Animal Nutrition Test 5 Flashcards
How many interactions are known to occur between pairs of minerals (if level of one is increased then digestibility, absorbability, or metabolizability of the other mineral is reduced)?
Over 45
How many mineral elements are required in the diet?
Good evidence for 20, many nutritionist think there’s more. The text says 22, but the specific 22 minerals can’t be nailed down from the reading)
When a mineral in the body has no function it’s called
An innocuous contaminant
Name the macrominerals
Mg2+ Na+ P (PO4) S Cl- Ca2+ K+
Name the microminerals
Si Mo Co Mn Zn Cu Se Cr I F Fe B
Example of mineral involved with hormones
Iodine is a part of the thyroxine hormone, which speeds up the body’s metabolism
Calcium constitutes what percent of bone wet weight?
9%
What percent of all body calcium is found in the bones and teeth? Soft tissues and blood?
99%, 1%
Minerals required for bone lengthening
Ca, P, Mg, F
Which vitamin is necessary for calcium transport across biological membranes?
D
Optimal dietary Ca:P ratios for nonruminants
1:1-2:1
How are fatty acids involved with Ca digestibility?
Fatty acids freed from fat digestion bind Ca, forming an indigestible fatty acid-Ca complex (similar to soap). This reduces Ca digestibility
Ca inhibits absorption of what mineral (besides P)?
Zn
Chronic Ca deficiency symptoms:
Rickets plus acute symptoms. Rickets is a disease of young growing animals which can also be caused by vit D deficiency or P imbalance
Acute Ca deficiency symptoms:
Muscle incoordination (wobbly walks), paralysis, even death. “Big head” disease in horses, various bone disorders
2 other names for calcium tetany
Milk fever
Parturient paresis
What species is milk tetany common in?
Dairy cattle, dogs, sows, and other species
When does milk fever usually occur?
Within the first 5 days after parturition (basically bc milk synthesis depletes the blood of calcium)
Problem with calcitonin and milk tetany
Female absorbs extra Ca during pregnancy and calcitonin helps deposit it in bones. But when lactation starts after giving birth, BLOOD calcium levels drop bc milk needs the calcium. The resulting low blood calcium stimulates parathyroid hormone production, but this is overridden by the calcitonin that is still present so blood can’t be released from bones, until several hours after the calcitonin was produced when it starts being destroyed. Then when the calcitonin is gone the danger of milk fever is gone, is the female lives that long
Modern and old-days treatment of milk fever
Modern: inject Ca, glucose, and Mg. The female will usually recover in less than 30 mins, but another injection may be needed to cure her
Old: reverse milk synthesis mechanism so the milk can be reabsorbed into body. This is done by inflating a cows udder with an air pump and a teat cannula and then sealing the teats with tape
Prevention of milk fever
- feed low calcium diet for 2 weeks before birth to stimulate parathyroid hormone, which will destroy calcitonin
- inject a big dose of vit D within 7 days prior to birth to stimulate extra ca absorption and therefore increase blood calcium levels (caution: if vit D is injected too soon then vit D toxicity, characterized by soft tissue and joint calcification, and milk fever may result)
What is the most versatile element found in livestock? Why?
P, it’s involved in almost every aspect of metabolism
What percent of all body P is found in the bones and teeth? Soft tissues and blood?
80%, 20%
Nearly all cells have P in them
Metabolic functions of P
- P combines with Ca to form crystals that resemble hydroxyapatite crystals, and these are components of hard tissues (therefore it’s indirectly controlled by same hormones as Ca bc it “follows” Ca)
- component of many enzymes (phosphoproteins)
- energy utilization (ATP for example)
- buffer in blood
- protein synthesis (P in RNA and DNA)
- lipid transport and metabolism and cell membrane structure (phospholipids)
Ca:P ratio in:
Monogastrics
Pigs
Laying hens
Growing chickens
Monogastrics: 1:1-1.5:1
Pigs: 1:1-1.2:1
Laying hens: much higher Ca bc egg shell is mostly Ca
Growing chickens: 2:1
Always check the current NRC or Extension Service recommendations
How much plant P is unavailable? Why?
