Vitamin A

Dr. Abdirahman Ali (MBBS)

 Introduction

 Vitamin A (retinol) is fat soluble vitamin found widely in

animal tissue

 Retinol and its naturally occurring relatives are member of a

large class known as retinoid

 There are now over 1000 new retinoid

 Vitamin A exists in two forms

◦ preformed vitamin A and
◦ provitamin form
 Continued…


Preformed vitamin A has several forms
◦ retinol (vit. A1) - most active and major natural form

◦ dehydroretinol (vit. A2) - Half the biological activity of

retinol

◦ retinyl esters - this is post absorptive storage and

transport form of vitamin A. [retinyl palmitate]
 It is mostly palmitic acid

 Provitamin A form – include all the carotenoid in

plant
ex. B-carotene, alpha carotene
 Metabolism

 Retinyl esters are released from dietary proteins via proteolysis

in the stomach by the action of retinyl ester hydrolases
 They join lipids and bile salts to form micelles for absorption
through the intestinal mucosa
 In the blood chylomicrons are broken down into apolipoprotein
B and E, which contain retinol esters [retinyl palmitate]
 Via a receptor mediated endocytosis, are then taken up by the
liver – release retinol esters
 Undergo further metabolism and eventually bind with RBP to be
stored
 About 50 to 85% of total body retinol is stored in the liver
◦ Released into plasma to reach target organs
 Sources

Source
 Fish liver oil
Carrot, raw
 Liver, ox
Mango
 Butter, cow’s
 Kidney, ox
Lettuce
 Egg, hen
 Chicken
Sweet potato, raw
 Milk, whole cow’s
 Milk, gout
Avocado, raw

Tomatoes, raw
 Continued…
 Cellular differentiation
-vitamin A is required for the maintenance of epithelial cells-
Bone growth –required for normal growth and remodeling of
bone
-controls appropriate balance of activity of osteoclasts
and osteoblasts
 Growth
 Reproduction –required for normal completion of pregnancy
and fetal development
 Causes

 Inadequate consumption of vitamin A rich

food
 Problem of absorption, like disorders

associated with fat malabsorption, such as

cystic fibrosis, cholestatic liver disease,
small bowel crohn’s, and pancreatic
insufficiency
 Repeated infections or diseases such as

measles or diarrhea
 Clinical manifestation

 Eye – functional retinal rod cell changes occur before structural

lesion
 Night blindness –failure of the eye to adapt to dim light
 Epithelial changes lead to-
 conjunctival xerosis –earliest lesion

 Bitot’s spots – foamy, bubbly, or cheesy accumulation

 xerosis of the cornea- haziness due to stromal infiltration,

epithelial keratinization and often early vascularization

 corneal ulcer followed by scar which is irreversible

 Keratomalacia – implies deformity and loss of corneal

substances leading to eye ball infection and corneal opacity
Corneal xerosis Keratomalacia
Vitamin E
 Vitamin E
Vitamin E refers to a group of fat-soluble
compounds that include both tocopherol and
tocotrienol. The vitamin is synthesized by plants,
and has eight different isoforms (Vitamers) divided
into two classes of four Vitamers each.
 α-Tocopherol
 α-Tocopherol is an important lipid-soluble

antioxidant.
 It performs its functions as antioxidant by

protecting cell membranes from oxidation. 

 This would remove the free radical intermediates
and prevent the oxidation reaction from
continuing.
 Sources
 The natural form of the vitamin is synthesized

only by plants and is found predominantly in

plant oils.

  Metabolism
 Absorption
 Absorption of vitamin E is highly dependent upon

the same processes that are utilized during fatty

acid digestion and metabolism. Bile acids are
considered formation essential for vitamin E
absorption and micelle.
 Storage
 Vitamin E is a lipid soluble vitamin and therefore

over 90% of total body vitamin E is found in the

adipose tissue.
 Excretion
 Vitamin E is excreted mainly via bile, urine, feces,

and the skin.

 Because of the poor intestinal absorption of

vitamin E, fecal excretion is the main route of

vitamin E elimination.
  Functions of vitamin E
 Vitamin E is integral part of cellular membranes

whose main role is to defend the cell against

oxidation.
1-Antioxidant.
2-Regulates oxidation reactions.
3-Cell-membrane stability.
4-Protect polyunsaturated fatty acids .
 The primary role of vitamin E within the body is

to function as an antioxidant.
  Deficiency 
 A deficiency of vitamin E is rare in humans

Vitamin E deficiency causes neurological

problems due to poor nerve conduction.
 Deficiency can also cause anemia due to

oxidative damage to red blood cells, retinopathy

 and impairment of the immune response.
 The existence of a lack of vitamin E is rare.
 If this occurs, it is manifested in specific cases,

that is, in the following three situations:

1-Persons with a difficulty of absorbing or secreting
bile or who suffer from fat metabolism-related
disease (celiac disease or cystic fibrosis)
2-Premature infants (with Very low birth weight,
VLB) who weigh <1,500 grams at birth
3-Persons with genetic abnormalities in alpha-
tocopherol transporter proteins.
Vitamin K
What is Vitamin K?
 Fat soluble compound
 Necessary for the synthesis of several proteins required for
blood clotting

1) Vit K 1
- natural form
- found in plants
- provides the primary source of vitamin K to
humans through dietary consumption

2) Vitamin K2 compounds
- made by bacteria in the human gut
- provide a smaller amount of the human
vitamin K requirement
Physiological Effects of Vitamin K
 Vitamin K serves as an
essential cofactor for a
carboxylase that catalyzes
carboxylation of glutamic
acid residues on vitamin K-
dependent proteins. These
proteins are involved in:

1) Coagulation
2) Bone Mineralization
3) Cell growth
Coagulation
 The transformation of liquid
blood into a solid gel
 Stops blood flow in the
damaged area
 Involves a cascade of
activation of plasma proteins
 These proteins are produced
in the liver
 Fibrin is the final protein
which produces a meshwork
to trap RBC and other cells
Vitamin K Dependent Proteins
 factor II (prothrombin)
 factor VII
 factor IX
 factor X
 protein C & protein S
Vitamin K Deficiency

Results in impaired blood clotting and, potentially, bleeding.

Vitamin K deficiency can result from:

 a lack of vitamin k in the diet

 disorders that reduce fat absorption
 Taking certain drugs, including anticonvulsants and some
antibiotics
 Use of coumarin anticoagulants
Symptoms of Vitamin K Deficiency

• Bruising from bleeding into the skin

• Nosebleeds
• Bleeding gums
• Bleeding in stomach
• Blood in urine
• Blood in stool
• Tarry black stool
• Extremely heavy menstrual bleeding
• In infants, may result in intracranial hemorrhage
Vitamin K Deficiency in Infants
Newborns are prone to vitamin K deficiency because…

1.Vitamin K and lipids are not easily transported across the

placental barrier
2.Prothrombin synthesis in the liver is an immature process in
newborns, especially when premature.
3.The neonatal gut is sterile, lacking the bacteria that is
necessary in Vit K synthesis.
4.Breast milk is not a good source of vitamin K

Results in a hemorrhagic disease called vitamin K deficiency

bleeding (VKDB)

This disease is associated with breastfeeding, maladsorption of

lipids, or liver disorders.
Physiology of Vitamin K Deficiency

END