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Vitamin Nutrition Syllabus
Spring 2004
Texas Ag. Experiment Station – Amarillo
Texas Tech University
West Texas A&M University
Instructor: C. Reed Richardson, Ph.D.
Professor and Director of the
Center for Feed Industry Research
and Education, Texas Tech University
Phone: (806) 742-2516
Fax:
(806) 742-4003
Email: [email protected]
Reference Text: Vitamins in Animal Nutrition by L.R. McDowell
Grading: Hour Exams (2) 35% each = 70%
Term paper (1)
= 30%
**Grade for the mineral/vitamin course will be calculated as 50% mineral
section plus 50% vitamin section.
Communication with students: All students are expected to have an e-mail
address. Term Papers and general correspondence will
be e-mailed to [email protected] Texas Tech
students may hand deliver term papers or use e-mail.
After grading, scores and comments will be returned
via email.
Hour Exams: Both hour exams will be closed book. The first exam will be given
during regular class time and the second exam given during the scheduled
time for final exams. For locations other than Texas Tech, exams will be
sent to a faculty/staff person at each location who will deliver exams to
the classroom and collect the completed exams. Each exam will be
comprehensive over material covered up to the exam date. The second
exam will cover only material after the first exam.
Term Paper: * It should be 8-10 double spaced pages and is due no later than the last
day of class, April 29Th. Format should be “Times New Roman”, 12
point font with 1.25 inch margins.
* Topic: Choose a vitamin or vitamin-like substance and develop
a subtopic that addresses one of the following six subject
areas:
1)
2)
3)
4)
5)
6)
chemical structure, properties, and antagonists
metabolism (digestion, absorption, and transport)
analytical procedures
functions in mammals and poultry
requirements
effects of deficiency
* Grading will be based on both depth and breadth of the paper. The reference text will
serve as a base to start the paper from, but should be greatly expanded in depth and
breadth to provide a clear, detailed understanding. There will be no duplication of
subtopics at a particular TTVN site since there are over 150 subtopics to choose from.
Tentative Schedule
DATE
March
TOPIC
4
Introduction; Classification; History
9
Fat Soluble Vitamins; Vitamin A
11
16 -18
April
May
Vitamin D; Vitamin E
Spring Vacation
23
Vitamin K; Vitamin C
25
Antioxidant vitamins ; Water soluble vitamins
30
Review and discussion (20 minutes); First Exam
6
Thiamin; Riboflavin
8
Riboflavin; Niacin
13
Vitamin B6; Panothenic acid
15
No class (Plains Nutrition Council Spring Conference)
20
Biotin; Folacin
22
Vitamin B12; Choline
27
Vitamin-like substances
29
Term Paper Due
7
Second Exam. (7:30 – 10:00 a.m.)
**Date and time for Texas Tech students, other locations to
be arranged during final exam week.
Main Cellul
ar Roles of B Vitamins Involved in
Metabolism of Carbohydrates, Proteins and Fats
Diet
Proteins
Carbohydrates
Fats
Body Cells
Free Fatty Acids
B2
B1
Glucose
Biotin
B2
PA
Niacin
B6
Biotin
Niacin
Amino Acids
B6
B12
Folacin
B6
B1
B2
Pyruvic
Acid
Acetyl
Co-Enzyme A
Niacin
Mitochondria
Krebs Cycle
B1
Folacin
B2
PA
Niacin
B12
Electrons (H+’s)
Excretion
ATP, H2O
C. R. Richardson, 1999
ANSC 5308
VITAMIN NUTRITION SECTION
LECTURE 1
INTRODUCTION
1.
Syllabus
2.
Definitions of vitamins
3.

Complex organic compounds required in small amounts

Required for essential life processes

Consist of a mixed group of compounds unrelated to each other

Some vitamins may deviate from the above definition (Vitamin C, Niacin, Vitamin
D)
Making sense of the role of vitamins in biological processes

Train yourself to visualize molecular events

Everything that occurs in the observable world has its basis in the unobservable
world of atoms and molecules

Develop a logical approach to solving

Apply the principles you learn to real-world situations

Let yourself be amazed by what you learn and curious about all there is still left to
learn

Optimum vitamin allowances

Vitamin controversies
problems . . .
CLASSIFICATION
1.
Fat soluble




2.
Vitamin A
Vitamin D
Vitamin E
Vitamin K
Associated with lipids
in feedstuffs; absorbed
along with dietary fats;
storage
Water soluble
 Vitamin C
 B complex – rapidly excreted
 Other
VITAMIN
SYNONYM
Fat Soluble
Vitamin A1
Vitamin A2
Retinol
Dehydroretinol
Vitamin D2
Vitamin D3
Vitamin E
Vitamin K1
Vitamin K2
Vitamin K3
Ergocalciferol
Cholecalciferol
Tocopherol
Phylloquione
Menaquione
Menadione
Water Soluble
Thiamin
Riboflavin
Niacin
Vitamin B6
Pyridoxamine
Pantothenic Acid
Biotin
Folacin
Vitamin B12
Choline
Vitamin C
Vitamin B1
Vitamin B2
VitaminPP, Vitamin B3
Pyridoxol, Pyridoxal,
Vitamin B5
Vitamin H
Vitamin M, Vitamin BC
Cobalamin
Gossypine
Ascorbic Acid
3.
Vitamin Nomenclature

Letters of the Alphabet

Designation of groups – the “B” group

System of suffixes – D2, etc.

Describing function or its source
1)
H (Biotin) – “Haut” German for “skin”
2)
K – Danish for “koagulation” (coagulation)
3)
Panothenic Acid – Greek for “pantos”

Rules for nomenclature by the Committee of Nomenclature of the American
Institute of Nutrition (CNAIN, 1981).
VITAMIN REQUIREMENTS
1.
Dietary needs differ widely among species
2.
Some vitamins are metabolic essentials, but not dietary essentials
3.
Ruminants usually satisfy their needs for B vitamins from feed and symbiotic
microorganisms
4.
Horses may meet most of their requirements for B vitamins from symbiotic
microorganisms
VITAMIN OCCURRENCE
1.
Vitamins originate primarily in plant tissue
2.
Vitamin B12 – occurs in plant tissue from microbial synthesis
3.
Vitamins A and D occur in plants as a provitamin (precursor)
4.
No precursors are known for any water soluble vitamins
5.
B vitamins are universally distributed in all living tissue
6.
Fat-soluble vitamins are completely absent from some tissue
HISTORY
1.
Late 1800’s and early 1900’s – chemically defined diets
2.
1860 Louis Pasteur / Justus Von Liebig – yeast studies
3.
Vitamin hypothesis
4.
1912 Casimer Funk proposed the “vitamin theory”

“vital amine”
5.
Later the term vitamin was coined
6.
1915 rat required two growth factors
7.

Fat-soluble A

Water-soluble B
1919 – Vitamin A
1922 – Vitamin D
1923 – Vitamin E
1926 – Thiamin
1926 – Riboflavin
1928 – Bacterial synthesis of B vitamins
1928 – Vitamin C
1930 – Panothenic Acid
1932 – Choline
1934 – Vitamin B6
1934 – Vitamin K
1935 – Niacin
1936 – Biotin
1943 – Folacin
1948 – Vitamin B12
The only disease a vitamin will cure is the one caused by a deficiency of that vitamin.
FACTORS THAT ADVERSELY AFFECT THE STABILITY OF VITAMINS
1.
Moisture
2.
Temperature
3.
Light
4.
Pressure
5.
Friction
6.
Trace minerals (Cu & Fe)
7.
Oxidizing and reducing agents
8.
pH
9.
Chemicals
10. Feed composition
VITAMIN DESIGN AND DELIVERY
1.
Crosslinking process (beadlet, insoluble in H2O)
2.
Coating
3.
Mixing with stable carriers
4.
Water flush into complete diet and rapid mixing and delivery
HOW TO ADD TO FEEDS
1.
Premix
2.
Manual weighing and hand addition
3.
Computer weighing and direct addition
4.
Sequence of batching ingredients
ANSC 5308
VITAMIN NUTRITION SECTION
LECTURE 2
FAT SOLUBLE VITAMINS
1.
A, D, E, and K
2.
Have some properties in common, yet each has a distinct physiological role
3.
Diversity of primary biological functions




4.
Excretion


5.
A – vision, and cellular differentiation
D – calcium absorption
E – antioxidant
K – blood clotting
Fat soluble – feces via the bile
Water soluble – rapid in urine
Excesses


6.
Composition


7.
Fat soluble – C, H, and O
Water soluble – C, H, O and some have N, S or Co
Absorption


8.
Fat soluble – A and D are toxic
Water soluble – relatively nontoxic
Fat soluble – passive diffusion
Water soluble – passive diffusion, but some by active process if low level in the
diet
Some deficiency signs of fat soluble may be related to function


D – required for Ca metabolism and deficiency results in bone abnormalities
Water soluble are much less specific and deficiency signs are difficult to relate to
function
1)
2)
Most result in – dermatitis, rough hair coat, poor growth, and reduced feed
efficiency
Several cause loss of pigment in hair; and anemia which is a deficiency of
hemoglobin
VITAMIN A
1.
May be most important from a practical standpoint
2.
Needed by all animals, including ruminants
3.
Found in plants as carotenoids (precursors)

4.
Higher in yellow and green plants
Deficiency – blindness in children throughout the world
CHEMICAL STRUCTURE AND PROPERTIES
1.
Vitamin A1 – retinol (C20 H30 O)

Replacement of alcohol group with aldehyde gives Retinal

Replacement with an acid gives retionic acid
2.
Vitamin A2 – (3, 4 –dehydroretinol)
3.
Since Vitamin A contains double bonds, it can exist in isomeric forms






all – trans
13 – cis
11 – cis
9 – cis
11, 13 – di-cis
9, 13 – di-cis
Biological Activity, %
Rats
Chicks
100
100
75
50
47
?
21
?
15
?
24
?
4.
Yellow carotenoids
Source
Relative
Rat-Biopotency
(All trans forms)
Plants/
animals
100
Plants/
animals
25
Gamma carotene
Less ubiquitous
14
Beta zeacarotene
Yellow corn
25
Cryptoxanthin
Yellow corn,
some fruits &
flowers
29
Beta carotene
Alpha carotene
Zeaxanthin
Lutein
(xanthophyll)
5.
6.
Corn, egg
yolk
0
Green leaves,
egg yolk
0
The most active form of Vitamin A and that most usually found in mammalian tissues is
all-trans

Cis can arise from trans but a marked loss on Vitamin A potency results
Pure Vitamin A has twice the potency of beta carotene

Only one molecule of Vitamin A is formed from one molecule of beta carotene
ANALYTICAL PROCEDURES
1.
Biological methods

