MICRONUTRIENTS

VITAMINS
 Coming from the Latin term Vita, meaning
‘Life’ and found to be chemically an ‘amine’,
vitamines were changed to the common term
we recognize today ‘vitamins’, once it was
found that not all vitamins were amines and
hence the ‘e’ was dropped.

 Nutritionally, they form a cohesive group of

organic compounds that are required in the
diet in small amounts (micrograms or
milligrams per day) for the maintenance of
normal health and metabolic integrity.
 For a compound to be considered a vitamin,
it must be shown to be a dietary essential.
Its elimination from the diet must result in a
more-or-less clearly defined deficiency
disease, and restoration must cure or
prevent that deficiency disease.
 There are two major classification of vitamins:
 Fat soluble vitamins
 Vitamin A (Retinol)
 Vitamin D (Cholecalciferol)
 Vitamin E (Tocopherol)
 Vitamin K
 Water soluble vitamins
 Vitamin B1 (Thiamin)
 Vitamin B2 (Riboflavin)
 Vitamin B3 (Niacin)
 Vitamin B5 (Pantothenic Acid)
 Vitamin B6 (Pyridoxine)
 Vitamin B7 (Biotin)
 Vitamin B9 (Folate)
 Vitamin B12 (Cobalamin)
 Vitamin C (Ascorbic Acid)
FAT SOLUBLE VITAMINS
 Fat Soluble vitamins are rich in aliphatic and
aromatic side chains, with less hydroxyl
groups for which they are primarily non-polar
and soluble only in lipids and fats and usually
requires to be transported in the body by
means of chylomicrons.
WATER SOLUBLE VITAMINS
 water soluble vitamins have more hydroxyl
and nitrogen in their structure, enabling
them to form more hydrogen bonds and
making them polar in nature. Therefore,
water soluble vitamins dissolve in water and
are usually excreted via urine from the body
when in excess, except for Vitamin B12 due its
complex structure
VITAMIN A: RETONOIDS AND
CAROTENOIDS
 Vitamin A deficiency is a serious problem of
public health nutrition, second only to protein-
energy malnutrition worldwide, and is probably
the most important cause of preventable
blindness among children in developing countries.

 In addition to primary deficiency of the vitamin,

secondary (functional) vitamin A deficiency
results from protein-energy malnutrition,
because of impaired synthesis of the plasma
retinol binding protein (RBP) that is required for
transport of the vitamin from liver reserves to its
sites of action.
 Significant sources of such preforms of
Vitamin A are carrots, tomatoes, peaches,
sweet potatoes, beef and cod liver. It’s a fat-
soluble vitamin, which consists of a 6
membered ring attached with an 11-carbon
side chain.
 Functions of Vitamin A:
 Promotes good eye sight by producing the pigment,
rhodopsin, in eye by means of Wald’s visual cycle.
 Retinoic acid acts a gene regulator, controlling the
biosynthesis of cholesterol, membrane glycoproteins
and glycosaminoglycans.
 Controls the rate of gluconeogenesis in the liver by
stimulating transcription of phosphor-enol pyruvate
carboxykinase enzyme.
 Involved in cellular differentiation of epithelial cells,
spermatogenesis and in the growth and development
of neoplasm.
 Reduces risk of cardiovascular diseases, due to
antioxidant traits of Beta carotene.
 Helps to maintain healthy teeth, skeletal and soft
tissues (Vitamin A).
 Known to help with immune function (Vitamin A).
 The main physiologically active forms of
vitamin A are retinaldehyde and retinoic
acid, both of which are derived from retinol.

 Retinaldehyde functions in the visual system

as the prosthetic group of the opsins, which
act as the signal transducers between
reception of light in the retina and initiation
of the nervous impulse.

 Retinoic acid modulates gene expression and

tissue differentiation, acting by way of
nuclear receptors.
ABSPORTION AND METABOLISM
 In plasma, the more hydrophobic carotenoids
are deep within chylomicrons or very low-
density lipoproteins, whereas the more polar
hydroxycarotenoids are at the surface, and
therefore potentially available for transfer
between plasma lipoproteins and uptake into
tissues.
 At physiological levels of intake, retinol uptake
into enterocytes is by facilitated diffusion from
the lipid micelles. When the transport protein in
the intestinal mucosal brush border cells is
saturated, there is also passive uptake of
retinol.
 Within the enterocyte, retinol is bound to
cellular retinol binding protein (CRBP II) and is
esterified by lecithin-retinol acyltransferase
(LRAT), which uses phosphatidylcholine as the
fatty acid donor.

 Then the retinyl esters enter the lymphatic

circulation and then the bloodstream (in
chylomicrons), together with dietary lipid and
carotenoids.