1/2-2/3
Phytic acid in plants binds P and the complex (phytate P) is indigestible to monogastrics, which don’t have phytase to free the P from phytic acid
The phytate P in animal manure is an environmental problem
P deficiency symptoms:
- Rickets in growing animals
- decreased appetite and anorexia
- reduced productivity
- abnormal eating or chewing called pica (chewing on wood and bones, eating soil, and a depraved appetite)
- long term effects in adults result in lameness and reduced bone strength
Percent of Mg bound in bones?
70%
Remember: in terms of largest mineral presence, it goes Ca>P>Mg>others
:)
Functions of Mg
- bone development and maintenance
- needed by enzymes for optimal activity (all enzymes that hydrolyze ATP need it)
- carb, fat, and protein metabolism (bc of bullet above)
Deficiency symptoms of Mg
- neuromuscular hyperirritability (muscle spasms)
- skin lesions
- calcium deposits in arteries, kidneys, and soft tissue (arteriosclerosis?)
- reduced microbial fermentation in rumen and cecum
- retracted head in calves
- anorexia and reduced productivity
- grass tetany
- bone abnormalities
4 other names for grass tetany
Wheat poisoning
Grass staggers
Lactation tetany
Winter tetany
Low blood Mg levels
Grass tetany typically occurs in:
Beef cattle that are grazing lush green pastures, especially when they’re lactating (losing Mg in milk) or those grazing heavily fertilized pastures and those is colder temperatures (shivering depletes Mg)
(The grass is typically adequate in Mg but due to poor Mg absorption, blood, bone, and muscle Mg levels are reduced. The poor absorption can be caused by too much P and protein in the grass, so analyzing the grass for Mg alone won’t give you any advanced warning of grass tetany)
Symptoms of grass tetany
Standing alone Loss of appetite Easy excitability Viscousness Grinding of teeth Salivation Incoordination Collapse Convulsions Coma Death (usually the first indication that you have grass tetany unless you check your heard 3 or more times a day)
How long after first grass tetany symptoms are observed does death usually occur?
6-20 hours
Grass tetany treatment
Injection of calculi-Mg solution under the supervision of a vet, only if the animal hasn’t gone into a coma yet
If the animal has been unable to walk for a few hours before the treatment, results aren’t usually favorable. Also relapses after treatment are usually fatal.
Grass tetany prevention
Really difficult to prevent in grazing livestock bc of all the variables
1) fertilized supplemented with Mg, works best with sandy soils. Expensive solution
2) give each cow 2 oz/day of MgO mixed into a range cube or with grain. Tastes super bad so it’s hard to get them to eat it
3) limit grazing time or feed hay at night
4) feed lots of grain but it’s expensive and defeats the purpose of grazing
5) can also feed Mg carbonate, MgCl, or MgP. The poorest source of Mg is MgO but it’s cheapest
Mg deficiency may play a role in ______ in humans and animals
Osteoporosis
Which 3 minerals work together to maintain the osmotic balance in intracellular and extracellular fluids?
Na, Cl, and K
Which 2 minerals cause an animal to exhibit deficiency symptoms the fastest if deficient from the diet? Why is this bad?
Na and Cl. This is bad bc very few feeds contain enough salt (except seaweed, fish meal, and whey that hasn’t been desalted)
Is K usually deficient in a normal diet?
No, both plant and animal product are usually very high in K. However, supplementation of ruminant animals has been beneficial in recent years (especially after shipping stress)
Where are Na, Cl, and K found in vivo?
Na: extracellular fluid (90%)
K: intracellular fluid (90%)
Cl: both inside and outside of cells
The Na:K makes an electrochemical gradient surrounding the cell, which regulates nerve impulses and muscle contractions, so these two things are impaired during deficiency of Na and K
(remember the sodium potassium pump)
GENERAL deficiency symptoms for Na, Cl, and K
Anorexia, reduced growth, unthrifty appearance, reduced productivity; and death
3 functions of Na
1) acid base regulation (93% of bases in the blood have sodium. Think of bicarbonate!)