Growth responses – rats or chicks


2.
Physicochemical methods

3.
Liver storage tests – various species
Cell changes in vaginal smears – rats
Color reactions
1) Carr-Price method (antimony trichloride)
2) Gas chromatography
3) Thin-layer chromatography
4) Spectrophotometric procedures
5) High-pressure liquid chromatography (HPLC)
Activity expressed



International units (IU)
U.S. pharmacopoeia units (USP)
1) IU = USP
IU defined as
1) 0.300 ug of Vitamin A alcohol (retinol), or
2) 0.550 ug of Vitamin A palmitate

One IU of Vitamin A activity = 0.6 ug of beta carotene
METABOLISM
1.
A number of factors influence digestibility of carotene





Type of forage (hay, silage, greenchop, or pasture)
Month of forage harvest
Species of plant
Plant dry matter
Season – higher in warmer months
2.
Appreciable amounts of carotene or Vitamin A may be degraded in the rumen – 40 to 70
%
3.
Absorption and transport


Conversion of beta carotene to Vitamin A occurs in intestinal mucosa
In most mammals the product absorbed is Vitamin A itself
1)
2)
Some species have ability to absorb dietary carotenoids – humans, cattle,
horses, and carp
In case of cattle there is a strong breed difference – Holstein vs. Guernsey and
Jersey
a) Difference may be due to – suitable receptor proteins, or micellar
solutions in intestinal lumen

Some Vitamin A derivatives are reexcreted into intestinal lumen via the bile
1) Retionic acid
2) Some retinol
3) Vitamin A glucuronides

Vitamin A alcohol (retinol) is transported in the blood by retinol binding protein
(RBP)
1) RBP is secreted by hepatic parenchymal cells, mol. wt. of 20,000 and has one
binding site for one molecule of retinol
2) 90% of plasma RBP is complexed to thyroxine-binding prealbumin
3) Storage and release of Vitamin A by the liver is under several forms of
homeostatic control
STORAGE
1.
Liver normally contains 90% of total body Vitamin A, remainder mostly in kidneys,
lungs, adrenals and blood

2.
Exceptions
1) Stomach oils of certain seabirds
2) Intestinal wall of some fish
3) Eyes of certain shrimp
Measurement of liver stores of Vitamin A at slaughter or in samples obtained by biopsy
is useful in studying Vitamin A status
FUNCTIONS
1.
Necessary for support of growth, health, and life of higher animals

In the absence of Vitamin A, animals cease to grow and eventually die
2.
The metabolic function of Vitamin A, explained in biochemical terms, is still
incompletely known
3.
Deficiency causes four different and probably physiologically distinct problems




Loss of vision
1) Due to failure of rhodopsin formation in the retina
Defects in bone growth
Defects in reproduction
1) Male – failure of spermatogensis
2) Female – resorption of the fetus
Defects in growth and differentiation of epithelial cells
REQUIREMENTS
1.
Requirements can be expressed as

IU per kilogram body wt. – on a daily basis


A unit of the diet
1) General practice is per unit of diet
Tables 2.1, 2.2, 2.3, 2.4, 2.7, and 2.8
DEFICIENCY SIGNS
1.
Ruminants











Reduced feed intake
Rough hair coat
Edema of joints and brisket
Lacrimation
Xerophthalmia (dry eye)
Night blindness
Slow growth
Diarrhea
Convulsive seizures
Improper bone growth
Blindness







2.
Low conception rates
Abortion
Stillbirths
Blind calves
Abnormal semen
Reduced libido
Susceptibility to respiratory and other infections
Swine

Principally nervous signs
1) Unsteady gait
2) Incoordination
3) Trembling of legs
4) Spasms
5) Paralysis

During reproduction and lactation
1) Failure of estrus
2) Resorption of young
3)
4)
5)
6)
7)
8)
9)
3.
Poultry





4.
Wobbly gait
Weaving and crossing of hind legs while walking
Dropping of the ears
Curving with head down to one side
Spasms
Inability to stand
Impaired vision
Slower growth
Lowered resistance to disease
Eye Lesions
Muscular incoordination
Other
Horses

Night blindness






5.
Lacrimation
Keratinization of the cornea and respiratory system
Reproductive difficulties
Capricious appetite
Progressive weakness
Death
Humans




Occurs in endemic proportions in many developing countries
Alcohol consumption results in liver Vitamin A depletion
Drugs such as phenobarbital or food additives such as butylated hydroxytoluene
(BHT), when combined with ethanol, results in greater depletion of liver Vitamin A
Deficiency is nearly always associated with
1) Protein-energy malnutrition
2) Parasitic infections
3) Intercurrent infections
VITAMIN D
4.
Thought of as the “sunshine vitamin”
5.
Two major natural sources:


6.
Ergocalciferol (D2) – occurs in plants
Cholecalciferol (D3) – occurs in animals
Synthesized in various materials when exposed to sufficient sunlight


Not needed in the diet with adequate sunlight exposure
Total confinement of animals leads to limited or no exposure to sunlight – poultry,
swine, other
7.
Deficiency – rickets in young; osteomalacia in adults
8.
Vitamin D functions as a hormone
CHEMICAL STRUCTURE and PROPERTIES
1.
Group of compounds that have antirachitic activity
2.
All sterols with Vitamin D activity have the same steroid nucleus, they differ only in the
side chain attached at carbon 17


UV light
Plant steroids  Ergosterol 
Vitamin D2 (Ergocalciferol)
Cholesterol or Squalene  7-Dehydrocholesterol
UV light


Vitamin D3 (Cholecalciferol)
Precursors have no antirachitic activity until the B-ring is opened between the 9-10
carbons by irradiation and a double bond formed between the 10 and 19 carbons
3.
Colorless crystals insoluble in water, but soluble in alcohol and organic solvents
4.
Destroyed by over-treatment with UV light and peroxidation (polyunsaturated fatty
acids)
5.
Vitamin D Activity:


RAT – D2 and D3 are equally active
BIRDS – D2 has only 1/10th the activity of D3
ANALYTICAL PROCEDURES
1.
Vitamin D analysis is complex because of so many isomers



2.
Standard method is biological assay
Only vitamin in which biological method is still used
Rats and chicks are assay animals of choice
1) Involves developing rickets
2) Then, adding Vitamin D for 7d, followed by a line test (deposition of calcium
salts) with silver nitrate
Physical and chemical methods include:



Ultraviolet absorption
Colorimetric procedures
Fluoresence spectroscopy



Gas chromatography
Competitive binding assays
High pressure liquid chromatography (HPLC)
METABOLISM
1.
Absorbed from the small intestine and requires bile salts


Only about 50% of a dose of Vitamin D is absorbed
D3 is produced by irradiation of 7-dehydrocholesterol with UV light from the sun
or and artificial source
1)
2)
3)
4)
5)
Once formed, 7-dehydrocholesterol is thermally isomerized to D3 over 2-3
days
Only about 15% 7-dehydrocholesterol in human skin is converted to D3
11-45 min. daily sunshine prevents rickets in chicks (longer exposure does not
increase D3 concentration)
90% of 7-dehydrocholesterol synthesis occurs in the epidermis
Rickets can be successfully treated by rubbing cod liver oil on the skin
6)
2.
Once D2 or D3 enters the blood, it circulates at relatively low concentrations






3.
Some D3 formed on the skin ends up in the digestive tract because of licking
of skin and hair
Probably a result of rapid accumulation in the liver
Liver hyroxylates the 25 carbon in the side chain to produce 25-OH Vitamin D
1) Major circulating form of Vitamin D
2) Conversion to 25-OHD3 takes place in the microsomes and the mitochondria
of the liver
Intestine and kidney also produce small amounts of 25-OHD3
25-OHD3 is transported to the kidney where it is converted to a variety of
compounds of which 1,25-(OH)2D3 is the most important
1,25-(OH)2D3 formed in the kidney is transported to the intestine, bones, or
elsewhere
1,25-(OH)2D3 is carefully regulated by parathyroid hormone in response to serum
Ca and P concentrations
Transport of 25–OHD3, and possibly 24,25–(OH)2D3 and 1,25-(OH)2D3 occurs on the
same protein

4.
This protein has a mol. wt. of 50,000 – 60,000 in humans
1) Single chain polypeptide
2) Called transcalciferin, or Vitamin D – binding protein (DBP)
Land animals and humans do not store large amounts of D, in contrast to aquatic species
which store much more




Much less storage than Vitamin A
Blood has the highest concentration; in pigs several-fold higher than in the liver
During times of deprivation, Vitamin D in tissues is released slowly
Transplacental movement of Ca increases dramatically during the last trimester of
gestation

A liberal intake of Vitamin D during gestation does provide a sufficient store in
newborn to prevent early rickets
FUNCTIONS
1.
Enhancement of intestinal absorption and mobilization, retention, and bone deposition of
calcium and phosphorus
2.
Recently, evidence suggest a role in immune cell functions
3.
Also, possible use of Vitamin D analogs in differentiation of myelocytic-type leukemias
and in the treatment of psoriasis
4.
1,25-(OH)2D3 works in relationship with thyrocalcitonin (calcitonin) and parathyroid
(PTH) hormones to control blood calcium and phosphorus levels

Calcitonin regulates high serum Ca levels by
1) Depressing gut absorption
2) Halting bone demineralization
3) Reasorption in the kidney

Vitamin D brings about an elevation of plasma Ca and P by stimulating pump
mechanisms in
1)
Intestine
2)
3)
5.
In 1963 it was demonstrated that Vitamin D regulated P absorption and transport, as
well as Ca

6.
P is transported against an electrochemical potential gradient involving sodium in
response to 1,25-(OH)2D3
Bone synthesis in young animals

7.
Bone
Kidney
Minerals are deposited on the matrix by an invasion of blood vessels that give rise
to trabecular bone
1) This process causes bones to elongate
2) During Vitamin D deficiency, this organic matrix fails to mineralize
3) 1,25-(OH)2D3 brings about mineralization
Vitamin D is involved with PTH in mobilization of Ca from bone to the extracellular
fluid compartment
8.
Another role of Vitamin D is in the biosynthesis of collagen in preparation for
mineralization

9.
Deficiency of Vitamin D causes inadequate cross-linking of collagen as a result of
low lysyl oxidase activity
Vitamin D functions in the distal renal tubules to improve Ca reabsorption
REQUIREMENTS
1.
Animals and humans do not have a nutritional requirement for Vitamin D if sufficient
sunlight is available
2.
Factors influencing dietary Vitamin D requirements include




Amount of Ca and P
Ratio of Ca and P
Availability of Ca and P
Species

3.
Sunlight radiation






4.
Contains only a small part of the UV range for Vitamin D synthesis
More potent in the tropics than in the arctic zones
More potent in summer than in winter
More potent at noon than in morning or evening
More potent at high altitudes
Provides most of its antirachitic powers during the 4 h around noon
Clouds, mist, smoke and air pollution screen out many UV rays

