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Animal Nutrition AnSc 315 > Vitamins and Minerals introduction > Flashcards

Vitamins and Minerals introduction Flashcards

1
Q

is vitamin/mineral nutrition important

A
  • critical for the health and growth of animals
  • it is important to know what role vitamins and minerals play in animal growth and physiology
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2
Q

what are fat soluble vitamins

A
  • thiamin (B1)
  • riboflavin (B2)
  • niacin (B3)
  • pantothenate (B5)
  • biotin (B7)
  • folic acid (B9)
  • vit B12 (cobalamin)
  • pyridoxine (B6)
  • vit c (ascorbate)
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3
Q

what are fat soluable vitamins

A
  • vitamins A D E K
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4
Q

what are common features of mineral nutrition

A

absorption: most microminerals form salt and other compounds which are relatively insoluable ( I and Se are exceptions) - not readily absorbed
transport: minerals often require carrier proteins for transport in the body ( synthesis of these proteins is important in regulation of mineral metabolism)

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5
Q

what is chelation

A
  • metal ions are reactive is they are chelated they will oxidise
  • metals form complexes with a well defined number of organis ligands ( can consist of neutral or anionic chemical groups, proteins and animo acids are common ligands
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6
Q

how are minerals stored

A
  • have significant storage so deficiency will not occur unless abset from diet from weeks to years (exception Na and K)
  • macrominerals (Ca P Mg) stored in bones
  • microminerals (Fe Cu Zn Se Cr and others) stored in liver
  • often associated with specific storage proteins
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7
Q

what are vitamins

A
  • organic nutrients required in small quantities for a variety of biochemical functions
  • generally, cannot be synthesized by the body and must be supplied in the diet
  • vitamin c is synthesised in liver by some animals but not enough
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8
Q

what are water soluble vitamins

A
  • all B vitamins are absorbed by passive absorbtion at high levels in the gut and by sodium dependent active transport at low levels in the gut
  • excesses are excreted in the urine
  • toxicity is rarely problem - but possible
  • storage is limited (apart from cobalamin B12) and they must be provided regularly
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9
Q

what is the difference between monogastrics and ruminants

A
  • rumen bacteria can synthesize B vitamins
  • monogastrics have some production of B vitamins in the ceca and hindgut but absorbtion in hindgut is limited
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10
Q

water soluability vitamines in horses

A

-normal horses can produce most of the B complex vitamins in adequate amounts in its intestinal tract
- young growing foals and horses under stress conditions (sick very hard work and racing) may benefit from B vitamin supplements

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11
Q

rabbits and coprophagy

A
  • rabbits practice coprophagy, two kinds of fecal matter one hard and one soft
  • cosumed directly from the anus
  • fermentation in the cecum and the practice of coprophagy provides the necessary aount of most B vitamins
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12
Q

what are fat soluable vitamins

A
  • non polar hydrophobic molecules
  • all are handled by the GI system in the same way as dietary fat
  • after absorbtion fat soluable vitamins are transported to the liver in chylomicrons
  • in contrast to water-soluable vitamins, fat soluable vitamins can be stored in the body : vitamins A D E K stored in liver , kidney
  • vitamin E stored in adipose tissue
  • not excreted in urine ; appear in bile and excreted in feces
  • because the body can store excess F-S vitamins, toxicity can occur (Vit A D)
  • vitamin D is actually not a true vitamin
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13
Q

electroyles

A
  • maintain osmotic and electrolytic environment in body fluids (maintaining protien function)
  • maintain NaK gradient between intracellular and extracellular environment
  • transport in nerve and muscel function
  • transport of molecules across cell membrane
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14
Q

what are electrolyte deficiency symptoms

A
  • Na: lethargy, loss of appetite, muscle weakness respiratory depression and areest
  • K : elevated blood pressure, muscle weakness, respiratory depression and cardiac arrest
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15
Q