2) reduced reproduction
3) osmotic balance (water follows Na into the sweat gland)
Only direct water pumps in vivo are in the:
Heart
Intestines (peristaltic motion)
Lymph system
Na deficiency symptoms
Reduced growth rate Reduced feed efficiency Reduced milk production Weight loss Drinking urine and licking the ground in salty areas
3 Cl functions
1) acid base regulation (associated with 66% of blood acids)
2) component of gastric juice (HCl and salts)
3) osmotic balance, especially of extracellular fluid
Cl deficiency symptoms
Depressed growth rate
Other symptoms are probably masked by Na deficiency symptoms which are very fast and overwhelming
5 K functions
1) muscle and nerve functions (heart lesions and irregular heartbeat can happen when deficient in K)
2) osmotic balance
3) acid base maintenance
4) enzyme reactions
5) helps cells absorb AAs and glucose
K deficiency symptoms
Abnormal EKGs Growth depression Unsteady gait Muscle weakness Depraved appetite (pica) and wool biting in sheep Emaciation and death
Why is S the odd man out in mineral nutrition?
It has unique ties to AAs
It’s not required in inorganic form by the body
S functions through its presence in organic metabolites. What is it used to make?
The chondroitin matrix of cartilage Taurine Heparin Cysteine Other organic constituents of the body Feathers, gizzard lining, and muscles of birds
How does S deficiency affect sheep?
Reduced wool growth
Reduced weight gain of sheep and cattle
This can occur when you feed NPN instead of protein without supplementing S! However, these effects are the effect of inadequate microbial nutrition on which the host depends for synthesis of organic metabolites, so they can’t be considered as direct effects of S deficiency
Is S toxicity a major problem? Why or why not?
No, the intestinal absorption of inorganic S compounds is low
Fe is needed for proper ____ to occur in cells
Metabolism
What percent of body Fe is found in hemoglobin? In myoglobin in muscles and hemoglobin in RBCs combined?
Over 50%; 60-80%
What 3 molecules can the iron in hemoglobin bind to?
Oxygen, CO, and water
CO2 is carried back from the tissues to the lungs but it’s not attached to the iron directly
Is there enough Fe to meet requirements in most feeds? In milk?
Yes, no (especially in sows milk so baby pigs are susceptible to Fe deficiency)
How much hemoglobin can blood alone carry vs blood with hemoglobin?
1/2 (causes death by suffocation)
What plays the determining role for the homeostasis of iron metabolism?
Absorption (no excretion method!)
The intestinal mucosal cells control the amount of iron entering the animals body
Fe deficiency symptoms
Anemia (microcytic, hypochromic)
Diarrhea
Oral and skin lesions (due to tissue anoxia)
Decreased cytochrome activity (only in sever deficiency)
The thumps in baby pigs
Describe the thumps
Baby pig has a marginal iron supply when it’s born that lasts for 5-6 days. Sows milk has low iron content (lowest of all livestock species) and rapidly growing piglets are using all of their body iron
The thumps symptoms
Pallor of the skin Labored breathing Rough hair coat Poor and reduced growth Respiratory infections
Treatment of the thumps
1) inject soluble Fe solution into piglet before 6 days of age and then 1-2 weeks later depending on the product being raised. This method guarantees the pig will get enough Fe
2) oral dose of Fe with a stomach tube at about 4-6 days
3) Fe supplement coated with something sweet or iron water in pig pen
4) give piglets a chunk of dirt
5) feeding iron chelated to AAs to sow may help, but just feeding Fe won’t
Copper functions
Required for:
Fe absorption synthesis of hemoglobin bone collagen formation elastin formation (blood vessels) nerve transmission
Copper deficiency symptoms