5.
Physiological effects
Thus, rickets has been called the first air pollution disease
Colors of hair coat and skin affect ultraviolet irradiation


More effective on exposed skin than through a heavy coat of hair
Less effective on dark-pigmented skin
1) White pigs resist Vitamin D deficiency twice as long as colored pigs
2)
6.
White humans, 20-30% of UV radiation is transmitted through the epidermis;
black humans, less than 5% is transmitted
Aging effect on production of Vitamin D3

In humans older than 20 years
1) Skin thickness decreases linearly with time
2) Aging decreases more than 2-fold the capacity of the skin to produce
previtamin D3
REQUIREMENTS
1.
Major species difference exist
2.
Humans are more like birds than like other mammals
3.
Growth rates were greater in children given 400 IU per day, although 100 IU is enough
to prevent rickets
4.
Table 3.1
DEFICIENCY
1.
All animals





2.
Failure of calcium salt deposition in the cartilage matrix
Failure of cartilage cells to mature, leading to accumulation rather than destruction
Compression of proliferating cartilage cells
Elongation, swelling, and degeneration of cartilage
Abnormal invasion of cartilage by capillaries
Outward signs of rickets




Weak bones cause curving and bending of bones
Enlarged hock and knee joints
Tendency to drag hind legs
Beaded ribs and deformed thorax
3.
Ruminants – clinical signs of deficiency







4.
Decreased appetite and growth rate
Digestive disturbances
Stiffness of gait
Labored breathing
Irritability
Weakness
Occasionally tetany and convulsions
Swine – clinical signs of deficiency







Poor growth
Stiffness
Lameness
Stilted gait
General tendency to “go down”
Loss of use of limbs
Frequent cases of fractures





5.
Poultry – clinical signs of deficiency





6.
Softness of bones
Bone deformities
Beading of the ribs
Enlargement and erosion of joints
Unthriftiness
Retarded growth
Rickets
Rest frequently in a squatting position
Disinclination to walk
Lame, stiff-legged gait
Horses – clinical signs of deficiency




Reduced bone calcification
Stiff and swollen joints
Stiffness of gait
Bone deformities


Frequent cases of fractures
Reduction in serum Ca and P
ASSESSMENT OF STATUS
1.
Poor production rates by animals
2.
Bone abnormalities in animals
3.
Diagnosis of rickets and osteomalacia


Serum calcium levels – 5 to 7 mg/100 ml
High serum alkaline phosphatase activity
ANSC 5308
VITAMIN NUTRITION SECTION
LECTURE 5
VITAMIN K
9.
Vitamin K was the last fat-soluble vitamin to be discovered
10. In contrast to the other fat-soluble Vitamins A, D, and E, which have multiple functions
and wide biological importance, Vitamin K appears to be limited in its function to:

Normal blood clotting mechanism

Suggested roles in identified Vitamin K dependent proteins
11. Because of the blood clotting function, Vitamin K was previously referred to as
the “coagulation vitamin”, “antihemorrhagic vitamin”, and “prothrombin factor”
12. Vitamin K is required for maintaining the function of the blood coagulation system in
humans and all investigated animals
13. Even though Vitamin K is synthesized by intestinal microorganisms, deficiency signs
have been observed under field conditions
14. Poultry and pigs are susceptible to vitamin K deficiency
15. In ruminants, a deficiency can be caused by ingestion of spoiled sweet clover hay, which
is a natural source of dicumarol (a Vitamin K antagonist)
16. Vitamin K is most required in human nutrition of infants because of insufficient
intestinal synthesis, and in adults under conditions where fat absorption is impaired
CHEMICAL STRUCTURE AND PROPERTIES
6.
Vitamin K is used to describe a group of quinone compounds that have characteristic
antihemorrhagic effects
7.
Vitamin K is a generic term consisting of 2-menthyl-1,4-naphthoquinone derivatives,
called menadione

8.
Various isomers differ in the nature and length of the side chain
There are three forms of Vitamin K

K1 – plant source (phylloquinone)
9.

K2 – animal (microbial) source (menaquinone)

K3 – synthetic source (menadione)
Vitamin K is a golden yellow viscous oil

Stable to heat

Labile to oxidation, alkali, strong acids, light, and irradiation
10. 5.



A number of Vitamin K antagonists exist
Dicumarol
Sulfonamides
Mycotoxins
ANALYTICAL PROCEDURES
5.
High Pressure liquid chromatography (HPLC) is highly suitable for Vitamin K analysis
6.
A classic biological assay for amount of Vitamin K is blood clotting time in the chick
METABOLISM
3.
Vitamin K is absorbed in association with dietary fats and requires bile salts and
pancreatic juice
4.
Unlike phylloquinone (K1) and menaquinones (K2), menadione bisulfites and phosphates
are relatively water soluble and are satisfactorily absorbed from low-fat diets
5.
Absorption of different forms of Vitamin K may differ greatly

Rats
1) 40% absorption of K1
2) 89% absorption of K3
Conclusion is K3 (menadione) is well absorbed and poorly retained while the
opposite is true for K1 (phylloquinone)
FUNCTIONS
10. Coagulation time is increased when Vitamin K is deficient

Plasma clotting factors VII, IX and X are dependent on Vitamin K for synthesis
1) These four blood-clotting proteins are synthesized in the liver in inactive
forms and then converted to biologically active forms by Vitamin K
REQUIREMENTS
7.
Vitamin K requirement in mammals is met by a combination of dietary intake and
microbial biosynthesis in the guts which involve E coli, and ruminal microbes
8.
Because of microbial synthesis a precise expression of Vitamin K requirements is not
feasible
9.
The adult human requirement for Vitamin K is extremely low, and a dietary deficiency
is rare in the absence of complicating factors
DEFICIENCY
5.
6.
All animals

Impairment of blood coagulation

Clinical signs include low prothrombin levels, increased clotting time, and
hemorrhaging
Ruminants

Deficiency is seen only in the presence of a metabolic antagonist, such as
dicumarol from moldy sweet clover
1)
2)
3)
7.
Swine

Deficiency was produced by using a sulfa drug and an antibiotic, and minimizing
coprophagy

In late 1960’s and early 1970’s there were numerous reports of bleeding disease of
young pigs on commercial diets
1)
8.
Condition is referred to as “hemorrhagic sweet clover disease”
Responsible for large animal losses
Dicumarol passes through the placenta and newborn animals may become
affected immediately after birth
This was overcome by Vitamin K medication
Poultry

Very young chicks are readily affected

Carryover from the parent hen to the chick has been demonstrated

Borderline deficiencies of Vitamin K often cause small hemorrhagic blemishes on
the breast, legs, wings, abdominal cavity, and intestine

Chicks show an anemia in part from blood loss, but also due to the development of
a hypoplastic bone marrow
VITAMIN C
1.
Scurvy, a potentially fatal condition resulting from inadequate Vitamin C (ascorbic
acid), has been known and feared since ancient times
2.
The prevention and cure of scurvy is associated with consumption of fresh fruits
(especially citrus)
3.
Vitamin C is synthesized by most species, exceptions being the primate
(including humans), guinea pigs, fish, fruit eating bats, insects, and some birds
4.
Animals that cannot synthesize this vitamin need a dietary source for their normal
maintenance
5.
The concept that the sole function of Vitamin C is to prevent scurvy has been revised in
recent years

Small quantities prevent scurvy; however, larger quantities may be needed to
maintain good health during
1) Adverse environment
2) Physiological stress
3)
Certain disease conditions
CHEMICAL STRUCTURE and PROPERTIES
1.
Vitamin C occurs in two forms



2.
Reduced ascorbic acid
Oxidized dehydroascorbic acid
Only the L isomer of ascorbic acid has activity
In foods the reduced form of Vitamin C may oxidize to the dehydro form which may
further oxidize to an inactive form called diketogulonic acid

This takes place readily and is accelerated by heat and light

Ascorbic acid is so readily oxidized to dehydroascorbic acid that other compounds
may be protected against oxidation

Vitamin C is used in canning of certain fruits to prevent oxidation changes that
cause darkening
3.
Vitamin C is the least stable, and therefore most easily destroyed, of all vitamins
4.
Reversible oxidation-reduction of ascorbic acid and dehydroascorbic acid is the most
important chemical property of Vitamin C and is the basis for its physiological activities
ANALYTICAL PROCEDURES
1.
Analysis of Vitamin C include biological, chemical, and physical methods

Biological test measures total amount of Vitamin C present in both forms
1)

Guinea pigs are often used
Chemical and physical methods require precautions to prevent oxidation
1)
Homogenize under N2 and avoid copper and other metallic ions
2)
7.
Dye methods are widely used
Both gas-liquid chromatographic (GLC) and high-pressure liquid chromatographic
(HPLC) methods have been developed for L- ascorbic acid determination
METABOLISM
1.
Vitamin C is absorbed similar to carbohydrates (monosaccharides)

Intestinal absorption requires Na+- dependent active transport
2.
Vitamin C is readily absorbed when quantities ingested are small, but limited intestinal
absorption occurs when excess amounts are ingested
3.
Absorbed Vitamin C readily equilibrates with the body pool of the vitamin
4.
No specific binding proteins for Vitamin C have been reported

Vitamin C may be retained by binding to subcellular structures
5.
Highest levels of Vitamin C are found in the pituitary and adrenal glands, with high
concentrations also in the liver, spleen, brain, and pancreas
6.
Vitamin C tends to localize around healing wounds
7.
Vitamin C is excreted in urine and sweat, with minimal losses in feces
FUNCTIONS
1.
The function of Vitamin C is related to its reversible oxidation and reduction
characteristics
2.
The exact role of this Vitamin in animals is not clearly known since a coenzyme form
has not been reported
3.
The most clearly established functional role for Vitamin C involves collagen
biosynthesis



Impairment of collagen synthesis in Vitamin C deficiency appears to be due to
lowered ability to hydroxylate lysine and proline
Proline is needed to form a stable extracellular matrix
Lysine is needed for formation of cross-links in the fibers
REQUIREMENTS
1.
A wide variety of plant and animal species can synthesize Vitamin C from glucose and
galactose
2.
Species that cannot synthesize Vitamin C lack the enzyme L-gulonolactone
DEFICIENCY
1.
Under practical feeding situations only humans, nonhuman primates, guinea pigs, and
fish will develop Vitamin C deficiency
2.
Farm animals synthesize Vitamin C from glucose in the liver or kidney
3.
Ruminants

Synthesize Vitamin C; however, clinical cases of scurvy have developed

Vitamin C stores are reduced in cold stress situations

More prone to deficiency than non-ruminants because dietary sources are rapidly
destroyed by ruminal microflora

Low Vitamin C levels may occur in winter and spring and tends to reduce general
resistance of the animal causing
1)
2)
3)
4)
4.
Swine
Infertility
Retained placenta
Low viability of progeny
And other economic losses
5.

