This document discusses vitamin D, including its types, metabolism, absorption, storage, functions, requirements, sources, deficiency, and toxicity. The two major forms are vitamins D2 and D3. Vitamin D is absorbed in the small intestine and transported to the liver and kidney where it is converted to its active form, 1,25-dihydroxyvitamin D. This active form regulates calcium and phosphorus absorption in the intestine and their deposition in bone. Requirements vary by species but adequate sunlight can meet animal requirements. Deficiency causes rickets in young animals due to poor bone mineralization.
vitamin d is one of the fat soluble vitamin on which there is great emphasis in the present scenario. it is present in breast milk in very minute amount so it is recommended that it must be supplemented right after birth to prevent it deficiency which in children can result in rickets. if not diagnosed and treated in time it may result in number of bony deformities . in adults besides oesteomalacia it is associated with n umber of non communicable diseases.
Vitamin D- Introduction , source, synthesis of vitamin D in body, absorption of vitamin D in the body , action of vitamin D,
vitamin D deficiency & toxicity, Dietary reference value,
vitamin d is one of the fat soluble vitamin on which there is great emphasis in the present scenario. it is present in breast milk in very minute amount so it is recommended that it must be supplemented right after birth to prevent it deficiency which in children can result in rickets. if not diagnosed and treated in time it may result in number of bony deformities . in adults besides oesteomalacia it is associated with n umber of non communicable diseases.
Vitamin D- Introduction , source, synthesis of vitamin D in body, absorption of vitamin D in the body , action of vitamin D,
vitamin D deficiency & toxicity, Dietary reference value,
A vitamin is an organic compound and a vital nutrient that an organism requires in limited amounts. An organic chemical compound (or related set of compounds) is called a vitamin when the organism cannot synthesize the compound in sufficient quantities, and it must be obtained through the diet; thus, the term "vitamin" is conditional upon the circumstances and the particular organism.
Hello
This ppt were on the basic information for synthesis of vitamin D and vitamin K in our body.
Along with their RDA , Source , biochemical function and disease state.
Thank you
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3. INTRODUCTION
“Sunshine Vitamin”
Fat soluble vitamin
Have antirachitic activity
1,25-dihydroxycholecalciferol, or 1 ,25-dihydroxyvitamin D3 or 1,25-dihydroxyvitamin D3,
is the hormonally active metabolite of vitamin D
Synthesised by various materials when they are exposed to sufficient sunlight
Vitamin D from the diet or dermal synthesis from sunlight is biologically inactive;
activation requires enzymatic conversion (hydroxylation) in the liver and kidney
In pure form occurs as colourless crystals that are insoluble in water but readily soluble
in alcohol & other organic solvents
Less soluble in vegetable oils
Can be destroyed by overtreatment with UV rays & peroxidation in presence of
rancidifying polyunsaturated fatty acids
4. FORMS OF VITAMIN D
Name Chemical composition
Vitamin D1 Mixture of molecular compounds of
ergocalciferol with lumisterol, 1:1
Vitamin D2 Ergocalciferol (made from ergosterol)
Vitamin D3 cholecalciferol(made from
7-dehydrocholesterolin the skin).
Vitamin D4 22-dihydroergocalciferol
Vitamin D5
sitocalciferol (made from
7-dehydrositosterol)
5. MAJOR FORMS
The two major forms are vitamin D2 or ergocalciferol, and vitamin D3 or
cholecalciferol
1. Ergocalciferol: derived from a common plant steroid, ergosterol, and is the usual
dietary source of vitamin D
2. Cholecalciferol: produced from animal products. 7-Dehydrocholesterol is derived
from cholesterol , synthesises in the body and present in large amount in skin,
intestinal wall and other tissues
Vitamin D3 (cholecalciferol) is more biologically active than vitamin D2
(ergocalciferol) in dairy calves
7. ABSORPTION AND CONVERSION FROM PRECURSORS:
Absorbed from the intestinal tract (ileum) associated with fats
Absorption require presence of bile salts, other natural lipids via chylomicron
into the lymphatic system (mammals) or portal system (birds)
Only 50% of an oral dose of vitamin D is absorbed
Sufficient vitamin D is usually produced by daily exposure to sunlight
Four factors influences the production of vit-D in skin:
Intensity of UV light
Wavelength of the UV light
