Iron

I.                    Storage form = ferritin (Iron + protein)

II.                 Functions

A.     Iron (heme) + protein (globulin) = hemoglobin

1.      Oxygen transport

B.     Myoglobin, muscle protein

C.     Enzyme activation (co-factor)

III.               Deficiency

A.     Iron deficiency anemia

1.      Fewer (#) red blood cells

2.      Less hemoglobin

3.      Pale mucus membranes

B.     Reduced appetite (pica)

C.     Diarrhea

D.     Labored breathing

E.      Rough hair coat

F.      Decreased growth

Newborn animals susceptible (pigs)

IV.              Toxicity

A.     Free Fe are very toxic

B.     Fe always associated with a protein

C.     2 Fe + 1 ß globulin protein (transferrin) = transferritin for Fe transfer

 

Selenium

I.                    Functions

A.     Component of glutathione peroxidase

1.      Protect against oxidation of PUFA

B.     Protect tissue from toxic substances

C.     Interrelationship with Vit. E

1.      Spare each other

II.                 Deficiency

A.     White muscle disease (stiff lamb disease)

B.     See Vit. E

III.               Toxicity

A.     Blind staggers or Alkali disease

1.      Emaciation

2.      Loss of hair

3.      Soreness and sloughing of hooves

4.      Blindness

5.      Death

 

Mineral

Main Functions

Deficiency Symptoms

Comments

Calcium (Ca)

Bone and teeth formation; blood coagulation; muscle contraction; nerve function; cell permeability; milk production; egg shell formation

Rickets (young); osteomalacia (adult); tetany; thin-shelled eggs; reduced egg production; hypocalcemia or milk fever in dairy cattle

Vitamin D involved in absorption and bone deposition; excess PO4 decreases absorption; excess Mg decreases absorption, replaces Ca in bone and increases Ca excretion; Ca:P ratio should be 1:1 to 2:1

Phosphorus (P)

Bone and teeth formation; phosphorylation; high-energy phosphate bonds; PO4 chief anion radical of intracellular fluid; PO4 important in acid-base balance

Rickets (young); osteomalacia (adult); reduced egg production

Vitamin D involved in renal reabsorption and bone deposition; excess Ca and Mg causes decrease in absorption; Ca:P ratio should be 1:1 to 2:1; in male ruminants, excess P may cause urinary calculi

Soduim (Na)

Major cation of extracellular fluid where it is involved in osmotic pressure and acid-base equilibrium; preservation of normal muscle cell irritability; cell permeability

Reduced growth; eye disturbances with corneal lesions; reproduction impairment (infertility in males, delayed sexual maturity in females)

Salt tocicity readily occurs in nonruminants with levels above 8% in diet; staggering gait, blindness, nervous disorders and hypertension

Chlorine (Cl)

Major anion involved in osmotic pressure and acid-base balance (chlorine shift); hydrochloric acid in digestion

Hypochloremic alkalosis (usually due to physiological disturbance such as vomiting rather than deficiency); reduced growth

Toxicity unlikely

Magnesium (Mg)

Enzyme activator primarily in glycolytic system; bone formation

Vasodilation; hyperirritability with convulsions, loss of equilibrium and trembling; tetany

Excess upsets Ca and P metabolism; toxicity not likely

Mineral

Main Functions

Deficiency Symptoms

Comments

Potassium (K)

Major cation of intracellular fluid where it is involved in osmotic pressure and acid-base balance; muscle activity

Hypokalemia; lethargic condition with high incidence of comas and death; diarrhea, distended abdomen and unitidy appearance

Excess reduces Mg absorption; Mg deficiency reduces K retention leading to K deficiency

Sulfur (S)

Sulfur-containing amino acids; SH group function in tissue respiration; component of biotin and thiamine

Primarily reduced growth effect due to sulfur amino acid requirement for protein synthesis

Toxicity unlikely

Iron (Fe)

Cellular respiration (hemoglobin, cytochromes, myoglobin)

Hypochromic-microcytic anemia (less than normal amount of hemoglobin and fewer red cells); anemia may be common in baby pigs unless Fe is supplied

Ca-P ratio influences absorption; Cu required for proper metabolism; pyridoxine deficiency decreases absorption

Copper (Cu)

Cofactor in several oxidation-reduction enzyme systems; hemoglobin synthesis; bone formation; maintenance of myelin of nerves; hair pigmentation

Fading hair coat or lack of wool; nervous symptoms or ataxia; lameness, swelling of joints and fragility of bones; anemia

Excess Mo or Zn inhibit its utilization and storage; toxcity occurs at levels above 250 ppm with much the same symptoms as deficiency

Zinc (Zn)

Component or cofactor of  several enzyme systems including peptidases and carbonic anhydrase; needed for bone and feather development

Poor hair or feather development and slipping of wool; rough and thickened skin or parakeratosis in swine

High Ca or phytate ties up Zn; excess Zn interferes with Cu metabolism and may cause anemia

Mineral

Main Functions

Deficiency Symptoms

Comments

Manganese (Mn)