Generally, Vitamin C is not formulated into diets (inconsistent data base showing
need)

If the need for Vitamin C exists in swine, the newly weaned pig would most likely
be deficient first
Poultry

Like swine, poultry do not normally need Vitamin C supplementation

However, the newly hatched chick may deficient because of
1)
2)
6.
Slow rate of synthesis
Stress
Humans

Deficiency causes scurvy, a disease characterized by multiple hemorrhages

Scurvy is preceded by
1) Lassitude
2) Fatigue
3) Anorexia
4) Muscular pain
5) General susceptibility to infection and stress
ANSC 5308
VITAMIN NUTRITION SECTION
LECTURE 6
ANTIOXIDANT VITAMINS
17. Vitamin E, Vitamin C and beta carotene (pro-vitamin A) are antioxidants

An antioxidant has the ability to stabilize highly reactive, potentially harmful
molecules called free radicals
18. Free radicals are generated during:

Cellular metabolism


Exposure to ingested or inhaled environmental pollutants
Metabolism of certain drugs
19. The generation of free radicals has been associated with damage to
membranes, enzymes, and the cell’s nuclear material
20. The antioxidant’s ability to destroy these highly reactive free radicals serves to protect
the structural integrity of cells and prevents the depletion of required nutrients or
matabolites
REFERENCES (ANTIOXIDANT VITAMINS)
11. The role of vitamins on animal performance and immune response. Symp. Proc.
Hoffman-LaRoche Inc., Nutley, NJ, March 11, 1987.
12. Halliwell, B., and J.M.C. Gutteridge. 1985. Free radicals and toxicology. In: Free
Radicals in Biology and Medicine. Basel:Karger, pp. 360-370.
13. Pryor, W.A. 1976. The role of free radical reactions in biological systems. In: Free
Radicals in Biology. London:Acad. Press, pp. 1-49.
WATER SOLUBLE VITAMINS
8.
Main cellular roles of B vitamins involved in metabolism of carbohydrates, proteins and
fats





9.
Metabolism of glucose and pyruvic acid
Metabolism of amino acids
Metabolism of free fatty acids
Production of acetyl co-enzyme A
Production of ATP
B vitamins are usually readily absorbed and excesses are excreted on a daily basis

Thus, needs must be met on a daily basis from dietary sources in non-ruminants,
and from a combination of dietary sources and microbial synthesis in ruminants and
horses
ANSC 5308
VITAMIN NUTRITION SECTION
LECTURE 7
THIAMIN
21. Thiamin also called: thiamine, aneurin(e), and Vitamin B1. First water-soluble vitamin
to be discovered
22. There is little chance of a thiamin deficiency for non-ruminant animals, including
humans, when diets contain whole cereal grain or starch roots
23. Thiamin deficiency in humans has occurred mostly in Asian countries when
highly milled (polished) rice is consumed
24. Intensification of ruminant feeding has resulted in nervous disorders that are responsive
to thiamin supplementation



High-concentrate diets
Management system changes
Increased levels of production
25. Thiamin deficiency disease beriberi is probably the earliest documented deficiency
disorder in humans (2600 B.C.)
26. No cure of beriberi was found until the 1880’s, where the incidence of beriberi was 32%
among sailors.
CHEMICAL STRUCTURE AND PROPERTIES
14. Thiamin consists of molecule of pyrimidine and a molecule of thiazole linked by a
methylene bridge

Contains nitrogen and sulfur

Isolated in pure form as thiamin hydrochloride

Sulfurous odor and bitter taste

Soluble in water, and insoluble in fat solvents

Very sensitive to alkali
1)
Thiazole ring opens at room temperature with pH above 7

In dry state, thiamin is stable at 100°C for several hours

Moisture greatly accelerates destruction and thus it is much less stable to heat in
fresh foods than in dry foods
15. Anti-thiamin activity is fairly common and includes structurally similar antagonists
(competitive inhibition)


Pyrithiamine
1)
Blocks the esterification with phosphoric acid
2)
Inhibits thiamin coenzyme cocarboxylase
Oxythiamine
1)

Likewise displaces cocarboxylase
Amprolium (coccidiostate)
1) Inhibits absorption of thiamin from the intestine
2) Also blocks the phosphorylation of thiamin
16. Thiaminase (enzyme) activity destroys thiamin activity by altering the structure of the
vitamin

“Chastek paralysis” in animals results from feeding raw fish that has a thiaminase
that splits the thiamin molecule into two components

Certain bacteria and molds also produce thiaminases

Bracken fern poisoning in horses results from antagonism to thiamin
ANALYTICAL PROCEDURES
10. Thiamin activity can be analyzed by biological, microbiological and chemical methods

Biological – based on curative ability for polyneuritis in pigeons, bradycardia in
rats, or growth in the chick, pigeon or rat.

Microbiological – fairly rapid but some organisms lack specificity for thiamin

Chemical – conducted by oxidation to thiochrome
1)
Shows blue fluorescence in ultraviolet light
2)
Widely used in foodstuffs and feeds
METABOLISM
6.
Readily digested and released from natural sources
7.
Must have sufficient production of hydrochloric acid in the stomach for digestion
8.
Phosphoric acid esters of thiamin are split in the intestine
9.
Free thiamin is easily absorbed in the duodenum
10. Ruminants absorb free thiamin from the rumen

But the rumen wall is not permeable for bound thiamin or thiamin contained in
rumen microorganisms
11. Horses can absorb thiamin from the cecum
12. Absorption

Both active transport and simple diffusion are involved in intestinal absorption
1)
Active sodium-dependent transport occurs at low concentrations
2)
Whereas, it diffuses passively at high concentrations

Absorption from the rumen is believed to be an active mechanism

Absorbed thiamin is transported via the portal vein to the liver with a carrier plasma
protein
13. Phosphorylation

Thaimin phosphorylation can take place in most tissues but particularly in the liver

Phosphorylation occurs under the action of adenosine triphosphate (ATP) to form
thiamin pyrophosphate (TPP)

TPP is the metabolically active form of thiamin

Total body thiamin
1)
80% - TPP
2)
3)
10% - thiamin triphosphate (TTP)
Remainder is thiamin monophosphate (TMP) and free thiamin
14. Animals need a regular supply of thiamin and unneeded intakes are excreted

The pig is somewhat of an exception and its tissues contain several times as much
thiamin as other species studied
1)
Can meet needs from body stores for up to two months
15. Excretion of absorbed thiamin is in both the urine and feces, and small amounts in
sweat
FUNCTIONS
11. Coenzyme

A principal function in all cells is as the coenzyme cocarboxylase (TPP)



In the Krebs cycle, energy production from carbohydrates, fats and proteins result
in products that require further breakdown and thiamin is involved
1)
Thiamin is the coenzyme for all enzymatic decarboxylations of -keto acids
2)
Thus, it functions in the oxidative decarboxylation of pyruvate to acetate
which combines with coenzyme A and enters the TCA cycle.
Two essential oxidative decarboxylation reactions in mammals
1)
Pyruvate  acetyl-CoA + CO2
2)
-Ketoglutaric acid  succinyl-CoA + CO2
TTP is required for the synthesis of:
1)
Ribose from glucose – needed for nucleotide formation
2)
NADPH from carbohydrates – essential to form fatty acids
12. Neurophysiology

Evidence shows a specific role of thiamin in neurophysiology that is independent of
its coenzyme function

Fatty acids and cholesterol are the major constituents of cell membranes
1)

Thiamin deficiency in cultured glial cells impairs their ability to synthesize fatty
acids and cholesterol
1)

Their synthesis would affect membrane integrity and function
The defect is related to reduced formation of key lipogenic enzymes
Possible mechanisms of action of thiamin in nervous tissue include:
1)
2)
Synthesis of acetylcholine which transmits neural signals
Participation in the passive transport of sodium of excitable membranes
3)
Reduction in activity of pentose phosphate pathway which reduces the
synthesis of fatty acids and metabolism of energy
REQUIREMENTS
10. Requirements in some species are difficult to establish

Synthesis by microflora in ruminants

Synthesis too far down the intestinal tract in non-ruminants for absorption

In horses only about 25% of free thiamin is absorbed from the cecum

In humans and most species other than ruminants and horses, thiamin synthesis and
absorption makes little contribution to body needs

In ruminants, total feed thiamin and ruminal synthesis must be considered together,
and the total need is yet to be defined.
DEFICIENCY
9.
The classic diseases, beriberi in humans and polyneuritis in birds represent a late stage
of the deficiency

Results from peripheral neuritis, perhaps from accumulation of carbohydrate
metabolism intermediates

Brain covers its energy requirements from glucose degradation

In addition to neurological disorders, the other main group of disorders involves
cardiovascular damage. Clinical signs include:
1)
2)
3)

Slow heart beat (bradycardia)
Enlargement of the heart
Edema
Of all the nutrients, a deficiency of thiamin has the most marked effect on appetite
1)
Must force-feed or inject thiamin to induce animals to resume eating
10. Ruminants

Because of extensive ruminal thiamin synthesis, the general conclusion is that
ruminants possessing a normally functioning rumen have no dietary requirement

Young calves and lambs have been shown to suffer from thiamin deficiency

Polioencephalmalacia (PEM), a thiamin responsive disease, occurs sporadically in
cattle, sheep, and goats
1)
The incidence of PEM is reported to be between 1 and 10% and mortality may
reach 100%
2)
Biochemical changes in animals include reduced tissue thiamin, dramatic
elevation in blood pyruvate, and lactate, and markedly reduced transketolase
activity
11. Swine – Clinical signs of deficiency



Reduced feed intake
Vomiting
Sharp reduction in weight gains
12. Poultry

Most susceptible to neuromuscular effects of thiamin deficiency

Clinical signs
1)
2)
3)
4)
Loss of appetite
Emaciation
Frequent convulsions
Other
13. Horses – Clinical signs


Reproductive failure in both sexes
Anorexia


Incoordination of hind legs
Other
14. Humans

Beriberi, a state in which both cardiac and nervous functions are disturbed
1)
Wet form – characterized by edema
2)
Dry form – characterized by peripheral neuritis, paralysis, and muscular
dystrophy
RIBOFLAVIN
6.
After the isolation of thiamin as the “Vitamin B” factor, riboflavin was the first growth
factor to be characterized from the remaining B-complex vitamins
7.
Riboflavin functions as a coenzyme in diverse enzymatic reactions as