what are electrolyte toxicity symptoms

A

Na: dehydration, seizure and coma
K: cardiac arrhythmia and death

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16
Q

what are the functions of calcium

A
  • bone strength and maintenance
  • maintain resting nerve potential
  • blood clotting
  • serve as 2nd messenger to relay info from outside to inside the cell
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17
Q

how does nerve function work

A
  • an action potential results in the open voltage gated ca channels resulting in an influx of ca
  • this triggers a series of events that results in the synaptic vesicles releasing their neurotrasnmitters
  • binding of the neurotransmitter with a receptor in the target cell results in the specific response
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18
Q

how does absorption of ca

A
  • calcium is absorbed by two distinct mechanism
  • active, transcellular absorption = upregulated to increase ca absorbtion when body ca stores are low
  • passive, paracellular absorption = occurs all the time and rate is dependent on dietary ca concentration
  • and solvent drag dependent on activation of sodium glucose co transporters 1 (SGLT-1) and Na/K ATPase (thus luminal glucose increase Ca absorption)
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19
Q

where does passive paracellular absorption of ca occur

A
  • in jejunum and ileum
  • when dietary calcium levels are moderate and high
  • Ca diffuses through tight junctions into the basolateral spaces around enterocytes and into blood
  • Up to 50% of absorption in monogastrics
  • less important in ruminants because rumen fluid dilutes ca in digesta
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20
Q

where does active transcellular absorption of Ca take place

A
  • in the duodenum, up regulated when body Ca stores are low
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21
Q

what is the three step process of active transcellular absorbtion of Ca

A
  1. facilitated diffusion of calcium into the enterocyte
  2. transport across the enterocyte
  3. active transport into extracellular fluid (ATP to ADP)
    - the step where this process is regulated is transport across the enterocyte, which is controlled by the amount of the carrier protein calbindin (vitamin D is dependent Ca binding proteins) present in the cell
    - synthesis of calbindin is controlled by Vitamin D
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22
Q

what is calbindin

A
  • vitamin D induces synthesis of calbindin
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23
Q

what is the transcellular absorbtion of Ca

A
  • passive and parcellular Ca transport takes place across the tight junctions and is driven by the electrochemical gradient for Ca
  • the ative form of vitamin D stimulates the individual steps of transcellular Ca transport by increasing the expression levels of the luminal Ca channels, calbindins and the extrusion systems
  • active and transcellular Ca transport is carries out as three step process.
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24
Q

what factors affecting Ca absorption

A
  • absorption is inhibited by compounds that form insoluable Ca salts
  • oxalates, phytates, phopshates form insoluable salts
  • undigestible fats for Ca soaps
  • a large part of ingested ca is not absorbed and is excreted in feces
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25
Q

how is calcium transported in blood

A
  • major ca binding factor in blood is gamma carboxyglutamate residues in serum protein (primary;y albumen)
  • the production of gamma carboxyglutamate residues on serum proteins is catalyzed by vitamin K
26
Q

how is Ca excretion

A
  • excreted by the kidneys - when Ca in serum is high; tightly regulated
  • secreted into intestinal lumen when calbindin is downregulated (epithelial cells are sloughed and unabsorbed Ca goes with them)
  • sweat (small amount)
27
Q

what is the correlation of ca metabolism and bone

A
  • body contains more ca than any other essential mineral
  • 99% of Ca in bones and teeth
  • skeletal calcium is in the form of hydroxyapatite
28
Q

bone remondeling

A
  • bone is constantly being remodeled
  • in humans approx. 500mg Ca may enter and leave bones each day
  • bone accretion remains constant in animals of a gieven age, decreases with age
  • bone reabsorption changes with Ca status and is a major factor in Ca homeostasis
  • two types of cells are responsible for removing and depositing Ca and P in bones
  • the activity of these cells is under hormonal regulation
29
Q

what is the difference between osteoclasts and osteoblasts

A
  • osteoclasts - removes CaP from bone
  • osteoblasts - deposit CaP in bone
30
Q