Hypochronic anemia Deformed bones Ruptured aorta Incoordination Paralysis and infertility in cows
Copper (toxicity) imbalance effects
Tissue necrosis
Jaundice
Brown liver (due to Cu accumulation)
Cobalt function
Contained in vitamin B12, similar to sulfur in Met and Cys, so functions are those listed in B12
Cobalt deficiency symptoms
Called “wasting disease”
Listless Anorexia Weight loss Normochromic anemia Death
Cobalt (toxicity) imbalance effects
Thyroid hyperplasia (like goiter but goiter is tied to iodine)
Anorexia
Nausea
Diarrhea
Iodine function
Contained in thyroxin hormone
Iodine deficiency symptoms
Goiter (enlarged thyroid gland)
Hairless piglets
Premature aging
Lowered basal metabolic rate
Iodine (toxicity) imbalance effects
Vasodilation
Skin lesions
Nausea
Hyperthyroidism
2-3 g per 70 Kg of body weight is fatal in humans
Zinc functions
Required by several enzymes such as:
Carbonic anhydrase
Phosphatase
Other enzymes
Important in carb and amino acid metabolism
Zinc deficiency symptoms
Skin lesions Anorexia Slow growth Stiff joints Reduced serum zinc Impaired taste and dwarfism in humans Parakeratosis in pigs
Zinc (toxicity) imbalance effects
Reduces copper absorption Dermatitis Corrosion of the GI tract Diarrhea Possibly death
Selenium function
Component of gluthathione peroxidase (removes toxic peroxides, interacts with vit E which is an antioxidant so it prevents peroxide formation)
Se deficiency symptoms
“White muscle disease”:
Liver necrosis
Atrophy of the pancreas
When deficient simultaneously with vit E, results in muscular dystrophy in calves and lambs
Se toxicity (imbalance) effects
Blind staggers and alkali disease in western states Hair loss from tail in cattle and horses Hooves slough off Reproduction failure Anorexia Death
Toxicity symptoms are noted with as little as 9 ppm se in diet
Molybedenum function
Component of enzymes like xanthine oxide
Mo deficiency symptoms
Anorexia
Poor growth
Mo (toxicity) imbalance effects
Diarrhea
Anemia
Stiffness
Treatment: feed Cu above the requirement as Cu reduced Mo toxicity and vice versa
F function
Strengthens bone and teeth
Helps prevent dental carries (1 ppm in water)
F deficiency symptoms
Weak bone and teeth structure
F (toxicity) imbalance effects
Bones and teeth lose normal color and become thickened and soft
Mottled enamel in children
2-5 ppm in water produce toxic results in children
Fluorine is a cumulative process
Chromium function
??
Required for body cells to be sensitive to insulin
Chromium deficiency symptoms
Impaired glucose tolerance (decreased insulin sensitivity, glucose not absorbed)
Cornea (eye) lesions
Anorexia
Poor growth
Chromium (toxicity) imbalance effects
Unknown
Silicon function
Calcification of chick bone and connective tissue
Silicon deficiency symptoms
Small joints
Growth depression
Silicon (toxicity) imbalance effects
Not fully understood.
Silicon in urine may be deposited in kidneys, bladder or urethra to form Calculi (water belly), but other factors besides silicon are involved
Sulfur function
Component of Met and Cys (S must be provided as these in nonruminant)
Sulfur deficiency symptoms
AA deficiency in nonruminant
Ruminant: reduced MCO fermentation, poor MCO growth in rumen, anorexia, and reduced productivity
S (toxicity) imbalance effects
Reduces Mo toxicity
May result in Mo and Cu deficiency
Manganese functions
Component of enzyme
Needed in collagen synthesis (so bone formation)
Mn deficiency symptoms
Anorexia Reduced productivity Delayed sexual maturity Poor blood clotting Weak egg shells and bones Perosis or slipped tendon in poultry
Mn (toxicity) imbalance effects
Depressed hemoglobin synthesis due to reduced iron absorption
Minerals most likely to be deficient in livestock rations:
Macro: Mg Na P Ca K (in ruminants)
Basically all macro besides S and Cl! “Magical NaP, Calvin Kline.”