 A small proportion of dietary retinol is oxidized

to retinoic acid, which is absorbed into the
portal circulation and bound to serum albumin.
Some retinyl esters are also transferred into
the portal circulation.
LIVER STORAGE AND RELEASE OF
RETINOL
 Tissues can take up retinyl esters from
chylomicrons, but most is left in the
chylomicron remnants that are taken up into
the liver by endocytosis.
 The retinyl esters are hydrolyzed at the
hepatocyte cell membrane, and free retinol
is transferred to the RER, where it binds to
apo-RBP.
 Holo-RBP then migrates through the smooth
endoplasmic reticulum to the Golgi and is
secreted as a1:1 complex with the thyroid
hormone binding protein, transthyretin
 METABOLIC FUNCTIONS OF VITAMIN A

 Vitamin A has four metabolic roles:

1. as the prosthetic group of the visual
pigments;
2. as a nuclear modulator of gene expression;
3. as a carrier of mannosyl units in the
synthesis of hydrophobic glycoproteins; and
4. in the retinoylation of proteins.
GENOMIC ACTIONS OF RETINOIC
ACID
 Retinoic acid has both a general role in
growth and a specific morphogenic role in
development and tissue differentiation.
 These functions are the result of genomic
actions, modulating gene expression by
activation of nuclear receptors. Both
deficiency and excess of retinoic acid cause
severe developmental abnormalities.
VITAMIN A DEFICIENCY
(XEROPHTHALMIA)
 Mild deficiency results in impaired dark
adaptation; as the deficiency progresses,
there is inability to see in the dark (night
blindness).
 the recycling of retinaldehyde to reform
rhodopsin is the rate limiting step in the
visual cycle.
 As the deficiency progresses, there is
keratinization of the cornea. At this stage,
the condition is still reversible
ASSESSMENT OF VITAMIN A
NUTRITIONAL STATUS
 An early sign of vitamin A deficiency is
impaired dark adaptation – an increase in the
time taken to adapt to seeing in dim light.
 Plasma Concentrations of Retinol and -
Carotene
Fatty fish such as tuna, salmon, dark green
vegetables, soy, egg yolk, beef liver are rich in
vitamin D. Sunlight has also been found to be a
source of vitamin D for humans, since the UV light
in sun rays, enables skin to make its own vitamin
D. However, sunscreens can damage 95% of the
skin’s ability to produce vitamin D, leading to
deficiency. There are two main forms of vitamins-
D3, known as cholecalciferol (the natural form
obtained from animal source in diet and sun) and
ergocalciferol (vitamin D2), which is synthesized in
the laboratory
TOXICITY OF VITAMIN A
1. The skin: excessive dryness, scaling and chapping of
the skin, desquamation, and alopecia.
2. The central nervous system: headache, nausea,
ataxia, and anorexia, all associated with increased
cerebrospinal fluid pressure.
3. The liver: hepatomegaly, hyperlipidemia, and
histological changes in the liver, including increased
collagen formation. Alcohol potentiates the
hepatotoxicity of vitamin A.
4. Bones: joint pains, thickening of the long bones,
hypercalcemia, and calcification of soft tissues, but
with reduced bone mineral density.High intakes of
vitamin A are associated with an increased rate of loss
of bone mineral density with age,
 VITAMIN D
 Vitamin D is not strictly a vitamin, rather it is
the precursor of one of the hormones involved
in the maintenance of calcium homeostasis
and the regulation of cell proliferation and
differentiation, where it has both endocrine
and paracrine actions.
 Dietary sources are relatively unimportant
compared with endogenous synthesis in the
skin by photolysis of 7-dehydrocholesterol;
problems of deficiency arise when there is
inadequate exposure to sunlight.
 Two compounds have the biological activity
of vitamin D: cholecalciferol, which is the
compound formed in the skin, and
ergocalciferol, which is synthesized by
ultraviolet (UV) irradiation of ergosterol.
 Vitamin D is a secosteroid – i.e., a steroid in
which the B-ring has undergone cleavage,
followed by rotation of the A-ring
 There are few rich dietary sources of vitamin
D, and the major source is usually
photosynthesis in the skin.

 Dietary vitamin D is absorbed in chylomicrons

and taken up rapidly by the liver as
chylomicron remnants are cleared from the
circulation.

 By contrast, vitamin D synthesized in the skin

is bound to plasma vitamin D binding protein
and is metabolized more gradually.
 Unlike the other fat-soluble vitamins, there
is little or no storage of vitamin D in the
liver, except in oily fish.
 The main storage of the vitamin seems to be
as plasma calcidiol, which has a half-life of
the order of 3 weeks
SYNTHESIS OF CALCIOL FROM 7-
DEHYDROCHOLESTEROL IN THE SKIN.
 Functions of Vitamin D:
 Vitamin D plays significant role in calcium homeostasis
(carried by 1, 25 dihydroxycholecalciferol).
 The activate form of vitamin D acts as a hormone,
regulating cell growth and differentiation such as for
immunoregulatory cells, epidermal cells and even for
malignant tumor cells.
 Responsible for proper calcification of bone, ithelps in
the mobilization of calcium and phosphate from the
bone.
 Regulates insulin secretion, parathyroid and thyroid
hormones.
 Associated with muscle function and posture stability
(Rejnmark, 2011).