how is Ca and P regulated

A
  • the importance of Ca in metabolism means its levels are precisely regulated
  • daily variation is rarely more than 3%
  • levels are regulated by ( parathyroid hormone, vitamin D and other hormones )
31
Q

parathyroid hormone

A
  • released by the parathyroid glands
  • parathyroid glands monitor blood Ca in the carotid artery
  • secretes PTH when Ca id down
  • rapid effects of PTH - increases Ca reabsorption across the renal glomerulus (decreases urinary Ca loss)
  • slower effects ( increased rate of intestinal absorption by stimulating production of active form of Vit D
  • increase the release of bone Ca stores (recruits osteoclasts )
32
Q

what is the effect of PTH on bone resorption

A

-PTH primary hormone regulating Ca resorption from bone
- PTH increases the numbers of osteoclasts
- this process takes days so is not used for short term regulation of calcium levels
- higher numbers of steoclasrs breaks down more bone and release Ca

33
Q

Vitamin D

A
  • not really a vitamin-acts as a hormone (synthesized in the body)
  • vitamin D precursors are found in plant and animal tissue
  • precursors are converted to vitamin D by sunlight UV on the skin
  • works with PTH regulated calcium and P metabolsim
34
Q

effects of Vitamin D on Ca metabolism

A
  • increase Ca absorption ( induces expression of calbindin in gut epithelial cells
  • increase P absorption
  • stimulated sunthesis of collagen and other bone matrix proteins by osteoblasts
  • in addition to its role in promoting bone formation stimulates bone resorption by osteoclasts and stimulates osteoclast recruitment
  • net effect is higher blood Ca concentrations
35
Q

what other hormones are involved

A
  • calcitonin = has the opposite effect of PTH
  • estrogen = regulates osteoclast and osteoblast populations
  • when estrogen levels low, more bone resorbed; leads to osteoporosis
  • supplimental estrogen prevents osteoporosis in postmenopausal women
36
Q

what are the phosphorus-functions

A
  • most abundant intracellular anion
  • structural: is essential part of mineral portion of bone
  • remaining 15-25% of P in solft tissues: component of cell membranes (phospholipids), metabolic ATP,RNA,DNA,NADP
37
Q

how is phosporus absorbed

A
  • most absorbed as inorganic form (PO43)
  • phosphosugars, phosphoprotein, phosphonucleotides are hydrolyzed to liberate inorganic P
  • absorption takes place in small intestine by: passive paracellular diffusion, active trancellular transport
  • active trancellular transport is responsive to
    production of 1,25 (OH)2-VitD3 is directly stimulated by low blood P
38
Q

P homeostasis

A
  • short term regulation of P is not as critical as for Ca
  • daily variations as much as 50%
  • the same 2 hormones that regulate Ca also regulate P in the body PTH, Vitamin D
39
Q

when P in the blood is low

A
  • stimulates 1,25 (OH)2-VitD3 production
  • decrease PTH secretion
  • increases intestinal absorption of P
  • increase serum P
40
Q

when P in the blood is high

A
  • increases PTH secretion and decrease 1,25 (OH)2-VitD3 production
  • PTH decreases renal resorption of P
  • decreases serum P
41
Q

Ca:P inbalances

A
  • the regulation of Ca and P works well if the Ca:P ratio in the diet between 1.2:1 to 2:1
  • these ratios result in maximal Ca absorption in monogastrics
  • excessive dietary P can interfere with Ca absorbtion in the SL
  • high dietary P levels leads to large fecal losses and bone reaption
42
Q

ca sources

A
  • normally insufficient in plant sources
  • normally add meat meal for protein/P, dicalcium phosphate for P and limestone or cacium carbonate to balance Ca:P ratio
  • Ca is cheap ; P is expensive
43
Q

calcium suppliments

A
  • limestone 35.8% Ca
  • calcium Ca rbonate 40%
  • oyster shells 38%
44
Q

calcium and phosphorus supplements

A

dicalcium phosphate 23% Ca and 18.2% P
bone meal 29% Ca and 13.6%

45
Q

mg suppliments

A
  • dolomite limestone
46
Q

P sources

A
  • inorganis = derived from mineral sources , decalcium phosphate
  • organis = derived from animal or plant sources
  • meat/bone meal-highly digestible
  • phytic acid major P source in plants but indigestible by animals
47
Q

phosphoruc mineral supplements

A
  • sodium phosphate 32%
  • monoammonium phosphate 12% P
  • phosphoric acid 23% P
48
Q