Micro: Mn (young chicks) Zn (animals fed high grain rations) Se (area dependent) I (area dependent) Fe (baby pigs)
Basically all micro besides Si, Mo, Co, Cu, Cr, F, and B “Man, zoinks, Selena! I feel…”
Is mineral toxicity ever a problem?
Yes, in several areas of the US it’s more of a problem than deficiency
How do you correct toxicities?
Mineral antagonisms
However, often the only solution is to dilute a feed with lots of the mineral with another feed that has little of the mineral
Feed formulation and or mixing errors can cause toxicities and deficiencies
5 methods commonly used to provide needed minerals to livestock:
1) adding free choice minerals in a self feeder (don’t mix in wrong ratio bc then the animal will have to eat too much to satisfy all mineral requirements! Also if one mineral is too high then toxicity or antagonism could occur)
2) adding free choice mineral salt plus a separate free choice feeder for Ca-P so animals can be more flexible in their consumption. (Some scientists think that animals will only eat what they need)
3) adding free choice salt, free choice Ca-P mix, free choice trace mineral mix. This gives the animal more flexibility especially if just salt is the limiting mineral
4) adding the needed minerals to a protein supplement such as a range cattle cube (cube of cottonseed meals, vitamins, salt, Ca, P, trace mineral cube). However, if the animal needs more of one mineral it has no way to get it without eating more range cube or supplement, which isn’t usually available
5) adding the complete mineral mix to a diet plus offering salt free choice. This allows the animal extra salt if they need it. Beef cattle feedlots and dairies usually use this method
Don’t mix minerals and vitamins together (unless chelated) for over _____ days. Why?
60-90; the minerals may oxidize or bind vitamins, making them both unavailable to the animal
Should you feed unneeded minerals? Why?
No, it’s costly and there is a chance of mineral antagonisms occurring
Why should you protect the mineral feeder from weather?
When rainwater accumulates in it, it will turn to brine and reduce consumption
How does a fresh supply of water affect mineral consumption?
It increases it
Why should aluminum be considered as required?
Al accumulates in regenerating bone
Al stimulates enzyme systems involved in succinate metabolism
Al has been reported to be essential in female rat fertility
Metabolic requirement unknown
Why should arsenic be considered as required?
Supplementation of As to purified diet has been reported to:
Increase growth of chicks
Decrease neonatal mortality in rats and goats
Improve birth weight
Why should cadmium be considered as required?
Rats fed little Cd show a growth depression when maintained in a metal free environment
Why should nickel be considered as required?
Dietary requirement reported for chicks
Deficiency reported in pigs, goats, rats, and sheep
Why should tin be considered as required?
Bc of a single report of a growth response to dietary Sn in rats kept in plastic isolators to prevent environmental contamination
Why should vanadium be considered as required?
Deficiency impairs reproductive efficiency
Beneficial effects of V on rats, chicks, and others have described tissue uptake and movement of V
V stimulates the rate of glucose transport into rat adipocytes
V ions mimic the effect of insulin on glucose oxidation in rat adipocytes
Why should barium be considered as required?
May be required for growth of some species
Why should barium be considered as required?
Might be required for growth of mice and chicks
Why should rubidium and cesium be considered as required?
May replace some of the vitamin K requirements
When did today’s vitamin nomenclature arise?
1990 in Journal of Nutrition
Who came up with the name “vitamin” and when?
Casimir Funk, 1912, vitamine. Vita=life, amine= contains N (he thought they all did). But then the “e” of amine was dropped when he realized that some don’t have N
Last group of nutrients to be discovered and quantified
Vitamin facts
- Throughout history, vitamin deficiencies have been a major cause of death in both humans and domesticated animals
- even though they’re only needed in minute quantities, when they’re missing or deficient productivity declines markedly
Are commercial vitamin supplements available? How expensive are they?