Flavin mononucleotide (FMN)
Flavin adenine dinucleotide (FAD)
8.
Riboflavin is required in metabolism of all plants and animals, and every plant
and animal cell contains the vitamin
9.
Adult ruminants do not require riboflavin. However, young ruminants require dietary
sources
10. One of the vitamins most likely to be deficient in typical swine and poultry diets
11. Likewise, human diets low in milk and eggs and leafy vegetables are likely to be
deficient in riboflavin
CHEMICAL STRUCTURE and PROPERTIES
5.
Riboflavin consists of a dimethylisoalloxazine nucleus combined with the alcohol of
ribose as a side chain
6.
Riboflavin exists in three forms:



Free riboflavin
Flavin mononucleotide (FMN)
Flavin adenine dinucleotide (FAD)
7.
Riboflavin is an odorless, bitter, orange-yellow compound that melts at 280°C
8.
It is only slightly soluble in water but readily soluble in dilute basic or strong acidic
conditions
9.
When dry it is not affected appreciably by light, but in solution it is quickly destroyed

Pasteurization of milk and exposure to light – 10 to 20% loss

Bottled milk in bright sunlight for 2 hours – 50 to 70% loss
FUNCTIONS
4.
Essential to the utilization of carbohydrates, protein and fat
5.
FMN and FAD combine with specific proteins to form active enzymes called
flavoproteins


Most flavoproteins contain FAD, and a few contain FMN
Riboflavin in these coenzyme forms acts as an intermediary in the transfer of
electrons in biological oxidation-reduction reactions

The enzymes that function aerobically are called oxidases, and those that function
anaerobically are called dehydrogenases

Flavoproteins function by accepting and passing on hydrogen, undergoing alternate
oxidation and reduction
6.
Although riboflavin is present mostly as flavoprotein enzymes FAD and FMN, the retina
of the eye contains free riboflavin in relatively large amounts.
REQUIREMENTS
3.
Riboflavin requirements decline with animal maturity and increase for reproductive
activity
4.
Microbial biosynthesis occurs in ruminants and thus affects requirements
5.
The utilization of riboflavin depends on diet composition


Slowly digested carbohydrates such as starch, cellulose or lactose increase
synthesis
Dextrose, fat and protein decrease intestinal production and increase dietary
requirements
DEFICIENCY
4.
Animals and humans are unable to synthesize riboflavin within tissues, thus needs are
met by dietary sources with some intestinal microbial synthesis
5.
A decreased rate of growth and poorer feed efficiency are common signs in all species
affected
6.
Ruminants

4.
Not a problem because ruminal microorganisms synthesize it in adequate amounts
Swine – clinical signs of deficiency





Impaired reproduction
Anorexia
Slow growth
Light sensitivity
Other
5.
Poultry



Curled-toe paralysis
Retarded growth
High mortality
10. Horses

Generally felt that riboflavin synthesis in the cecum and colon provides some of the
horse’s requirement

Horses fed low-riboflavin diets have demonstrated anorexia, severe weight loss,
general weakness and poor growth
11. Humans

Clinically, riboflavin deficiency is usually observed in conjunction with
deficiencies of other B vitamins

Clinical features include dermatitis around the nose and mouth, soreness and
burning of the mouth and tongue, glossitis (flattening followed by disappearance of
the papilla of the tongue)
ANSC 5308
VITAMIN NUTRITION SECTION
LECTURE 8
NIACIN
27. Niacin exerts its major effects through its role in the enzyme system for cell respiration
28. Niacin deficiency results in the disease pellagra in humans, and black tongue in dogs
29. The requirement for niacin in non-ruminants has been established, however
exact requirements are difficult to determine since it can be synthesized from
the amino acid tryptophan
30. Supplemental niacin may provide substantial benefits under some feeding systems, even
though it has been accepted that there is no dietary requirement in ruminants for B
vitamins including niacin
CHEMICAL STRUCTURE AND PROPERTIES
17. Chemically, niacin is one of the simplest vitamins
18.
Nicotinic acid and nicotinamide correspond to 3-pyridine carboxylic acid and its amide,
respectively
19. The term niacin is used as a generic descriptor of pyridine 3-carboxylic acid and
derivatives exhibiting the same qualitative biological activity of nicotinamide
20. Nicotinic acid and nicotinamide (niacinamide) possess the same vitamin activity, the
free form is converted to the amide in the body
21. Nicotinamide functions as a component of two coenzymes


Nicotinamide adenine dinucleotide (NAD, formerly called DPN)
Nicotinamide adenine dinucleotide phosphate (NADP, formerly called TPN)
ANALYTICAL PROCEDURES
11. Microbiological determination is the most sensitive and is the preferred method

Lactobacillus plantarum responds to both forms of the vitamin

Whereas, leuconostoc mesenteroides measures only nicotinic acid
METABOLISM
16. Effectively absorbed by diffusion at either low or high doses
17. By employing the gastrointestinal tube technique, niacin was shown to be equally
absorbed from both the stomach and the upper small intestine in humans
18. Blood transport of niacin is associated mainly with the red blood cells
19. Niacin rapidly leaves the bloodstream and enters kidney, liver, and adipose tissues
20. Although niacin coenzymes are widely distributed in the body, no true storage occurs
TRYPTOPHAN-NIACIN CONVERSION
1.
2.
The amino acid tryptophan is a precursor for the synthesis of niacin

Synthesis in the body, and evidence that synthesis takes place in the intestine

Synthesis occurs in the developing chick embryo
Metabolic requirement for niacin can be met from tryptophan in the diet if:


3.
Sufficient quantity of tryptophan
Efficient conversion of tryptophan
Protein, energy, riboflavin and Vitamin B6 nutritional status and hormones affect
conversion of tryptophan to niacin
4.
It is suggested that pellagra is not simply a disease of niacin deficiency but a disease of
tryptophan metabolism
5.
Factors that affect efficiency of conversion

Levels of tryptophan intake, low levels – high conversion

Energy restriction, high conversion

Pregnacy in women, increses conversion

Amino acid imbalance due to excess leucine

Animal species
1)
Humans: 60 mg of tryptophan for 1 mg of niacin synthesis
2)
Rats:
35 – 50 mg of tryptophan for 1 mg of niacin synthesis
3)

Cats:
no conversion
4) Ducks: no conversion
Picolinic acid carboylase in livers of various species has a very close inverse
relationship to dietary niacin requirement
1)
Cat and duck have so much of the enzyme that they cannot convert any dietary
tryptophan to niacin (excess tryptophan is catabolized to carbon dioxide and
water)
FUNCTIONS
13. The major function of niacin is in the coenzyme forms of nicotinamide, NAD and
NADP
14. Enzyme containing NAD and NADP are important links in a series of reactions
associated with carbohydrate, protein and lipid metabolism, especially energy
metabolism
15. More than 40 biochemical reactions have been identified that have paramount
importance, particularly for the:



Skin
Gastrointestinal tract
Nervous system
16. NAD and NADP – containing enzymes play key roles in oxidation-reduction reactions
by serving as hydrogen transfer agents in conjunction with a second hydrogen-carrying
system, the riboflavin coenzymes



The transfer of hydrogen is reversible and sterospecific
NADP has an important role in the synthesis of fats and steroids
Both NAD and NADP are involved in degradation and synthesis of amino acids
REQUIREMENTS
11. There is a wide variation in niacin requirements generally due to the conversion of
tryptophan to niacin
2.
Factors that influence niacin requirements

Genetics – meatier, faster-growing animals

Increased production levels

Ability to synthesize niacin from tryptophan

Stress and subclinical disease level

Exposure to feces (coprophagy)

Handling and processing of feeds

Amino acid imbalances

Earlier weaning

Molds and antimetabolites in feeds
DEFICIENCY
15. All animals

A deficiency of niacin is characterized by severe metabolic disorders in the skin
and digestive organs
1)

First sign to appear are loss of appetite, retarded growth, weakness, digestive
disorders, and diarrhea
Three D’s: diarrhea, dermatitis, death
16. Ruminants

Dietary requirement for niacin does not exist as long as the level of tryptophan is
near 0.2% of the diet

For calves, a diet free of niacin and low in tryptophan resulted in deficiency signs
of:
1)
2)
3)
4)
Sudden anorexia
Severe diarrhea
Dehydration
Sudden death
17. Swine

Niacin is expected to be deficient in typical swine diets, particularly when corn,
which is low in available niacin and tryptophan is fed

Wide variation has been observed
1)

Occasionally animals appear to thrive with no niacin, and others appear to
vary in their requirement
Niacin deficient pigs have inflammatory lesions of the gastrointestinal tract
18. Poultry

Deficiency results in black tongue, a condition characterized by inflammation of
the tongue and mouth cavity

Clinical signs include:
1)
2)
3)
Bowing of the legs
Poor feathering
Dermatitis on the feet and head
19. Horses

No requirements for niacin have been established for the horse and a deficiency has
not been reported
20. Humans

The similarity of niacin deficiency signs between the dog and humans has been
important because the dog is the laboratory animal to identify niacin deficiency


Traditionally niacin deficiency in humans has been equated with pellagra
3)
Skin changes
4)
Lesions of the mucous membranes of the mouth, tongue, stomach, and
intestinal tract
5)
Changes in nervous origin
Earliest symptoms of pellagra is inflammation and soreness of the mouth followed
by bilateral symmetrical erythema on all parts of the body exposed to sunlight
1)
Common sites are surfaces of the extremities, face and neck
2)
Lesions are also found at sites of constant irritation such as under the breast,
scrotum, axilla, and perineum
3)
Tongue is swollen and beefy red
ANSC 5308
VITAMIN NUTRITION SECTION
LECTURE 9
VITAMIN B6
31. Vitamin B6 refers to a group of three compounds:




Pyridoxol (Pyridoxine)
Pyridoxal
Pyridoxamine
Their activity is equivalent in animals but not in various microorganisms
32. Vitamin B6 is involved in many enzymes during metabolism of proteins, fats, and
carbohydrates. The vitamin is particularly involved in various aspects of protein
metabolism.
33. It is generally considered that common feed ingredients for poultry and swine
diets contain adequate amounts of Vitamin B6
34. There is evidence of low Vitamin B6 status in the human population, especially for
young and pregnant, or lactating women
CHEMICAL STRUCTURE AND PROPERTIES
22. Vitamin B6 is a relatively simple compound with three substituted pyridine derivatives
that differ only in the functional group in the 4-position