Concentration of 7-dehydrocholesterol present in the skin
melanin in skin (skin colour)
8. CONT…
Cholecalciferol is produced by irradiation
of 7-dehydrocholesterol with UV light
During exposure to sunlight, UV rays
photolyze 7-dehydrocholesterol
(provitamin D3) to previtamin D3
Previtamin D3 undergoes a thermally
induced isomerization to vitamin D3
cholecalciferol formed by the UV
irradiation of 7-dehydrocholesterol in the
skin is absorbed and transported by the
blood, primarily bound to gamma-
globulin, and becomes immediately
available for further metabolism
9. CONVERSION OF METABOLICALLY ACTIVE FORM
In the liver, the microsomal system
hydroxylates the 25-position carbon in the side
chain to produce 25-hydroxy-vitamin D3 [25-
(OH)D3]
25-(OH)D3 is then transported to the kidney on
the vitamin D transport globulin, where it can
be converted in the proximal convoluted cells
to 1,25-dihydroxy-vitamin D [1,25-(OH)2D3]
1,25-(OH)2D3 is then transported to the
intestine, bones or elsewhere in the body,
where it is involved in the metabolism of
calcium and phosphorus
Hormonal form, 1,25-(OH)2D3, is the
metabolically active form of the vitamin that
functions in intestine and bone
10. Production of 1,25-(OH)2D3 is very carefully regulated by parathyroid hormone (PTH)
in response to serum calcium and phosphate (PO4
3-) concentrations
Under calcium stress, PTH activates renal mitochondrial 1-alpha-hydroxylases,
which convert 25-(OH)D3 to 1,25-(OH)2D
Regulation of the vitamin D endocrine system occurs through stringent control of
the activity of the renal 1 alpha-hydroxylase. Thus, the production of the hormone
1,25-(OH)2D3 can be modulated according to the calcium needs
High plasma 1,25-(OH)2D3 concentration has an inhibitory effect on renal 1-alpha-
hydroxylase and a stimulatory effect on tissue 24- and 23-hydroxylases
In mammals vitamin D, 25-(OH)D3, and possibly 24,25- 1,25-(OH)2D3 and 1,25-
(OH)2D3 are all transported on the same protein, called transcalciferin, or vitamin D-
binding protein (DBP)
CONT…
11. STORAGE
Principal stores of vitamin D occur in blood and liver,
but it is also found in lungs, kidneys and elsewhere in
the body
During times of deprivation, vitamin D in these
tissues is released slowly, thus meeting vitamin D
needs of the animal over a longer period of time
Excretion of absorbed vitamin D and its metabolites
occurs primarily in feces with the aid of bile salts
A liberal intake of vitamin D during gestation does
provide a sufficient store in newborns to help prevent
early rickets
13. FUNCTIONS
Primary function of vitamin D is to elevate plasma calcium and phosphorus
for normal mineralization of bone as well as other body functions
There is a regulatory role of vitamin D (1,25-(OH)2D3 ) in
immune cell functions,
release of insulin in relation to glucose challenge and
reproduction in both males and females
Hormones, thyrocalcitonin (calcitonin) and PTH, function in a delicate relationship
with 1,25-(OH)2D3 to control blood calcium and phosphorus levels
Vitamin D elevates plasma calcium and phosphorus by stimulating specific ion
pump mechanisms in the intestine, bone and kidney
14. CONT…
1,25-(OH)2D3 regulates gene expression through its binding to tissue-specific
receptors and subsequent interaction between the bound receptor and the DNA
A heterodimer of the vitamin D receptor (VDR) and a vitamin A receptor (RXR) within
the nucleus of the cell as the active complex for mediating positive transcriptional
effects of 1,25-(OH)2D3 The two receptors (vitamins D and A) selectively interact with
specific hormone response elements composed of direct repeats of specific
nucleotides located in the promoter of regulated genes
The complex that binds to these elements actually consists of three distinct
elements:
the 1,25-(OH)2D3 hormonal ligand,
the vitamin D receptor (VDR) and
one of the vitamin A (retinoid) X receptors (RXR)
15. INTESTINAL EFFECTS
Stimulates active transport of calcium and phosphorus across intestinal epithelium
Parathyroid hormone indirectly stimulates intestinal calcium absorption by
stimulating production of 1,25-(OH)2D3 under conditions of hypocalcemia
1,25-(OH)2D3 is transferred to the nucleus of the intestinal cell, it interacts with the
chromatin material and 1,25-(OH)2D3 specific RNAs are elaborated by the nucleus, a
specific proteins by ribosomes are translated, it increases calcium and phosphorus
absorption.
In the intestine, 1,25-(OH)2D3 promotes synthesis of calbindin (calcium-binding
protein, CaBP) and other proteins and stimulates calcium and phosphorus
absorption.