Yes, they’re inexpensive
Define vitamin
Any group of a feed constituent essential in small quantities to maintain life but not themselves supplying energy (although some are very involved in intermediary metabolism)
They regulate many body reactions, but don’t become part of the body structure
Are vitamins inorganic or organic?
Organic! But they’re not carbs, fat, or protein
4 fat soluble vitamins:
K, A, D, E
12 water soluble vitamins
Ascorbic acid (vit C) Thiamin (B1) Riboflavin (B2) Niacin (B3) Pyridoxine (B6) Cyanocobalamin (B12) PABA (para-aminobenzoic acid) Pantothenic acid Biotin Choline Myoinositol Folic acid (folacin)
Note: myoinositol and PABA are both made by normal gut microbes in animals and people. Under normal conditions, there isn’t evidence for a dietary requirement. Some nutritionists still refuse to put them on the list of water soluble vitamins
Vitamins are added to feed components based on:
1) Vitamin activity found in the vitamin source (expressed as International Units, I.U., or US pharmaceutical units, USP, per Kg diet)
So IU/Kg or USP/Kg
These systems take into consideration the vitamins chemical structure (several of the vitamins are available in a variety of molecular structures that vary in vitamin activity) and also the digestibility and absorbability of the vitamin
2) weight (not ideal bc digestibility, absorbability, and activity are variable, but it works if these things are known)
What are 3 substances that are usually chemically related to biologically active vitamin forms?
Antivitamins, vitamin antagonists, and pseudovitamins
The problem: these don’t have vitamin activity but the body can’t tell that they’re not actual vitamins. In addition, antagonists refuse to be replaced by the proper substances, which can shut down metabolism
Chemical composition of fat vs water soluble
Fat soluble: made of C,H, and O
Water soluble: CHO and also either N, S, or Co
Occurrence of fat vs water soluble vitamins
Fat soluble: plants in the precursor form (provitamins)
Water soluble: not in provitamin form (Trp can be convert to niacin but isn’t considered a provitamin)
Physiological action of fat vs water soluble vitamins
Fat: associated with regulation of structural units including building, maintenance, and physiological action
Water: B vitamins play a variety of very important roles in intermediary metabolism. Energy transfer cannot occur without them
Absorption of fat soluble vs water soluble
Fat: absorbed along with lipid from the gut
Water: absorbed with water across the small intestine
Storage of fat vs water soluble vitamins
Fat: can be stored in the fat tissue of the body. The storage increases with the intake and can actually reach toxic levels in the body. It can be extensive enough to allow animals to survive, even flourish, on fat-soluble vitamin deficient diets for a long time (even months) without showing deficiency symptoms
Water: only stored in the body for a very short term use. A 2-4 day storage is as good as it gets. Therefore, a constant dietary source is much more important. B12 is the exception, there’s significant B12 storage
Excretion of fat vs water soluble vitamins
Fat: excreted in feces
Water: B vitamins are generally excreted via the kidney into urine. B12 is also excreted via bile
Synthesis of fat vs water soluble vitamins
Fat: A, D, and E aren’t made by microbes and must be supplemented in many rations
Water: rumen microbes can make the water soluble vitamins and vitamin K, so these don’t need supplementation
Source of vitamin A
- B-carotene precursor found in green and yellow plants
- corn 1/8 value of green forage
- milo devoid
- fish oil (good source)
- yellow fat
- liver (polar bear)
Synthetic costs 2 cents/10^6 IU
Animal storage in vit A
Substantial reserves may be stored in body fat and liver if diet permits (results in yellow fat)
Stability of vit A
Destroyed by oxidation (hay curing)