Ca vit D P deficiency

A
  • similar symptoms for all three nutrients
  • difficult to distinguish one another without doing blood chemistry
49
Q

cage layer fatigue

A
  • occurs in laying hens at peak production
  • due to high requirement for Ca for egg shell formation
  • causes bone deformities, fractures and paralysis
  • pullets should be fed high Ca to build up reserves and proper Ca P and Vit D levels should be maintained in the diet
50
Q

vitamin D deficiency

A
  • rickets and osteoporosis
  • potential issue in piglets raised indoors
  • limited transfer ascross the placenta, and colostrum is low
51
Q

vitamin D deficieny in humans

A
  • very common nutrients deficiency in canada pre WWll
  • now we fortify milk vit d
52
Q

P deficiency

A
  • rickets in young animals osteoporosis in elderly
  • some differences = osteomalacia and poor pigmentation in older animals
  • abnormalitites of erythrocytes, leukocytes and platelets
  • pica depraved appetite where animals consume dirt, chew on pen materials
53
Q

toxicity

A
  • Ca toxicity does not occur normally
  • excess ca is simply not absorbed
  • P toxicity is rare - usually due to kidnet failure
  • Vit D - calcification of soft tissue, avoid megadoses of vitamin D
54
Q

vitamin k

A
  • for many years it was beleived that vit k was only involved in blood clotting
  • now recognized the vit k is a cofactor in the synthesis of carboxyglutamic acid
  • gla resides in responsible for binding Ca in a range of proteins
  • upon binding with Ca becomes activated leading to a series of reaction important in the clotting cascades
  • deficiency of vit k can reduce bone density
55
Q

poisoning with k antagonists

A
  • many of the populatr rodenticides act by inducing a vitamin K deficiency
  • warfarin and dicoumarol interfere with recycling of vitamin k and thereby lead to vitamin k deficiency
  • a singler feeding on poison bait can kill not only the rodent, but cause bleedin disease in dogs or cats that subsequently ingest them
56
Q

physiologcal effects of vitamin K

A
  • gamma carboxylation of glutamic acid residue in proteins
  • proteins are = blood coagulation, bone mineralization, cell growth
57
Q

vitamin k and blood clotting

A
  • some clotting factors require Ca to bind for activation
  • ca only bind after the gamma carboxylation of specific glue residues in these proteins
  • these are called vitamin k dependent proteins
58
Q

vitamin k and bone density

A
  • vitamin k promotes bone density by the gamma carboxylation of glutamte in the hormone osteocalcin
  • vit k deficiency in associated with osteoporosis
59
Q

vit k deficiency

A
  • newborn infants have no stores of vit k
  • if a supplement is not provided, hemorrhagic disease of newborns can result
  • usually given an injection of 1mg vitamin k at birth
  • not observed in swine
60
Q

sweet clover poisoning in ruminants

A
  • sweet clover contains coumarin
  • in spoiled or damaged clover the coumarin is converted to dicoumarin which blocks the vit k cycle
  • stiffness, lameness, swellings beneath the skin (hematomas and blood clots) blood in urine or milk
  • prevention, sweet clover that is poiled r moldy should not be fed
  • treatment = vit k injections or blood transfusions
61
Q

sources of vit k

A
  • plants or bacteria
  • intestinal synthesis is important; ruminants dont normally require addition vit k
  • high levels of feed antibiotics may reduce vit k synthesis
  • synthetic source menadione
  • synthetic vit k susceptible to oxidation if exposed to sunlight, loisture, choline or trace elements

Animal Nutrition AnSc 315 (12 decks)

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