Influence magnesium (Mg) absorption as well as calcium and phosphorus balance
16. BONE EFFECTS
Plays role in mineralization of bone as well as demineralization or mobilization of
bone mineral
In vitamin D deficiency, this organic matrix fails to mineralize, causing rickets in the
young and osteomalacia in adults
mobilization of calcium from bone to the extracellular fluid compartment
This function is shared by PTH, requires metabolic energy, and presumably
transports calcium and phosphorus across the bone membrane by acting on
osteocytes and osteoclasts
biosynthesis of collagen in preparation for mineralization
17. KIDNEY EFFECTS
Vitamin D functions in the distal renal tubules to improve calcium reabsorption and
is mediated by the calcium-binding protein, calbindin
99% of the renal-filtered calcium is reabsorbed in the absence of vitamin D and PTH
1% is under control of hormonal agents
Without intact PTH, vitamin D increases renal loss of P
18. FUNCTIONS OF VITAMIN D BEYOND BONE MINERALIZATION
More than 50 genes have been reported to be transcriptionally regulated by 1,25-
(OH)2D3
Embryonic development of the chick
Vitamin D treatment stimulated yolk calcium mobilization and the vitamin D-
dependent Ca+2-binding protein, calbindin, is present in the yolk sac
1,25-(OH)2D3 is also essential for the transport of eggshell calcium to the embryo
across the chorioallantoic membrane
1,25-(OH)2D3 also inhibits growth of certain malignant cell types
Inhibit proliferation of leukemic cells, breast cancer cells and colorectal cells
Deficiency of vitamin D may promote prostate cancer
19. REQUIREMENTS
With adequate direct exposure to sunlight, ruminants
do not have an absolute dietary requirement
Vitamin D becomes nutritionally important in the
absence of sufficient sunlight
factors influencing dietary vitamin D requirements
include
(1) amounts and ratio of dietary calcium and
phosphorus
(2) bioavailability of calcium and phosphorus
(3) species; and
(4) physiological state of the animal
Rickets has been called the first air pollution disease
21. SOURCES
Precursors ergosterol in plants and 7-
dehydrocholesterol in animals
Ergocalciferol occurs naturally in some mushrooms
and cholecalciferol occurs naturally in fish
The principal source of vitamin D in the diets of farm
animals is vitamin D2 (ergocalciferol) produced by the
action of UV light on the ergosterol in forage
Green, uncured forages are poor sources of vitamin D
Saltwater fish and their oils are extremely rich
sources of vitamin D
Vitamin D3 is the principal source of supplemental
vitamin D for livestock and poultry diets
23. DEFICIENCY
Rickets, the primary vitamin D deficiency disease,
is a skeletal disorder of young, growing animals
generally characterized by decreased concentration of
calcium and phosphorus in the organic matrices of
cartilage and bone
In the adult animal, osteomalacia is the counterpart of
rickets. Cartilage growth in adult ceased, and thus a
decreased concentration of calcium and phosphorus in
the bone matrix
Symptoms of rickets include the following skeletal
changes:
I. weakened long bones, resulting in curvature and
deformation;
II. Enlarged, painful hock and knee joints;
III. General stiffness of gait, arched back and a
tendency to drag hind legs; and
IV. Beaded ribs and deformed thorax
24. CONT…
Osteomalacia in adults
There is progressive demineralization of bones eventually results in fractures and
breaks
symptoms such as reduced performance, hypocalcemia and reproductive failure
Other clinical signs of vitamin D deficiency in ruminants are decreased appetite and
growth rate, digestive disturbances, stiffness of gait, labored breathing, irritability,
weakness and occasionally tetany and convulsions
skeletal symptoms: enlargement of joints, slight arching of the back, bowing of legs,
with erosion of joint surface causing difficulty in locomotion
25. VITAMIN D DEFICIENCY IN CATTLE
Normal range of plasma 25-(OH)D3 in cattle is 20 to 50
ng/ml
Clinical signs in calves involving the skeleton begin with
thickening and swelling of the metacarpal or metatarsal
bones
As the disease progresses, the forelegs bend forward or
sideways.
In severe or prolonged deficiency, the force exerted by
normal muscle tension results in bending and twisting
of long bones and the characteristic bone deformity.
Enlargement of bone ends (epiphyses) from deposition
of excess cartilage, giving the characteristic “beading”
effect along the sternum at the point of attachment of
the ribs
26. CONT…
In calves, the mandible becomes thick and soft, and
in the worst cases, calves have difficulty eating
There can be slobbering, inability to close the
mouth and protrusion of the tongue
Joints (knee and hock) become swollen and stiff,
the pastern straight and the back arched
In severe cases, synovial fluid accumulates in the
joints
Posterior paralysis may also occur as the result of
fractured vertebrae
The advanced stages of the disease are marked by
stiffness of gait, dragging of the hind legs,
irritability, tetany, labored and rapid breathing,
weakness, anorexia and cessation of growth
27. CONT…
Calves born to vitamin D-deficient dams may be born dead, weak or deformed
Older animals with osteomalacia, bones become weak and fracture easily, and
posterior paralysis may accompany vertebral fractures.