This is why new corn has activity but 1 year old corn doesn’t
In vivo functions of vitamin A
Vision
Epithelium integrity of eye and respiratory, alimentary, reproductive, and urogenital tract
Bone formation
Vit A deficiency symptoms
Night blindness or total blindness Diarrhea due to poor nutrient absorption Pneumonia Bladder stones Sterility Fetus absorption Crooked bones Bone overgrowth
Vit A toxicity symptoms
Skin disorder
Hair loss
Fragile bone
Vitamin D sources
Ergosterol precursor
Found in plants
7-dehydrocholesterol precursor found in animals
Both animal and plant sources require sunlight to be converted to active form
Fish oil and sun cured plants are excellent sources
Animal storage of vit D
Some in liver
Stability of vitamin D
Good
In vivo functions of vit D
Calcium absorption
D2 works in all species except poultry
Poultry require D3
Vit D deficiency symptoms
Rickets (soft bones) due to poor ca absorption Weakness Poor egg production Anorexia Reduced growth
Toxicity symptoms of vit D
Hypercalcificstion of heart, kidney, and joints
Especially toxic to human infants
Vit E sources
Germ of cereal grains
Green forage
Vit E storage
Large amounts can be stored in fat and liver
Stability of vit E
Low, easily oxidized
In vivo functions of vit E
Antioxidant, functions with Se to detoxify perioxides
Cell membrane stability
Vit E deficiency symptoms
Membrane damage
Brain lesions in chicks
Degeneration of testes in rats, so it’s a cure for rat impotence
Vit E toxicity symptoms
None in most species, nausea in humans
Vit K storage
Bacterial synthesis in the rumen and large intestine (for all but poultry, nonruminants have to practice coprophagy to get the benefit)
Green leafy materials, liver, fish, eggs
Commercial sources (menadione)
Vit k storage
Some in liver
Stability of vit K
Fairly stable.
Actively reduced by dicumerol found in spoiled sweet clover (dicumerol used at rat poison), therefore animals fed spoiled sweet clover need higher vit K intake to offset the dicumerol effect
In vivo functions of vit K
Required for rapid blood coagulation (needed for prothrombin formation which is necessary for proper clot formation)
Vit K deficiency symptoms
Hemorrhage
Reduced clotting time
Anemia
Weakness
Toxicity symptoms of vit K
Relatively nontoxic
Thiamin (B1) sources
Good sources include bacteria, forages, and other feedstuffs
Animal storage of thiamin
Low (3-9 days)
Thiamin stability
Destroyed by moist heat
Raw fish contain thiaminase that lowers thiamin activity and can precipitate deficiency symptoms
In vivo functions of thiamin
Carb metabolism
Thiamin deficiency symptoms
Edema Anorexia Diarrhea Weakness Convulsions Brain lesions Paralysis Reduced growth Polyneritis in poultry Polioencephalonalacia in cattle Increased blood lactate and pyruvate levels
Toxicity symptoms of thiamin
Relatively nontoxic
Riboflavin (B2) sources
Plants Yeast Milk Eggs Liver
Most nonruminant diets contain inadequate amounts so always add to nonruminant diet
Stability of Riboflavin
Good except destroyed by blue and violet light (riboflavin activity of milk in glass bottles and exposed to sunlight is reduced to 0 in about 8 hours)
In vivo functions of riboflavin
Component of FAD in electron transport chain
Energy metabolism
Protein metabolism
Deficiency symptoms of riboflavin
Curled toe paralysis and leg paralysis in chicks
Crooked legs, dermatitis, and reproductive failure in swine
Dermatitis in man
Ruminant deficiency unknown
Anorexia and reduced growth
Toxicity symptoms of riboflavin
Relatively nontoxic
Niacin (B3) sources
Leafy materials Vasodilation Distillers products Cereals are generally a poor source 60 mg tryptophan and 1 mg niacin (expensive though)
Animal storage of niacin
Poor
Stability of niacin
Very stable
In vivo functions of niacin
Hydrogen transport (NAD) in glycolysis Diarrhea Dermatitis Energy metabolism Synthesis
Deficiency symptoms of niacin