Thought to be an activator of enzyme systems involved in oxidative phyosphorylation, amino acid metabolism, fatty acid synthesis and cholesterol metabolism; bone formation (organic matrix); growth and reproduction

Poor growth; shortened long bones; impaired reproduction (testicular degeneration of males, defective ovulation of females); perosis or slipped tendon in poultry

Excess Ca and P decreases absorption; toxicity unlikely

Cobalt (Co)

Component of vitamin B12; needed by rumen bacteria for growth and vitamin B12 synthesis

Anemia (varies from normocytic-normochromic to megaloblastic or macrocytic); deficiency in ruminants causes reduced appetite, reduced growth and body weight and eventually death

Related in vitamin B12; toxicity unlikely

Iodine (I)

Thyroxine formation

Goiter; stillbirths; hairless pigs or wool-less lambs at birth

Long-term intake of high amounts of I reduces thyroid uptake of I

Selenium (Se)

Component of the enzyme glutathione peroxidase, which reduces peroxides arising from tissue lipid oxidation; thus, protects against cellular membrane damage by the peroxides; functions are closely related to that of vitamin E

Excudative diathesis  (chicks); muscular dystrophy (white muscle disease); cattle stiff lamb disease-sheep; liver necrosis (pigs, rats)

Chronic toxcity yields blind staggers at 10-20 ppm or alkali disease at 5-10 ppm; acute toxcity occurs at 20 ppm and above; sudden death; SO4 protector against toxcity

Molybdenum (Mo)

Purine metabolism; stimulates microbial activity in rumen

Lack of conversion of xanthine to uric acid but not likely to be deficient in natural diet

Excess interferes with Cu activation of enzymes; causes anemia and diarrhea; SO4 protects against toxcity

Fluorine (F)

Traces protect against teeth decay

Excesses of F are of more concern than deficiencies in livestock production

Levels above 5-10 ppm block vital oxidative enzymes by interfering with Mn; causes bone deformities enamel defects and organ degeneration; Ca and Al salts protect against toxcity; F is a cumulative poison so toxicity may not be noted for some time

 

INTEGRATION OF METABOLISM

Well Fed State:

Glucose is the source of energy for the brain

AA to liver for protein

Excess AA used for energy - trans- and de-amination (­ urea synthesis)

Fats go to adipose tissue

CHO for NADPH production

Starvation:

Nothing coming for the diet

Sources of nutrients:

Fat (stored in adipose tissue)

Glycogen (liver & muscle)

Brain uses glucose, but not muscle

Early starvation, muscle uses ketone (FA, but limited number available)

Can only break down so much protein - only 25-30% of muscle an be broken down.

Brain can be eventually forced to used ketone bodies for energy 

 

Hormones

Insulin: Polypeptide (51 AA) - produced by b cells of Islets of Langerhans in Pancreas. Anabolic (synthesize glycogen, triglycerides, protein)

Regulation: of secretion (what stimulates secretion)

1. High blood glucose (hyperglycemia) after a meal

2. High blood amino acids after a meal

 

Metabolic effects - due to binding to receptors in liver, muscle, adipose tissue.

1. CHO Metabolism - Prevent hyperglycemia by ¯ blood glucose

a. Increase glucose transport into adipose and muscle cells

b. Increase glycolysis (glucose ® acetyl-CoA)

c. Decrease gluconeogenesis in the liver

d. Increase glycogen synthesis in liver and muscle

2. Lipid Metabolism Promotes lipogensis (triglyceride synthesis in adipose tissue)

a. Increase fatty acid synthesis: 1) Acetyl-CoA from glucose (glycolysis); 2) NADPH from glucose

b. Increase triglyceride synthesis

c. Increase triglyceride storage in adipose tissue

 3. Amino Acid Metabolism Reduce blood AA increasing synthesis

a. Increase entry of AA to liver and muscle cells

b. Increase protein synthesis

c. Increase degradation of surplus AA

d. ­ Urea cycle activity

Insulin

Glucagon: Polypeptide (29 AA) produced by a cells of Islets of Langerhans in Pancreas. Catabolic - favors breakdown of glygogen in liver, mobilization of fatty acids, protein degradation, and gluconeogenesis (oppose the action of insulin)

Regulation: - Low blood glucose (hypoglycemia) after overnight or prolonged fast.

Metabolic Effects - due to binding to receptors in liver & adipose tissue ONLY!!

1. CHO Metabolism - Prevent hypoglycemia by ­ mobilization and synthesis of glucose

a. Increase glycogen breakdown in liver (NOT muscle = no receptors)

b. Increase gluconeogenesis by activating key gluconeogenic enzymes

2. Lipid Metabolism - promotes lipolysis (breakdown)

a. Increase triglyceride breakdown - release free FA

b. Increase mobilization of FA and uptake by the liver

c. Increase b -oxidationin liver - ­ Acetyl-CoA

d. Increase ketone body formation

3. Amino Acid Metabolism - lowers AA concentration in the blood

a. Increase uptake of AA by the liver for gluconeogenesis

b. Other hormones (cortisol) ­ degradation of muscle protein, release AA into blood

glucagon