Alcohol (pyridoxine or pyridoxal)
Aldehyde (pyridoxal
Amine (pyridoxamine)
23. Pyridoxine is the predominant form in plants, whereas pyridoxal and pyridoxamine are
generally found in animal products
24. Two additional Vitamin B6 forms found in foods are the coenzyme forms of pyridoxal
phosphate (PLP) and pyridoxamine phosphate
25. Metabolically active Vitamin B6 is mainly as PLP and to a lesser degree pyridoxamine
phosphate
26. Exposure to light, especially in neutral or alkaline media, is highly destructive
27. Forms of Vitamin B6 are colorless crystals soluble in water or alcohol, commercial
preparation is the hydrochloride salt of the alcohol form, pyridoxine hydrochloride
28. Several Vitamin B6 antagonists exist

Deoxypridoxine – used in experiments to accelerate deficiency

Isonicontic acid hydrazide (isoniazid) – used in tuberculosis treatment
1)
Used to clarify functions of enzymes dependent on PLP

Thiosemicarbazide and hydralazine-antihypertensive drugs

Penicillamine – used to remove body copper in copper poisoning and Wilson’s
disease

L-Dopa – antiparkinson drug

Oral contraceptives

Hydrazic acid – present in linseed oil meal from flax
METABOLISM
21. Vitamin B6 forms are bound to feed proteins and must be split off through digestive
processes for absorption to occur
22. Vitamin B6 compounds are first dephosphorylated in the small intestine and then
absorbed
23. After absorption, B6 compounds rapidly appear in the liver, where they are mostly
converted into pyridoxal phosphate
24. Both niacin (as an NADP-dependent enzyme) and riboflavin (as the flavoprotein
pyridoxamine phosphate oxidase) are important for conversion of Vitamin B6 forms and
phosphorylation reactions
FUNCTIONS
17. Vitamin B6 in the form of PLP plays on essential role in the interaction of amino acid,
carbohydrate, and fatty acid metabolism, and the energy producing citric acid cycle
18. Over 50 enzymes are already known to depend on Vitamin B6 coenzymes
19. Pyridoxal phosphate is involved in amino acid metabolism through:





Transamination
Decarboxylation
Deamination
Desulfhydration
Clevage or synthesis of amino acids
20. Some other important reactions that Vitamin B6 is involved in include:






Synthesis of niacin from tryptophan
Conversion of linolenic to arachidonic acid (this function is controversial)
Glycogen breakdown to glucose 1-phosphate
Synthesis of epinephrine and norepinephrine
Incorporation of iron in hemoglobin synthesis
Synthesis of globulins, which carry antibodies
REQUIREMENTS
12. Because of microbial synthesis, ruminants have no dietary requirement, with the
exception of young animals that don’t have a fully developed rumen
13. The horse has considerable synthesis in the large intestine (cecum) but adequate
absorption is controversial
14. Breed of animal and environmental temperature influence Vitamin B6 requirements

Breed differences – chick research

Temperature differences – rat research
15. Quantity of dietary protein affects requirement for B6 in both animals and humans
 Increased on high protein diets
DEFICIENCY
21. Characteristics of Vitamin B6 deficiency are retarded growth, dermatitis, epileptic-like
convulsions, anemia, and a partial alopecia
22. Because of the predominant function of Vitamin B6 in protein metabolism, the following
may result:

Fall in nitrogen retention

Feed protein is not well utilized

Nitrogen excretion is excessive

Impaired tryptophan metabolism
23. Ruminants
4.

No deficiency signs have yet been observed in mature ruminants

Essential for young calves when selected experimental diets are used
Swine – clinical signs of deficiency

Poor appetite

Microcytic hypochromic anemia

Epileptic-like fits or convulsions

Other
16. Poultry – clinical signs of deficiency

Poor appetite and grow slowly

Squat with wings slightly spread and head resting on the ground

Abnormally excitable
17. Horses – no deficiency has been reported

Some researchers believe that racehorses need Vitamin B6 supplementation
1)
Intensive training
2)
High proportion of protein in their diets
18. Humans

High proportion of the human population receives inadequate dietary Vitamin B6,
particularly young and pregnant, or lactating women

Clinical signs of deficiency include
6)
Hypochromic microcytic anemia
7)
Loss of weight
8)
Vomiting
9)
Hyperirritability
10) Other
PANTOTHENIC ACID
1.
Pantothenic acid is found in two enzymes, coenzyme A and acyl carrier protein which
are involved in many reactions in carbohydrate, fat, and protein metabolism
2.
Although this vitamin occurs in practically all feedstuffs, the quantity present is
generally insufficient for optimum performance of poultry and swine and other nonruminant species
3.
There are no reports of deficiency in adult ruminants because of microbial synthesis
4.
Pantothenic acid deficiency occurs rarely in humans
CHEMICAL STRUCTURE AND PROPERTIES
1.
Pantothenic acid is an amide consisting of pantoic acid joined to -alanine
2.
The free acid of the vitamin is a viscous, pale yellow oil readily soluble in water and
ethyl acetate

The oil is extremely hygroscopic and is easily destroyed by acids, bases, and heat
3.
Maximum heat stability occurs at pH 5.5-7.0
4.
Calcium pantothenate is the pure form of the vitamin used in commerce
5.
Pantothenic acid is optically active, and only the dextrorotatory form d-pantothenic acid
is effective as a vitamin
METABOLISM
1.
Pantothenic acid is found in feeds in both bound (largely as coenzyme A) and free forms
2.
Pantothenic acid is absorbed from the intestinal tract, probably by diffusion

Little information is available on digestion, absorption, and transport of the vitamin
3.
Within tissues pantothenic acid is converted to coenzyme A
FUNCTIONS
1.
The most important function of coenzyme A is to act as a carrier mechanism for
carboxylic acids


2.
Such acids when bound to coenzyme A have a high potential for transfer to other
groups and are referred to as active
The most important of the reactions is the combination of coenzyme A with acetate
to form active acetate
1)
It is used directly by combining with oxaloacetic acid to form citric acid,
which enters the Krebs citric acid cycle
2)
This enables two-carbon fragments from fats, carbohydrates, and certain
amino acids to form acetyl coenzyme A and enter the citric acid cycle
Coenzyme A also functions as a carrier of acyl groups in enzymatic reactions involved
in synthesis of fatty acids, cholesterol, and sterols
3.
In the form of active acetate, acetic acid can also combine with choline to form
acetylcholine
4.
Coenzyme A has an essential function in lipid metabolism

Fatty acids are activated by formation of the coenzyme A derivative

Degradation by removal of acetate fragments in beta oxidation
1)
5.
These fragments may directly enter the citric acid cycle or combine to form
ketone bodies
When pantothenic acid is deficient, the incorporation of amino acids into the blood
albumin fractions is inhibited, and there is a reduction in the titer of antibodies
REQUIREMENTS
1.
When energy density of diets is increased, intake is reduced so that higher dietary
concentrations of pantothenic acid and other vitamins are required

2.
3.
4.
Increasing energy in diets for broilers from 2870 to 3505 kcal/kg resulted in a
19.1% decrease in pantothenic acid
Antibiotics have a sparing effect on the pantothenic acid requirement

Aureomycin – weanling pigs

Penicillin – turkey poults
In ruminants, synthesis by ruminal microflora is:

Reduced by diets high in cellulose

Increased by diets high in easily soluble carbohydrates
There are interrelationships with other vitamins on pantothenic acid requirements



Vitamin B12 – sparing effect
Vitamin C – sparing effect
Biotin – related to utilization
DEFICIENCY
1.
2.
All animals

Clinical signs take many forms and differ from one animal species to another

Deficiency does occur under certain feeding programs for animals, however, clear
cut deficiency symptoms in humans are rarely found in practice
Ruminants

Not required in the diet of adult ruminants

Deficiency in the calf results in scaly dermatitis around the eyes and muzzle
3.
4.
Swine

Many swine diets are borderline in supplying pantothenic acid and many are
deficient in the vitamin

A characteristic sign of deficiency is a locomotor disorder in the hindquarters
termed goose stepping

Insufficient quantities pantothenic acid may result in complete reproductive failure
in females
1)
Sows become pregnant but do not farrow or show signs of pregnancy
2)
Macerating feti in the uterine horns in all cases
Poultry

Reduced egg production

Reduced hatchability

In young chicks a deficiency of pantothenic acid is difficult to differentiate from a
biotin deficiency – both cause severe dermatitis
5.
Horses – no deficiency has been reported
6.
Humans

Deficiency does not occur under natural conditions except when associated with
severe malnutrition

Deficiency results in burning feet syndrome
ANSC 5308
VITAMIN NUTRITION SECTION
LECTURE 10
BIOTIN
35. For many years it was believed that supplemental biotin was not required in swine and
poultry diets because of wide distribution in feedstuffs and synthesis by intestinal
microflora

However, in the mid 1970’s, field cases of deficiency were found under modern
production systems

On the basis of these findings nutritionists have had to reexamine the role of biotin
36. Humans and animals may become deficient after consumption of excessive quantities of
raw eggs

Raw eggs contain a biotin complexing factor (avidin)
37. Children may be biotin deficient due to inborn errors of metabolism

Respond dramatically to high-level dietary supplementation
CHEMICAL STRUCTURE AND PROPERTIES
29. Biotin has a sulfur atom in its ring (like thiamin) and a tranverse bond across the ring
30. Biotin has a rather unique structure with three asymmetric carbons and therefore eight
different isomers are possible

Only one isomer has vitamin activity, d-biotin
31. Biotin crystallizes from water solution as long, white needles
32. It is soluble in dilute alkali and hot water. Its melting point is 232-233 C
5.
Biotin is inactivated by:





Rancid fats
Choline
Formaldehyde
Nitrous acid
Ultraviolet radiation
6.
Oxidation converts biotin to sulfoxide or sulfone
7.
Strong agents result in sulfur replacement by oxygen to produce oxybiotin
METABOLISM
25. Biotin exists in natural feedstuffs in both bound and free forms

Bound form is about one-half biologically available

Biotin is often bound to lysine in protein of animal tissues and plant seeds

Free biotin occurs in fruit, milk, and vegetables
26. Biotin is absorbed as the intact molecule in the first half of the small intestine
27. Limited information is available on biotin transport, tissue deposition, and storage in
animals and humans
28. Biotin is transported as a free water-soluble component of plasma, is taken up by cells
via active transport, and is attached to its apoenzymes
29. All animal cells contain some biotin, with larger quantities in liver and kidneys

Intracellular distribution is associated with biotin-dependent enzymes
(carboxylases)
30. Biotin excretion in urine and feces together often exceeds total intake

Biotin producing microorganisms in intestinal tract
FUNCTIONS
21. Biotin is an essential coenzyme in carbohydrate, fat, and protein metabolism

Conversion of carbohydrate to protein and vice versa

Maintaining normal blood glucose levels when carbohydrate intake is low

Transports carboxyl units

Fixes carbon dioxide (as bicarbonate) in tissue

Serves as a prosthetic group in enzymes
1)
Linked covalently to -amino group of a lysyl residue of the biotin-dependent
enzyme
22. Specific biotin-dependent reactions in carbohydrate metabolism

