 (animal) or methyl-B12 (human) via transcobalamines

Role in body

• Adenosyl-B12 → cofactor of Me-malonyl-CoA mutase

• Methyl-B12 → cofactor methionine synthase

Toxicity

• not toxic

Deficiency

• nerve problems

antioxidant vitamins

1. Vitamin E

2. Vitamin C

Antioxidant vitamins: vitamin E

• toxicity !!

antioxidant vitamins: vitamin C

toxicity because it becomes pro-oxidative!! → interferes with synthesis of collagen

Vitamin K

source

• plant: phylloquinones

• bacteria: menaquinones

• synthetic: menadion

Function

• prothrombin = role in blood clotting

• osteocalcin = skeleton

• carboxylation glu-residues increases Ca-binding properties

New nutrients