Vitamin D refers to a group of fat soluble secosteroids responsible for enhancing intestinal absorption of calcium, iron, magnesium, phosphate and zinc

1. Vitamin - D
Dr. T. Poongodi Vijayakumar
Dept. of Food Science & Nutrition
Periyar University
Salem-11
Tamil Nadu

2. Introduction
• Vitamin D refers to a group of fat-
soluble secosteroids responsible for
enhancing intestinal absorption
of calcium, iron, magnesium, phosphate
and zinc.

3. PRECURSOR D VITAMER
Ergosterol D2 (Ergocalciferol)
7-Dehydrocholesterol D3 (cholecalciferol)
22,23-dehydroergosterol D4
7-Dehydrositosterol D5
7-Dehydrostigmasterol D6

4. CHEMISTRY
• The chief structural prerequisite of compounds serving as D provitamins is
the sterol structure which has been opened B ring that contains a D5,6
conjugated double bond. No vitamin activity is possessed by the compound
until the B ring is opened.
• This occurs as a result of exposure to ultraviolet light. In addition, vitamin
activity is dependent on the presence of a hydroxyl group at carbon3 and
upon the presence of conjugated double bonds at the 10-19, 5-6 & 7-8
positions.
• If the location of these double bonds is shifted, vitamin activity is
substantially reduced. A side chain of a length atleast equivalent to that of
cholesterol is also a prequisite for vitamin activity. If the side chain is
replaced by a hydroxyl group, for ex vitamin activity is lost.
• The potency of the various D vitamins is determined by the side chain.
• D5 for ex with its branched 10- carbon side chain, is much less active with
respect to the calcification of bone cartilage than is D3 with its 9- membered
sidechain.
• Structurally to four - ring called compounds
cyclopentanoperhydrophenanthrenes, from which they were derived by a
photochemical reaction.

5. PHYSICAL CHARACTERISTICS
• Under normal conditions, D3 is more stable than D2; however, both
compounds undergo oxidation when exposed to air for period of 24
to 72 hrs.
• In acid solutions, the D vitamins are unstable.
• All the D vitamins are moderately soluble in fats, oils & ethanol, and
very soluble in fat solvents such as chloroform, methanol and ether.
• Other chemical alteration can result in decreased vitamin potency as
well. Saturation of any of the double bonds or the substitution of a
chloride, bromide, or mercaptan residue for the hydroxyl group
attached to carbon 3 results in a loss of activity.

6. BIOPOTENCY
• The comparative potency of the D vitamers depends on several
factors : (1) the species consuming the vitamers ; and (2) the
particular function assessed.
• The activated forms of D3 (25- hydroxy and 1,25-
dihydroxycholecalciferol) are far more potent than their parent
vitamer D3. The synthetic analog of D3, 1α – hydroxycholecalciferol,
likewise has 5 to 10 times the potency of cholecalciferol.
• The analog 3- deoxy-1,25- dihydroxycholecalciferol is far more
active as an agent to promote intestinal calcium uptake than as an
agent to promote bone calcium mobilisation. This is also true for the
analog, 25- hydroxy-5,6- cholecalciferol.

7. DIGESTION & ABSORPTION
• Vitamin D3 (cholecalciferol) from the diet is absorbed from micelle, in association with
fat and with the aid of bile salts, by passive diffusion into the intestinal cell. About
50% of dietary vitamin D3 is absorbed. Although the rate of absorption is most rapid in
the duodenum, the largest amount of vitamin D is absorbed in the distal small
intestine.
• Absorption takes place primarily in the jejunum and ileum. The vitamin is absorbed in
either the hydroxylated or the nonhydroxylated form.
• Within the intestinal cell, vitamin D is incorporated primarily into chylomicrons (long
chain fattyacids), which then enter the lymphatic system with subsequent entry into
the blood. Chylomicrons transport about 40% of the cholecalciferol in the blood,
although some vitamin D may be transferred from the chylomicron to DBP (Vitamin D
Binding Protein) for delivery to extra hepatic tissues. Chylomicrons remnants deliver
the vitamin to the liver.
• Cholecalciferol reaching the liver either by way of chylomicrons remnants or by DBP
typically is metabolized by a couple of different hydroxylases to generate the active
form of the vitamin.
• In the liver 25- hydroxylase functions in the mitochondria to hydroxylate
cholecalciferol at carbon 25 to form 25-OH(vitamin)D3, also called calcidiol or 25-OH
cholecalciferol.

8. • Following hydroxylation in the liver, 25-OH D3 bound to DBP is released into
the blood and taken up by tissues, especially the kidney. Specifically, DBP-
25-OH D3 complex binds to megalin on the plasma membrane of the kidney
and is transported into the renal cells. In the kidney, a second hydroxylation
of 25-OH D3 occurs at position 1, resulting in 1,25- (OH)2 D3 (also called
1,25-dihydroxycholecalciferol or calcitriol)
• Once synthesized, calcitriol is released from the kidney and bound to DBP
for transport in the blood. DBP is one of the major proteins in the blood; the
protein transports 1,25- (OH)2 D3 along with other metabolites to various
target tissues.
• Dietary phosphorus intake affects calcitriol production by 1-hydroxylase. A
high intake of phosphorus causes a decrease in serum 1,25-(OH)2D3,
whereas a low phosphorus intake stimulates its production.

9. EXCRETION
• Calcitriol hydroxylation at carbon 24 generates the metabolite 1,24,25-
(OH)2D3 which may be further oxidized to 1,25-(OH)2 24- oxo D3.
Subsequent reactions including side chain clevage, yield calcitroic acid.
• Other vitamin D metabolites are also formed after hydroxylation and
oxidation. These other vitamin D metabolites may be conjugated and then
excreted primarily in the bile.
• Most vitamin D metabolites (more than 70%) are excreted in the feces, with
lesser amount excreted in the urine.

10. PHYSIOLOGICAL FUNCTIONS
• ABSORPTION OF CALCIUM FROM DIGESTED FOOD
• REABSORPTION OF PHOSPHATE IN THE RENAL TUBULE
• CALCIFICATION OF OSTEOBLAST CELLS OF GROWING SKELETAL
STRUCTURES
• CALCIUM HOMEOSTASIS
• CALCITRIOL AND INTESTINE
• CALCITRIOL AND KIDNEY
• CALCITRIOL AND BONE
• CELL DIFFERENTIATION , PROLIFERATION AND GROWTH