Carboxylation of pyruvic acid to oxalascetic acid

Conversion of malic acid to pyruvic acid

Interconversion of succinic acid and propionic acid

Conversion of oxalocuccinic acid to -kelogultaric acid
23. Role of biotin in protein metabolism

Transcarboxylation in degradation of various amino acids

Deficiency of biotin hinders the conversion of deaminated leucine to oxaloacetate

Synthesis of citrulline from ornithine
24. Role of biotin in fat metabolism

Catalyzes the addition of CO2 to acetyl-CoA to form malonyl-CoA
1)

This is the first step in the synthesis of fatty acids
Deficiency in rats inhibits arachidonic acid synthesis from linoleic acid
REQUIREMENTS
19. Microorganisms contribute to the animal and human requirements

Supply provided may be variable and undependable
20. In poultry, it has been shown that polyunsaturated fats, Vitamin C, and other B vitamins
may influence the demand for biotin
21. Biotin is rapidly destroyed as feeds become rancid

Pure biotin is inactivated by 96% in presence of linoleic acid

In presence of Vitamin E, biotin destruction was only 40%
DEFICIENCY
24. Most dramatic clinical sign of biotin deficiency is severe dermatitis
25. Biotin is also important for normal function of the thyroid and adrenal glands, the
reproductive tract, and the nervous system
26. Ruminants

No evidence for a biotin deficiency has been produced in animals with functional
rumens

In calves, hindquarters pralysis has been reported in calves
27. Swine – clinical signs of deficiency

Alopecia (hair loss)

Dermatitis

Transverse cracking of the hooves

Other
28. Poultry – clinical signs of deficiency

Reduced growth rate and poorer feed efficiency

Disturbed and broken feathering

Dermatitis

Leg and beak deformities
29. Horses

Biotin is synthesized in the lower digestive tract of horses

Hoof integrity for a number of cases has been reported to improve as a result of
biotin supplementation
30. Humans

Except in infants, there is no evidence of biotin deficiency in humans

Intake through foods is good due to the ubiquitous nature of the vitamin and
benefits from microbial synthesis
FOLACIN
1.
Folacin is a general term used to describe folic acid and related compounds that exhibit
the biological activity of folic acid
2.
High incidence of deficiency in pregnant women

Affects 1/3 of all pregnant women in the world (both in developed and
undeveloped countries)

Causes megaloblastic anemia

3.
1)
Large red blood cells that are poor in carrying oxygen
2)
Associated with poor diet selection
Common in women 16 to 40 years old
In animals, folacin needs are met mostly by dietary sources and intestinal bacterial
sysnthesis

However, it is a feed additive of general use in poultry diets

Being reevaluated for supplementation of young swine
CHEMICAL STRUCTURE AND PROPERTIES
1.
Pure folic acid is pteroylmono-glutamic acid

Consists of glutamic acid, p-aminobenzoic acid (PABA), and a pteridine nucleus
2.
PABA portion of folic acid was once thought to be a vitamin
3.
If folacin requirement is met, there is no need to add PABA to the diet
4.
Folacin in natural feedstuffs is conjugated with varying numbers of extra glutamic acid
molecules

Generally 1 to 9 glutamates long

Poly glutamate forms (usually 3 to 7 glutamyl residues) are natural coenzymes
abundant in every tissue
5.
Synthetic folacin (folic acid) is in the monoglutamate form
6.
There are more biologically active forms of folacin than any other vitamin


About 100 different compounds
No. 5 and 10 nitrogens are associated with a formyl or methyl group
7.
Easily degraded by light and ultraviolet radiation
8.
A wide variety of folacin analogs have been prepared, principally for anticancer and
antimicrobial therapy
METABOLISM
1.
The enzyme for hydrolysis of pteroylpolyglutamate is -carboxypeptidase known as
folate conjugase
2.
The sequence of intestinal absorption of conjugated folate is mucosal or luminal uptake
followed by hydrolysis to simple folate
3.
Conjugase activity is inhibited by low pH


Orange juice (citric acid)
Drugs
4.
Zinc Transport is significantly decreased when folacin is present in intestinal lumen and
folacin transport is likewise decreased with the presence of zinc
5.
Specific folate-binding proteins (FBPs) exist in many tissues and body fluids and affect
bioavilability



Serum
Milk
Leukemic granulocytes

Other
FUNCTIONS
1.
Folacin is indispensable in the transfer of single-carbon units in various reactions

A role analogous to that of pantothenic acid in the transfer of two-carbon units

One-carbon units of formyl, forminino, and methyl groups

One-carbon units:
1)
Bound to folacin by tetrahydrofolic acid (THF)
2)
Generated mostly during amino acid metabolism
3)
Used in interconversions of amino acids (serine and glycine)
4)
Used in purine and pyrimidine synthesis (cell division)
2.
In folacin deficiency, histidine cannot be completely transformed to glutamate and a
hydrofolic acid resulting in an intermediate (formiminoglutamic acid) being excreted in
the urine

3.
4.
Used for diagnosis of early deficiency
Relationship of folacin and Vitamin B12

Vitamin B12 regulates the methyl trap theory

Vitamin B12 deficiency decreases the formation of methionine from homocysteine
and methyl-THF
Folacin is needed to maintain the immune system

Probably mediated through a reduction in DNA synthesis, resulting in impaired
nuclear division
REQUIREMENTS
1.
Species differ markedly in their requirements
2.
Poultry and humans (and other primates) develop deficiencies on low dietary folacin
3.
Self-synthesis is dependent on dietary composition
4.

Higher needs for high protein diets

Higher needs when simple sugars are high in the diet

Dietary fiber sources (xylan, wheat bran and beans) stimulate folacin synthesis

Sulfa drugs in diets increase requirements

Aflatoxins (moldy feed) inhibit microial intestinal synthesis
The more rapid the growth or production rates, the greater is the need for folacin
because of its role in DNA synthesis
DEFICIENCY
1.
Folacin deficiency has occurred in many animals species, with megalogblastic anemia
and leukopenia (reduced number of white cells) being constant findings
2.
In some animals (chick, guinea pig, and monkey) deficiency can be readily induced by
low folacin diets
3.
In other animals (dog, rat and pig) intestinal microflora meet requirements
4.
Ruminants

5.
Swine

6.
Synthesis occurs in the rumen
Until recently, deficiency occurred only when sulfa drugs were fed
Poultry – clinical signs of deficiency
7.

Poor feather development (folacin and lysine are required for feather pigmentation)

Decreased egg production
Horses

Synthesis occurs in intestinal tract

Deficiency has been reported in a diet lacking fresh grass for months
8. Humans

Probably the most common vitamin deficiency in the world

Adolescent girls have a greater nutritional requirement in relation to body size that
adult women

In older people, utilization of polyglutamate forms is lower compared to younger
people

Clinical signs include:
1)
2)
3)
4)
5)

Pallor
Weakness
Forgetfulness
Sleeplessness
Bouts of euphoria
Often associated with chronic alcoholism
ANSC 5308
VITAMIN NUTRITION SECTION
LECTURE 11
VITAMIN B12
38. Vitamin B12 was the last vitamin discovered (1948) and the most potent of the vitamins.
39. It is synthesized in nature only by microorganisms
40. Non-ruminant animals and humans that eat only plant foods are susceptible to Vitamin
B12 deficiency
41. Discovery of this vitamin was dramatic and involved microbiologists, biochemists,
nutrition scientists and physicians in various laboratories
CHEMICAL STRUCTURE AND PROPERTIES
33. Vitamin B12 is a complex structure
C63 H88 O14 N14 PCo. It is called cyanocobalamin

It belongs to the corrinoid group of compounds that have a corrin nucleus

However, numerous other corrinoids do not possess Vitamin B12 activity

The name cobalamin is used for compounds that have the cobalt atom in the center
of the corrin nucleus

Cyanide is attached to the cobalt atom and thus the name cyanocobalamin
34. The cyanide can be replaced by other groups and are referred to as “pseudo” Vitamin
B12 complexes or B12 – like factors




OH (hydroxycobalamin)
H20 (aquacobalamin)
NO2 (nitrocobalamin)
CH3 (methylcobalamin)
35. Vitamin B12 is a dark-red, hygroscopic substance, freely soluble in water and alcohol
36. It is the heaviest of all vitamins with a molecular weight of 1354
METABOLISM
31. Vitamin B12 in the diet is bound to food particles which are released by the combined
effort of low pH and peptic digestion

The released B12 is then bound to a nonintrinsic factor – cobalamin complex
32. The B12 remains bound to nonintrinsic protein until pancreatic proteases (i.e. trypsin)
partially degrade the nonintrinsic factor protein and thus enables B12 to become bound
exclusively to an intrinsic factor

Patients with pancreatic insufficiency absorb B12 poorly

Malabsorption is completely corrected by pancreatic enzymes or purified trypsin
33. Intrinsic factor is a glycoprotein (nucoprotein) synthesized by the parietal cells of the
gastric mucosa

Intrinsic factor concentrates from one animal do not always increase B12 absorption
in other species

Intrinsic factor has been identified in humans, monkey, cattle, swine, rat, rabbit,
hamster, fox, lion, tiger and leopard

Intrinsic factor has not yet been detected in dog, horse, sheep, chicken, guinea pig,
and a number of other species
34. About 3% of ingested cobalt is converted to Vitamin B12 in the rumen. Only 1 –3% of
Vitamin B12 produced in the rumen is absorbed.
FUNCTIONS
25. Vitamin B12 is essential for reactions that involve transfer or synthesis of one-carbon
units, such as methyl groups
26. A general function of B12 is to promote red blood cell synthesis and to maintain nervous
system integrity
27. A deficiency of either folacin or B12 leads to impaired cell division and alterations of
protein synthesis
28. A deficiency of B12 will induce a folacin deficiency by blocking utilization of folacin
derivatives
29. Overall synthesis of protein is impaired in vitamin B12 deficient animals

Affects methionine reformation from homocysteine

Principal reason for the growth depression
30. Propionate metabolism

Propionate is a three-carbon compound and must be converted to succinate to enter
the TCA cycle
1)
To add the one carbon unit requires methymalonyl-CoA isomerase (mutase)
which is a B12 requiring enzyme
31. Another important function of Vitamin B12 is in maintaining glutathione and sulfhydryl
groups of enzymes in the reduced state
REQUIREMENTS
22. Excess protein increases the need for B12 as does performance levels
23. The B12 requirement seems to depend on the levels of choline, methionine and folacin in
the diet and B12 is interrelated with Vitamin C metabolism
24. A reciprocal relationship occurs between B12 and pantothenic acid in chick nutrition,
with pantothenic acid sparing the B12 requirement
25. Dietary need depends on intestinal synthesis and tissue reserves at birth
26. Requirement for Vitamin B12 in ruminant diets is closely related with their requirement
for cobalt

