CONTENTS
 Introduction
 Types
 Metabolism & Absorption
 Storage
 Functions
 Requirements
 Sources
 Deficiency
 Toxicity
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
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)
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
METABOLISM
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)
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
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
 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…
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
FUNCTIONS
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
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)
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
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
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
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
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
REQUIREMENTS
Animals Requirements IU/kg
Beef cattle 275
Dairy cattle
Growing bulls 300
Lactating 1000
Goat 1400
Chicken 250-300
Sheep 555
Swine 200
Cats 500
Dogs 221
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
 Vitamin D2 concentration in feedstuffs
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
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
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
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
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
 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
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
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
 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
 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
EXCESS
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
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
Summery:
Vitamin D

Vitamin D

  • 2.
    CONTENTS  Introduction  Types Metabolism & Absorption  Storage  Functions  Requirements  Sources  Deficiency  Toxicity
  • 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 VITAMIND 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  Thetwo 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
  • 6.
  • 7.
    ABSORPTION AND CONVERSIONFROM 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 isproduced 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 METABOLICALLYACTIVE 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 of1,25-(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 storesof 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
  • 12.
  • 13.
    FUNCTIONS  Primary functionof 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 regulatesgene 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  Stimulatesactive 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  Playsrole 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  VitaminD 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 VITAMIND 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 adequatedirect 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
  • 20.
    REQUIREMENTS Animals Requirements IU/kg Beefcattle 275 Dairy cattle Growing bulls 300 Lactating 1000 Goat 1400 Chicken 250-300 Sheep 555 Swine 200 Cats 500 Dogs 221
  • 21.
    SOURCES  Precursors ergosterolin 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
  • 22.
     Vitamin D2concentration in feedstuffs
  • 23.
    DEFICIENCY  Rickets, theprimary 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 inadults  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 DEFICIENCYIN 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 bornto 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 calciumdecreases 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 DEFICIENCYIN 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, lowergrowth 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
  • 33.
  • 34.
    TOXICITY  For cattleand 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 ofleaves 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
  • 36.

Editor's Notes

  • #7 Consider talking about: Interactive pathway Photochemistry Synthesis in the skin Evolution Industrial synthesis
  • #12 Consider talking about: Interactive pathway Photochemistry Synthesis in the skin Evolution Industrial synthesis
  • #13 Consider talking about: Bone health
  • #20 Consider talking about: Interactive pathway Photochemistry Synthesis in the skin Evolution Industrial synthesis
  • #22 Consider talking about: Interactive pathway Photochemistry Synthesis in the skin Evolution Industrial synthesis
  • #24 Consider talking about: Interactive pathway Photochemistry Synthesis in the skin Evolution Industrial synthesis
  • #34 Consider talking about: Effect of excess