This document discusses vitamin D, including its sources, biochemical effects, and related diseases. It summarizes that vitamin D aids in calcium and phosphorus absorption in the intestine and bone mineralization. Deficiencies can cause rickets in children and osteomalacia in adults, resulting from insufficient mineralization of bones. Toxicity from oversupplementation can lead to excessive calcification.

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Introduction
Sources of dietary vitamin d
Formation of vitamin d
Biochemical effects of vitamin d
Vitamin d related diseases
rickets
osteomalacia
Toxicity
hypervitaminosis D
Requirements RDA
References

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Sunshine vitamin.
Vitamin D are a group of sterols that have
hormone like function.
Production of vitamin D is directly proportional to
sunlight and inversely proportional to melanin
pigmentation of skin.
Commercially vitamin is derived from the fungus
ergot.
Two forms
D2 ergocalciferol
D3 cholecalciferol

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Not found naturally in many foods
Synthesized in body
Natural sources including cod-liver oil. Fatty fish
species like eel catfish, salmon, tuna. Egg yolk also
contains vit D
Milk contains moderate quantity of the vitamin.
Mushrooms also gives greater amounts of vitamin D
when exposed to sunlight immediately after
harvesting fungi and yeast which possess vitamin D
precursor ergo sterol
Vitamin D is also available from fortified food when
supplemented with required nutrients such as bread
cereal, margarine oil, milk pastries, yogurt etc.

6. The major biologic function of vitamin D is to maintain
normal blood levels of calcium and phosphorus.
Vitamin D aids in the intestinal absorption of calcium and
phosphorous
It promotes bone mineralization in concern with a number
of other vitamins, minerals, and hormones.
It maintains normal cellular growth and function.
Stimulates renal tubular transport of Ca and P

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Although the body can obtain vit d from the diet the
major source of this prohormone is its production in
the skin from 7-dehydrocholestrol. It is located
primarily in the malpighian layer of the skin.
Upon exposure to UV light it is photo chemically
converted to previtamin D, which then isomerizes to
vitamin D over a period of several days.
Once formed vitamin D is preferentially removed
from the skin into the circulatory system by the
blood transport protein for vitamin D, the vitamin Dbinding protein (DBP)

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In liver:- Cholecalciferol is first transported to liver
–hydroxylation at 25th position-25 hydroxy
cholecalciferol-by the enzyme 25 hydroxylase
Note:- 25 hrdroxy cholecalciferol is the major
transport form in plasma
In kidney:-hydroxylated at 1st position-by 1 alpha
hydroxylase-1,25dihydroxy cholecalciferol is
generated.
Since it has 3 hydroxyl groups its also called
calcitriol-active form of vitamin d

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Vitamin D is best absorbed when ingested with
lipids. Vitamin D will be incorporated into micelles
and these will be absorbed by the intestine by
passive diffusion.
In the intestinal cells, chylomicrons will be
formed, and these will enter the lymphatic system
and enter the plasma.
Vitamin D will then be transported to the liver by
chylomicron remnants and to specific target with
the help of carrier vitamin D binding protein (DBP)
or transcalciferin.

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Vitamin D and intestinal absorption of calcium
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Effect of vitamin D in bone
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Effect of vitamin D in renal tubules

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Calcitriol promotes the absorption of calcium and
phosphorous from the intestine.
In the brush bordered surface ca is absorbed
passively. From the intestinal cell to
blood, absorption of calcium needs energy.
Calcitriol enters the target cell and binds to a
cytoplasmic receptor. The hormone-receptor complex
interacts with DNA and causes derepession and
consequent transcription of specific genes that code
for calbindin.
Due to the increased availability of calcium binding
protein, the absorption of calicum is increased.

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Mineralization of bone is increased by
increasing the activity of osteoblasts.
Calcitriol stimulates osteoblasts which secrete
alkaline phosphatase.
Due to this enzyme the local concentration of
phosphate is increased. The ionic product of
calcium and phosphorous increases, leading to
mineralization.

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Calcitriol increases the reabsorption of calcium
and phosphorous from renal tubules, therefore
both minerals are conserved.

14. Causes
 Inadequate supply
 Impaired absorption as in obstructive jaundice and
steatorrhea. High phytate content in diet may also
reduce the absorption of vitamin.
 Secondary to abnormality of vitamin D activation.
Liver and renal diseases may retard the
hydroxylation reactions.
 Secondary to abnormalities in renal absorption of
phosphates.
 Secondary to end organ resistance

15. Seen in children.
Insufficient mineralization of bone.
Bones become soft and pliable.
Features
 Delayed milestones
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Delayed closure of anterior fontanellae
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Delayed dentition
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Deformities of bones
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Decreased serum calcium

16. Bone deformities
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Frontal bossing
Weight bearing bones are bent
Rachitic rosary
Pigeon chest
Knock-knee
Bowed legs
Harrison’s sulcus- transverse depression passing
outwards from the costal cartilage to axilla. This is
due to the indentation of lower ribs at the site of
the attachment of diaphragm

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Classical vitamin D deficiency rickets- cured by
giving vitamin d in the diet
Hypophosphatemic rickets-result from defective
renal tubular reabsorption of phosphate.
Supplementation of vitamin D or its active form along
with phosphate is found to be useful.
Vitamin d resistant rickets-found to be associated
with fanconi syndrome where the renal tubular
reabsorption of bicarbonate, phosphate, glucose, and
amino acids are also deficient. Metabolic acidosis is
associated. Supplementation of vitamin D, phosphate
and bicarbonate are beneficial.

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Renal rickets-in kidney diseases even if vit D is
available calcitriol is not synthesized. These
cases will respond to administration of
calcitriol.
End organ refractoriness to 1,25-DHCC will also
lead to rickets. Either a decrease in the
number of cytosolic receptor or a structurally
abnormal receptor is noticed. The bone
diseases has been found to respond to mega
doses of calcitriol (35mg/day)

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Seen in adults
Bones are softened due to insufficient
mineralization and increased osteoporosis.
Involves generalized reductions in bone density and
the presence of pseudo fractures especially of the
spine, femur and humerus
Clinical features
 Muscular weakness and bone tenderness
 Increased softness of bones
 Greater risk of fractures particularly of the wrist
and pelvis
 Bowing of long bones

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Excessive exposure to sunlight does not lead to
overproduction of vitamin D. Toxicity is inevitably the
result of overdosing on vitamin D supplements.
Doses above 1500 I.U/ day for a very long periods may
cause toxicity
Excessive formation of vitamin D metabolites enhances the
calcification of various tissues along with bones

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Intense thirst
Difficulty in speaking
Confusion
Weight loss
Hypokalemia
Metabolic alkalosis
Arterosclerosis or
hardening of arteries
occurs due to calcification
of blood vessels
Nephrocalcinosis deposition
of ca in kidneys
Nephrolithiasis deposition
of ca in renal tubules

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Preschool children =10 microgram (400 I .U/ day)
Older children and adults=5 to 10 microgram (200
I.U)/ day
Pregnancy and lactation=10 microgram (400 I. U)/
day
Persons between ages 50-60 =400 I.U/ day
Senior citizens above the age of 60= 600 I.U /day