Fat Soluble Vitamins:

A, D, E, K

STEFANIA WIDYA S.
Fat Soluble Vitamins
SLIDE 2
• Being insoluble in the watery GI juices, the fat-soluble vitamins
require bile for their digestion and absorption.
• Upon absorption, fat-soluble vitamins travel through the
lymphatic system within chylomicrons before entering the
bloodstream, where many of them require protein carriers for

Overview transport.
• The fat-soluble vitamins participate in numerous activities
throughout the body, but excesses are stored primarily in the
liver and adipose tissue.
• By the same token, because fat-soluble vitamins are not readily
excreted, the risk of toxicity is greater than it is for the water-
soluble vitamins.

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Vitamin A and Beta Caroten
 The Vitamin A
• Vitamin A was the first fat-soluble vitamin to be
recognized. A century later, vitamin A and its precursor,
beta-carotene
• Three different forms of vitamin A are active in the body:
retinol, retinal, and retinoic acid. Collectively, these
compounds are known as retinoids.
• Foods derived from animals provide compounds (retinyl
esters) that are readily digested and absorbed as retinol in
the intestine. Foods derived from plants provide
carotenoids
• The most studied of the carotenoids is beta-carotene,
which can be split to form retinol in the intestine and
liver. Beta-carotene’s absorption and conversion are
significantly less efficient than those of the retinoids.
• The cells can convert retinol and retinal to the other active
forms of vitamin A as needed. The conversion of retinol
to retinal is reversible, but the further conversion of
retinal to retinoic acid is irreversible
Digestion and Absorption
Vitamin A SLIDE 5
Animal Plant
Product Product

Gaster Protein binding Pepsin

Carotenoid

Duodenum Caroten dioxigenase

Retinil ester
Hydrolase Free Caroten Retinaldehide

Free Retinol

Retinol
Micelle
complex
Liver
Enterocytes

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Conversion of Vitamin A in the Body
SLIDE 6
Several proteins participate in the
digestion and absorption of vitamin A.
After absorption via the lymph system,
vitamin A eventually arrives at the liver,
where it is stored. There, a special
transport protein, retinol-binding protein
(RBP), picks up vitamin A from the liver
and carries it in the blood. Cells that use
vitamin A
have special protein receptors for it, and
its action within each cell may differ
depending on the receptor. For example,
retinoic acid can stimulate cell growth in
the skin and inhibit cell growth in tumors

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Role of Vitamin A
SLIDE 7
Vitamin A is a versatile vitamin, known to regulate the expression of several hundred genes.
Its major roles include:
• Promoting vision
• Participating in protein synthesis and cell differentiation, thereby maintaining the health of epithelial tissues
and skin
• Supporting reproduction and growth
• Antioxidant
As mentioned, each form of vitamin A performs specific tasks.
• Retinol supports reproduction and is the major transport and storage form of the vitamin.
• Retinal is active in vision and is also an intermediate in the conversion of retinol to retinoic acid
• Retinoic acid acts like a hormone, regulating cell differentiation, growth, and embryonic development.

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Vitamin A Deficiency
SLIDE 8
• Vitamin A status depends mostly on the adequacy of vitamin A stores, 90% of
which are in the liver.
• Vitamin A status also depends on a person’s protein status because retinol-
binding protein
• Deficiency symptoms would not begin to appear until after stores were
depleted—one to two years for a healthy adult but much sooner for a growing
child.
• Vitamin A deficiency is a major nutrition problem in many developing
countries.
• An estimated 250 million children worldwide have some degree of vitamin A
deficiency and thus are vulnerable to infectious diseases and blindness.
Effect of Vitamin A Deficiency:
• About 1 to 2 percent of them become blind every year, half of them dying 1. Infectious diseases
within a year of losing their sight. 2. Night blindness
• Routine vitamin A supplementation and food fortification can be a lifesaving 3. Blindness (xerophtalmia)
intervention 4. Keratinization