In dairy cattle, milk production may be decreased and estrus inhibited by
inadequate vitamin D
The visible signs of vitamin D deficiency in dairy cows are similar as rickets in
calves. Stiffness in limbs and joints, difficult to walk, lie down and get up.
The knees, hocks, and other joints become swollen, tender and stiff. The knees often
spring forward, the posterior joints straighten, and the animal is tilted forward on
her toes.
The hair coat becomes coarse and rough appearance of unthriftiness
In advance cases, the spine and back often become stiff, arched and humped.
Hypocalcemia, either milk fever (parturient hypocalcemia) or unexplained lactational
hypocalcemia and paresis
28. Milk fever (parturient paresis) is a metabolic
disease characterized by hypocalcemia at or near
parturition in dairy cows
milk fever is a failure of calcium homeostasis
Milk fever is related to factors such as
(a) previous calcium and phosphorus intakes;
(b) previous vitamin D intake;
(c) dietary ratios of potassium, chloride, magnesium,
sulfur and sodium; and
(d) age and breed of cow
29. CONT…
serum calcium decreases from a normal 8 to 10 mg to 3 to 7 mg (average 5 mg)
cow is observed lying on her sternum with her head turned sharply toward her flank in a
characteristic posture
If treatment is delayed, paresis will progress into coma, which becomes progressively deeper,
leading to death
intravenous calcium boro-gluconate is an extremely effective treatment
Aged cows are at the greatest risk of developing milk fever
Jersey cattle are generally more susceptible than Holsteins
Parturient paresis can be prevented effectively by feeding a low-calcium and adequate-
phosphorus diet for the last several weeks prepartum, followed by a high-calcium diet after
calving
increased PTH and 1,25-(OH)2D3 concentrations resulted in “prepared” and effective
intestinal absorption and bone resorption of calcium at parturition
low calcium diets, anionic diets and PTH administration all increase renal 1-alpha
hydroxylase activity, resulting in increased production of 1,25-(OH)2D3 and prevention of
milk fever
30. VITAMIN D DEFICIENCY IN SHEEP AND GOATS
Vitamin D deficiency has been observed in young
lambs or goat kids kept in complete confinement
without access to sun-cured roughage
Clinical signs of vitamin D deficiency in sheep and
goats are similar to those of cattle, including rickets in
young animals and osteomalacia in adults
Parturient paresis occurs in ewes
31. Poor growth, stiffness, lamness, stilled gait, tendency to
go down, frequent fractures, softness of bones, bone
deformities, bending of ribs, enlargement and erosion of
joints and unthriftiness
VITAMIN D DEFICIENCY IN SWINE
32. Rickets, lower growth rate, egg production and hatchability
Severe weakness of legs
Beak is rubbery
Skeletal distortions
Endochondral ossification defects
Blackening of wings in red or buff-coloured breeds of
chicken
In layers deficiency causes thickening of egg shell or
decrease in production
VITAMIN D DEFICIENCY IN POULTRY
34. TOXICITY
For cattle and sheep, the upper safe dietary level for short-term exposure is 25,000
IU per kg (11,364 IU per lb) of diet
vitamin D3 is 10 to 20 times more toxic than vitamin D2when provided in excess
amounts
Serum calcium concentration is elevated due to increases in bone resorption and
intestinal absorption of calcium
Inflammation, cellular degeneration and progressive calcification. Diffuse
calcification affects joints, synovial membranes, kidneys, myocardium, pulmonary
alveoli, parathyroid glands, pancreas, lymph nodes, arteries, conjunctivae a
Common observations of vitamin D toxicity are anorexia, extensive weight loss,
brachycardia, reduced rumination, depression, polyuria, muscular weakness, joint
pain and stiffness, elevated blood calcium and lowered blood phosphate
concentrations
35. CONT…
Ingestion of leaves of the shrub Solanum
malacoxylon by grazing animals causes
enzootic calcinosis in Argentina and Brazil,
where the disease is referred to as “enteque
seco” and “espichamento,” respectively
Calcinogenic factor in S. malacoxylon is a
water-soluble glycoside of 1,25-(OH)2D
The sterol is released during digestion,
which results in a massive increase in the
absorption of dietary calcium
In practice, vitamin D toxicity is unlikely