Dietary requirement: 0.07 to 0.20 ppm
27. A ruminant may require more Vitamin B12 than a non-ruminant animal of comparable
size

Propionic acid utilization
DEFICIENCY
31. The result of Vitamin B12 deficiency in humans is a megalablastic anemia (pernicious
anemia) and neurological lesions
32. In animals, anemia is not characteristic of a Vitamin B12 shortage

B12 functions as a growth factor and reduced growth is observed when deficient
33. Ruminants – clinical signs of deficiency

Poor appetite and growth

Muscular weakness

Poor general condition
34. Swine – clinical signs of deficiency

Poor appetite and growth

Variable feed intake

Dramatic growth decline
35. Poultry – clinical signs of deficiency

Reduced body weight gain, feed intake and feed conversion

Perosis may occur when diet lacks choline, methionine, or betaine

Reduced hatchability
36. Horses

Not required for mature horses
37. Humans

Pernicious anemia and degenerative changes in the nervous system
1)
Either B12 or folacin will cure the anemia
2)
Only B12 will prevent degenerative changes in the nervous system
3)
Results in stiffness of limbs, progressive paralysis, mental disorders, diarrhea,
and finally death
CHOLINE
4.
Choline is tentatively classified as one of the B-complex vitamins

5.
However, it does not entirely satisfy the strict definition of a vitamin
1)
Can be synthesized in the liver
2)
Is required in the body in greater amounts
3)
Functions as a structural constituent rather than as a coenzyme
4)
Also existence of choline in essential body constituents was recognized long
before the first vitamin was discovered
Regardless of classification, choline is an essential nutrient for all animals and a required
dietary supplement for swine and poultry
CHEMICAL STRUCTURE AND PROPERTIES
9.
Choline is widely distributed in nature as free choline, acetylcholine, and more complex
phospholipids

It is an integral part of lecithins and thus occurs in all plant and animal cells
FUNCTIONS
5.
Metabolic essential for building and maintaining cell structure
6.
Plays an essential role in fat metabolism in the liver
7.
Essential for the formation of acetylcholine
8.
Source of labile methyl groups
REQUIREMENTS
5.
Choline requirements are influenced by dietary methionine, betaine, myo-inositol,
folacin, and Vitamin B12
6.
Choline and methionine are the two principal methyl donors functioning in animal
metabolism

Provide biologically labile methyl groups that can be transferred within the body
1)
Transmethylation occurs between choline and methionine through
intermediates
Methyl (from methionine) + ethanolamine  choline
Methy (from choline) + homocystome  methionine
DEFICIENCY
9.
Common signs include poor growth, fatty livers, perosis, hemorrhagic tissue, and
hypertension
10. Ruminants

Choline under certain conditions of high-concentrate feeding (feedlot cattle) may
be limiting in the diet

Choline may increase milk fat percentage in dairy cows
11. Swine

Fatty infiltration of the liver

Spraddled hindleg in young pigs
1)
2)
Suggests a strong genetic component
Started to appear as swine producers began to decrease feed allowances given
sows during gestation
12. Poultry

Growth retardation and perosis result from choline deficiency in young poultry
13. Horses

No deficiencies have been reported
14. Humans

Dietary choline may arrest cirrhosis of the liver and reverse the fatty infiltration
1)

Inconclusive
Choline supplements may be useful in preventing age related memory deficits and
certain neurological diseases
ANSC 5308
VITAMIN NUTRITION SECTION
LECTURE 11
VITAMIN B12
42. Vitamin B12 was the last vitamin discovered (1948) and the most potent of the vitamins.
43. It is synthesized in nature only by microorganisms
44. Non-ruminant animals and humans that eat only plant foods are susceptible to Vitamin
B12 deficiency
45. Discovery of this vitamin was dramatic and involved microbiologists, biochemists,
nutrition scientists and physicians in various laboratories
CHEMICAL STRUCTURE AND PROPERTIES
37. Vitamin B12 is a complex structure
C63 H88 O14 N14 PCo. It is called cyanocobalamin

It belongs to the corrinoid group of compounds that have a corrin nucleus

However, numerous other corrinoids do not possess Vitamin B12 activity

The name cobalamin is used for compounds that have the cobalt atom in the center
of the corrin nucleus

Cyanide is attached to the cobalt atom and thus the name cyanocobalamin
38. The cyanide can be replaced by other groups and are referred to as “pseudo” Vitamin
B12 complexes or B12 – like factors




OH (hydroxycobalamin)
H20 (aquacobalamin)
NO2 (nitrocobalamin)
CH3 (methylcobalamin)
39. Vitamin B12 is a dark-red, hygroscopic substance, freely soluble in water and alcohol
40. It is the heaviest of all vitamins with a molecular weight of 1354
METABOLISM
35. Vitamin B12 in the diet is bound to food particles which are released by the combined
effort of low pH and peptic digestion

The released B12 is then bound to a nonintrinsic factor – cobalamin complex
36. The B12 remains bound to nonintrinsic protein until pancreatic proteases (i.e. trypsin)
partially degrade the nonintrinsic factor protein and thus enables B12 to become bound
exclusively to an intrinsic factor

Patients with pancreatic insufficiency absorb B12 poorly

Malabsorption is completely corrected by pancreatic enzymes or purified trypsin
37. Intrinsic factor is a glycoprotein (nucoprotein) synthesized by the parietal cells of the
gastric mucosa

Intrinsic factor concentrates from one animal do not always increase B12 absorption
in other species

Intrinsic factor has been identified in humans, monkey, cattle, swine, rat, rabbit,
hamster, fox, lion, tiger and leopard

Intrinsic factor has not yet been detected in dog, horse, sheep, chicken, guinea pig,
and a number of other species
38. About 3% of ingested cobalt is converted to Vitamin B12 in the rumen. Only 1 –3% of
Vitamin B12 produced in the rumen is absorbed.
FUNCTIONS
32. Vitamin B12 is essential for reactions that involve transfer or synthesis of one-carbon
units, such as methyl groups
33. A general function of B12 is to promote red blood cell synthesis and to maintain nervous
system integrity
34. A deficiency of either folacin or B12 leads to impaired cell division and alterations of
protein synthesis
35. A deficiency of B12 will induce a folacin deficiency by blocking utilization of folacin
derivatives
36. Overall synthesis of protein is impaired in vitamin B12 deficient animals

Affects methionine reformation from homocysteine

Principal reason for the growth depression
37. Propionate metabolism

Propionate is a three-carbon compound and must be converted to succinate to enter
the TCA cycle
1)
To add the one carbon unit requires methymalonyl-CoA isomerase (mutase)
which is a B12 requiring enzyme
38. Another important function of Vitamin B12 is in maintaining glutathione and sulfhydryl
groups of enzymes in the reduced state
REQUIREMENTS
28. Excess protein increases the need for B12 as does performance levels
29. The B12 requirement seems to depend on the levels of choline, methionine and folacin in
the diet and B12 is interrelated with Vitamin C metabolism
30. A reciprocal relationship occurs between B12 and pantothenic acid in chick nutrition,
with pantothenic acid sparing the B12 requirement
31. Dietary need depends on intestinal synthesis and tissue reserves at birth
32. Requirement for Vitamin B12 in ruminant diets is closely related with their requirement
for cobalt

Dietary requirement: 0.07 to 0.20 ppm
33. A ruminant may require more Vitamin B12 than a non-ruminant animal of comparable
size

Propionic acid utilization
DEFICIENCY
38. The result of Vitamin B12 deficiency in humans is a megalablastic anemia (pernicious
anemia) and neurological lesions
39. In animals, anemia is not characteristic of a Vitamin B12 shortage

B12 functions as a growth factor and reduced growth is observed when deficient
40. Ruminants – clinical signs of deficiency

Poor appetite and growth

Muscular weakness

Poor general condition
41. Swine – clinical signs of deficiency

Poor appetite and growth

Variable feed intake

Dramatic growth decline
42. Poultry – clinical signs of deficiency

Reduced body weight gain, feed intake and feed conversion

Perosis may occur when diet lacks choline, methionine, or betaine

Reduced hatchability
43. Horses

Not required for mature horses
44. Humans

Pernicious anemia and degenerative changes in the nervous system
4)
Either B12 or folacin will cure the anemia
5)
Only B12 will prevent degenerative changes in the nervous system
6)
Results in stiffness of limbs, progressive paralysis, mental disorders, diarrhea,
and finally death
CHOLINE
6.
Choline is tentatively classified as one of the B-complex vitamins

7.
However, it does not entirely satisfy the strict definition of a vitamin
5)
Can be synthesized in the liver
6)
Is required in the body in greater amounts
7)
Functions as a structural constituent rather than as a coenzyme
8)
Also existence of choline in essential body constituents was recognized long
before the first vitamin was discovered
Regardless of classification, choline is an essential nutrient for all animals and a required
dietary supplement for swine and poultry
CHEMICAL STRUCTURE AND PROPERTIES
10. Choline is widely distributed in nature as free choline, acetylcholine, and more complex
phospholipids

9.
It is an integral part of lecithins and thus occurs in all plant and animal cells
FUNCTIONS
Metabolic essential for building and maintaining cell structure
10. Plays an essential role in fat metabolism in the liver
11. Essential for the formation of acetylcholine
12. Source of labile methyl groups
REQUIREMENTS
7.
Choline requirements are influenced by dietary methionine, betaine, myo-inositol,
folacin, and Vitamin B12
8.
Choline and methionine are the two principal methyl donors functioning in animal
metabolism

Provide biologically labile methyl groups that can be transferred within the body
2)
Transmethylation occurs between choline and methionine through
intermediates
Methyl (from methionine) + ethanolamine  choline
Methy (from choline) + homocystome  methionine
DEFICIENCY
15. Common signs include poor growth, fatty livers, perosis, hemorrhagic tissue, and
hypertension
16. Ruminants

Choline under certain conditions of high-concentrate feeding (feedlot cattle) may
be limiting in the diet

Choline may increase milk fat percentage in dairy cows
17. Swine

Fatty infiltration of the liver

Spraddled hindleg in young pigs
3)
4)
Suggests a strong genetic component
Started to appear as swine producers began to decrease feed allowances given
sows during gestation
18. Poultry

Growth retardation and perosis result from choline deficiency in young poultry
19. Horses

No deficiencies have been reported
20. Humans

Dietary choline may arrest cirrhosis of the liver and reverse the fatty infiltration
1)

Inconclusive
Choline supplements may be useful in preventing age related memory deficits and
certain neurological diseases