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 Vitamin A Toxocity
SLIDE 9
• Symptoms of toxicity begin to develop when all the binding proteins are swamped, and free vitamin
A damages the cells.
• Toxicity is a real possibility when concentrated amounts of preformed vitamin A in foods derived
from animals, fortified foods, or supplements is consumed.
• Children are most vulnerable to toxicity because they need less vitamin A and are more sensitive
to overdoses.
• Beta-carotene, which is found in a wide variety of fruits and vegetables, is not converted efficiently
enough in the body to cause vitamin A toxicity; instead, it is stored in the fat just under the skin.
Although overconsumption of beta-carotene from foods may turn the skin yellow, this is not
Effect of Vitamin A Toxocity
harmful.
1. Bone defect
• In contrast, overconsumption of beta-carotene from supplements may be quite harmful. 2. Birth defect
• In excess, this antioxidant may act as a prooxidant, promoting cell division and destroying vitamin
A.
• Furthermore, the adverse effects of beta-carotene supplements are most evident in people who drink
alcohol and smoke cigarettes.

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Vitamin A Recommendation
SLIDE 10
Because the body can derive vitamin A from various retinoids and carotenoids, its content in foods and its
recommendations are expressed as retinol activity equivalents (RAE).

1 μg RAE = 1 μg retinol
= 2 μg beta-carotene (supplement)
= 12 μg beta-carotene (dietary)
= 24 μg of other vitamin A precursor
carotenoids

Most food and supplement labels report their vitamin A contents using International Units (IU)
• IU retinol = 0.3 μg retinol or 0.3 μg RAE AKG Vitamin A:
• 1 IU beta-carotene (supplement) = 0.5 IU retinol or 0-6 mo = 375 mcg Pregnant : +300 mcg
0.15 μg RAE 7mo-3y0 = 400 mcg Lactating : +350 mcg
• 1 IU beta-carotene (dietary) = 0.165 IU retinol or 0.05 4-6 yo = 450 mcg
μg RAE 7-9 yo = 500 mcg
• 1 IU other vitamin A precursor carotenoids = 0.025 μg 10-18 yo = 600 mcg
RAE 19->80 yo = 500 mcg

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Source of Vitamin A
SLIDE 11

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 SLIDE 12

Vitamin D

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The Vitamin D
• Vitamin D (calciferol) is different from all the other nutrients in that the body
can synthesize it, with the help of sunlight, from a precursor that the body
makes from cholesterol.
• Therefore, vitamin D is not an essential nutrient; given enough time in the
sun, people need no vitamin D from foods.
• Ultraviolet rays from the sun hit the precursor in the skin and convert it to
previtamin D3. This compound diffuses from the skin into the blood and is
converted to its active form with the help of the body’s heat.
• The biological activity of the active vitamin is 500- to 1000-fold greater than
that of its precursor.
• Regardless of whether the body manufactures vitamin D or obtains it directly
from foods, two hydroxylation reactions must occur before the vitamin
becomes fully active.
• First, the liver adds an OH group, and then the kidneys add another OH
group to produce the active vitamin
Role of Vitamin D
SLIDE 14
Though called a vitamin, the active form of vitamin D is actually a hormone. Like vitamin A, vitamin D has a binding protein that
carries it to the target organs—most notably, the intestines, the kidneys, and the bones. All respond to vitamin D by making the
minerals needed for bone growth and maintenance available.
Vitamin D in Bone Growth
• Vitamin D’s special role in bone health is to assist in the absorption of calcium and phosphorus, thus helping to maintain blood
concentrations of these minerals.
• The bones grow denser and stronger as they absorb and deposit these minerals.
• Vitamin D raises blood concentrations of bone minerals in three ways.
 When the diet is sufficient, vitamin D enhances their absorption from the GI tract.
 When the diet is insufficient, vitamin D provides the needed minerals from reabsorption by the kidneys and
 mobilization from the bones into the blood.
• The vitamin may work alone, as it does in the GI tract, or in combination with parathyroid hormone, as it does in the bones
and kidneys