Pellagra in humans Dementia Lesions on tongue, lips, and mouth Nausea Black tongue in dogs Anorexia Reduced growth
Pyridoxine (B6) sources
Cereal grains
Yeast
Bacteria
Legumes
Animal storage of pyridoxine
Poor
Stability of pyridoxine
Very stable
In vivo functions of pyridoxine
Fat, carb, and protein metabolism
Antibody formation
Deficiency symptoms of pyridoxine
Deficiencies are rare
Anemia Dermatitis Staggering gait Convulsions Anorexia Reduced growth
Toxicity of pyridoxine
Nontoxic
Pantothenic acid sources
Soybean meal
Yeast
Bran-rich cereals
Corn and meat are poor sources
Animal storage of pantothenic acid
Poor
Stability of pantothenic acid
Fair
In vivo functions
Fat, carbs, and protein metabolism
Constituent of coenzyme A
Pantothenic acid deficiency symptoms
Goose stepping in pigs Dermatitis Eye matting Paralysis Hair loss Fatty liver Anorexia Poor growth Burning feet syndrome in humans
Pantothenic acid toxicity symptoms
Nontoxic
Biotin sources
Synthesized in rumen and intestines
Avidin found in egg white ties up biotin and can result in deficiency in animals fed egg white
Animal storage of biotin
Poor
Stability of biotin
Very stable
In vivo functions of biotin
Fat, carbs, and protein metabolism
Carboxylation reactions
Biotin deficiency symptoms
Dermatitis Hair loss Feather loss Depression Foot lesions Fatty liver in birds Impaired leg coordination Paralysis in hindquarters of swine Anorexia Reduced growth
Toxicity symptoms of biotin
None
Choline sources
Animal and plant products
Methionine can serve as a methyl donor
Choline storage
Poor
Choline stability
Fair
In vivo functions of choline
Cell structure (membranes) Fat metabolism Methyl donor
Choline deficiency symptoms
Most likely in poultry
Fatty liver Growth depression Perosis in poultry Anorexia Reduced growth
Choline toxicity symptoms
None
Folic acid sources
Liver Legumes Tankage Yeast Bacteria Soybean meal
Folic acid storage
Poor
Folic acid stability
Poor
Folic acid in vivo functions
Carb and protein metabolism
Nucleic acid synthesis
Folic acid deficiency symptoms
Anemia Intestinal upsets Growth depression Anorexia Reduced growth
Folic acid toxicity symptoms
None
Cyanocobalamin (B12) sources
Plants devoid
Protozoa and bacterial products are good sources
Liver contains some if animal fed adequate diet
Feces are rich in B12 (cow manure factor)
B12 animal storage
Poor
B12 stability
Fair
In vivo functions of B12
Nucleic acid synthesis
Carb and protein synthesis
Propionic acid metabolism
Maturation of RBCs
B12 deficiency symptoms
Pernicious anemia
Anorexia
Reduced growth
Vitamin C sources
Citrus fruits
Green leafy veggies
Tomatoes
Vitamin C storage
Poor
Vitamin C stability
Good
Vit C in vivo functions
Formation and maintenance of intercellular material in some species
Has a role in a various redox reactions in living cells
Vit C deficiency symptoms
Human, pig, bat, some birds and some fish:
Swollen, bleeding gums
Increased oxidation of vit C which increases the requirement
Loosening of teeth
Weak bones
Vit C toxicity symptoms
Possibly kidney stones
PABA sources
Plants are good sources
Liver
PABA animal storage
Poor
PABA stability
Good
PABA in vivo functions
Enhances growth of microbes and chicks
PABA deficiency symptoms
Very rare in livestock
Poor growth in chicks
Inositol sources
Plants
Inositol storage
Poor except in sharks
Inositol stability
Good
Inositol in vivo functions
Cures alopecia in mice
Inositol deficiency symptoms
Very rare in most livestock feeding situations
In general, vitamins promote:
General health and vigor, and are involved in mechanisms to fight stress and disease in the animal such as antibody synthesis
Main vitamins that are deficient in ruminants
A and probably D in special circumstances
Main vitamins that are deficient in swine
Riboflavin Niacin Pantothenic acid B12 Choline A D Possibly E
Main vitamins that are deficient in poultry
All vitamins except:
C
Inositol
PABA
Main vitamins that are deficient in horses
A
D
E
Thiamin