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Vitamin D Deficiency
SLIDE 15
• Factors that contribute to vitamin D deficiency include dark skin, breastfeeding without
supplementation, lack of sunlight, and not using fortified milk.
• Consequently, a vitamin D deficiency creates a calcium deficiency and increases the risks of
several chronic diseases.
• Vitamin D–deficient adolescents may not reach their peak bone mass.
• Low blood calcium due to a vitamin D deficiency can also trigger seizures

Akibat Defisiensi Vit D:

1. Riketsia  tulang tidak dapat melakukan kalsifikasi secara sempurna sehingga terjadi
retadasi pertumbuhan dan kelainan skeletal
2. Osteomalasia  tulang menjadi lunak, rapuh, fleksibel, dan cacat
3. Osteoporosis

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Vitamin D Toxicity
SLIDE 16
• The amounts of vitamin D made by the skin and found in foods are well within the safe limits
set by the UL.
• Supplements containing the vitamin in concentrated form should be kept out of the reach of
children and used cautiously, if at all, by adults.
• Excess vitamin D raises the concentration of blood calcium.
• Excess blood calcium tends to precipitate in the soft tissue, forming stones, especially in the
kidneys where calcium is concentrated in an effort to excrete it.
• Calcification may also harden the blood vessels and is especially dangerous in the major
arteries of the brain, heart, and lungs, where it can cause death

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Vitamin D Requirement
SLIDE 17
Adequate Intake
Adults = 5 μg/day (19–50 yr)
= 10 μg/day (51–70 yr)
= 15 μg/day (>70 yr)
Upper Level = 50 μg/day
AKG (2013)
1-64 yr = 15 μg/day
> 64 yr = 20 μg/day

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 SLIDE 18

Vitamin E

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 The Vitamin E
• Vitamin E is a fat-soluble antioxidant and one of the body’s primary defenders against
the adverse effects of free radicals.
• Its main action is to stop the chain reaction of free radicals producing more free
radicals. In doing so, vitamin E protects the vulnerable components of the cells and
their membranes from destruction.
• Most notably, vitamin E prevents the oxidation of the polyunsaturated fatty
acids, but it protects other lipids and related compounds (for example, vitamin A) as
well.
• Accumulating evidence suggests that vitamin E may reduce the risk of heart disease
by protecting low-density lipoproteins (LDL) against oxidation and reducing
inflammation that lead to the development of heart disease.
• Alpha-tocopherol is the only one with vitamin E activity in the human body.
 Absorption and Utilization of Vitamin
E
• Tocopherols and tocotrienols are absorbed unchanged from the small
intestine, in micelles with other dietary lipids, and incorporated into
chylomicrons.
• The major route of excretion is in the bile, largely as glucuronides and other
conjugates.
• There are two mechanisms for tissue uptake of vitamin E.
• Lipoprotein lipase releases the vitamin by hydrolyzing the triacylglycerols in
chylomicrons and VLDLs,
• while separately there is uptake of low-density lipoprotein (LDL)-bound
vitamin E by means of LDL receptors.
Vitamin E Deficiency
• A primary deficiency of vitamin E (from poor dietary intake) is rare;
deficiency is usually associated with diseases of fat malabsorption such as cystic
fibrosis.
• Without vitamin E, the red blood cells break open and spill their contents,
probably due to oxidation of the polyunsaturated fatty acids in their
membranes.
• This classic sign of vitamin E deficiency, known as erythrocyte
hemolysis, is seen in premature infants, born before the transfer of vitamin
E from the mother to the infant that takes place in the last weeks of pregnancy.
• Prolonged vitamin E deficiency also causes neuromuscular dysfunction
involving the spinal cord and retina of the eye. Common symptoms
include loss of muscle coordination and reflexes and impaired vision and speech.
Vitamin E Toxicity
• the liver carefully regulates vitamin E concentrations. Toxicity is rare, and
vitamin E appears safe across a broad range of intakes.
• The UL for vitamin E (1000 milligrams) is more than 65 times greater than
the recommended intake for adults (15 milligrams).
• Extremely high doses of vitamin E may interfere with the blood-clotting action
of vitamin K and enhance the effects of drugs used to oppose blood clotting,
causing hemorrhage.
Sources of Vitamin E
• Vitamin E is widespread in foods. Much of the vitamin E in the diet comes
from vegetable oils and products made from them, such as margarine and
salad dressings.
• Because vitamin E is readily destroyed by heat processing (such as deep-fat
frying) and oxidation, fresh or lightly processed foods preferable sources.
• Prior to 2000, values of the vitamin E in foods reflected all of the
tocopherols and were expressed in ‘milligrams of tocopherol equivalent’
• These measures overestimated the amount of alpha-tocopherol.
• To estimate the alpha-tocopherol content of foods stated in tocopherol
equivalents, multiply by 0.8
Vitamin K
The Vitamin K
• Like vitamin D, vitamin K can be obtained from a nonfood source.
• Bacteria in the GI tract synthesize vitamin K that the body can absorb.
• Vitamin K acts primarily in blood clotting
• Vitamin K also participates in the metabolism of bone proteins, most notably
osteocalcin. Without vitamin K, osteocalcin cannot bind to the minerals that
normally form bones, resulting in low bone density
Absorption and Utilization of Vit K
• About 80% of dietary phylloquinone is normally absorbed into the
lymphatic system in chylomicrons, and is then taken up by the liver from
chylomicron remnants and released into the circulation in VLDLs.
• Intestinal bacteria synthesize a variety of menaquinones, which are
absorbed to a limited extent from the large intestine, again into the
lymphatic system, cleared by the liver, and released in VLDLs.
Role of Vitamin K in the Body
• Vitamin K is essential for the activation of several of these proteins, among
them prothrombin, made by the liver as a precursor of the protein thrombin
 Vitamin K Deficiency
• primary deficiency develops in response to an inadequate dietary intake whereas
a secondary deficiency occurs for other reasons
• A primary deficiency of vitamin K is rare, but a secondary deficiency may occur
in two circumstances.
• First, whenever fat absorption falters, as occurs when bile production fails, vitamin
K absorption diminishes.
• Second, some drugs disrupt vitamin K’s synthesis and action in the body:
antibiotics kill the vitamin K–producing bacteria in the intestine, and
anticoagulant drugs interfere with vitamin K metabolism and activity.
• Excessive bleeding due to a vitamin K deficiency can be fatal.
Vitamin K Toxicity
• Toxicity is not common, and no adverse effects have been reported with high
intakes of vitamin K. Therefore, a UL has not been established.
• High doses of vitamin K can reduce the effectiveness of anticoagulant drugs
used to prevent blood clotting.

Source of Vitamin K
• vitamin K is made in the GI tract by the billions of bacteria that normally reside
there.
• Once synthesized, vitamin K is absorbed and stored in the liver. This source
provides only about half of a person’s needs.
• Vitamin K–rich foods such asgreen vegetables and vegetable oils can easily
supply the rest.
Assignment
Make a paper with this topic :
1. Absorption, utilization, and metabolism of vitamin A
2. Role of Vitamin A in vision, protein synthesis, growth, immune system, and reproduction
3. Effect of deficiency and toxicity of Vitamin A
4. Absorption, utilization, and metabolism of Vitamin D
5. Role of Vitamin D in bone mineralization
6. Absorption, utilization, and metabolism of Vitamin E
7. Role of Vitamin E as antioxidant
8. Absorption, utilization, and metabolism of Vitamin K
9. Role of Vitamin K in blood clotting
10.Food source of fat soluble vitamin
That’s all. Thank you very much! 
Any Questions?