Phosphorus

Physiological Roles
Tissue Distribution of Phosphorus
Metabolism, Absorption, and Excretion
Homeostatic Control of Phosphorus
Interaction with Other Elements
Phosphorus Requirements
Deficiency of P
Phosphorus Excess

I.  Physiological Roles

  1. Phosphorus has more known functions than any other mineral element in the animal body. It is located in every cell of the body and is vitally concerned in many metabolic processes
  2. Phosphorus plays a major role, along with Ca, in formation of bones and teeth
  3. Phosphorus, in combination with other elements, is involved in maintenance of osmotic and acid-base balance
  4. A component of nucleic acids which are important in genetic transmission and control of cellular metabolism
  5. Carbohydrates such as glucose are absorbed from the intestinal mucosa and phosphorylated compounds
  6. Fatty acids are transported throughout the body as phospholipids
  7. Phosphorus is a component of and activator of many enzyme systems
  8. Energy transfer inside living cells.  Practically every energy transfer inside living cells involves the forming and breaking of chemical bonds between phosphorus and carbon or carbon-nitrogen compounds
    1. Low-energy phosphates
      1. Glucose-6-phosphate and triose phosphate are vital intermediates to the glycolysis scheme of energy metabolism
      2. Low energy phosphates liberate 2-3 Kcal/mole on hydrolysis
    2. High energy phosphate bonds
      1. Energy liberated by catabolism is not used directly by cells
      2. It is applied instead to the formation of ester bonds between phosphoric acid residues and certain organic compounds
      3. Energy transfer inside living cells involves the forming or breaking of these ester linkages
        1. Adenosine triphosphate (ATP)
          – The most important high-energy phosphate compound
          – Upon hydrolysis to ADP, it liberates energy directly to such processes as muscle contraction, active transport, and synthesis of many chemical compounds
          – Loss of another phosphate to form AMP liberates more energy
        2. Guanosine triphosphate (GTP)
        3. Cytidine triphosphate (CTP)
        4. Uridine triphosphate (UTP)
        5. Inosine triphosphate (ITP)
        6. Creatine phosphate in muscle
      4. Relatively large amounts of energy (10-12 Kcal/mole) are released when high-energy bonds are hydrolyzed

II.  Tissue Distribution of Phosphorus

  1. Phosphorus is located in every cell of the body
  2. The skeleton contains 80% of the total phosphorus in the body
  3. The remaining 20% is distributed throughout the soft tissues

III.  Metabolism, Absorption, and Excretion

  1. See Ca section for bone metabolism of Ca and P
  2. Phosphorus in the form orthophosphate is absorbed primarily in the upper small intestine
  3. Transit by the small intestine consists of both an active and passive process
    1. The active process is separate and distinct from that associated with Ca transport
    2. When P intake is low, active transport is stimulated via the vitamin D pathway (see J. Dairy Sci. 69:604.1986)
    3. Low plasma P will stimulate 1,25(OH)2D synthesis independent of Ca influences
    4. The resulting increase in 1,25(OH)2D stimulates the intestine to absorb P more efficiently
    5. At higher luminal P concentrations, active transport of P is saturated and passive absorption predominates

IV.  Homeostatic Control of Phosphorus

  1. The greater the need, the more efficient the absorption (see above)
  2. When normal to high dietary P is consumed, P absorption is almost directly related to amount in the diet
  3. In nonruminants the kidney is a major route of P excretion
  4. In ruminants, the salivary glands supplant the kidney as the major route of P excretion
    1. Flow of saliva in cattle is 25-290 l/d
    2. This contributes 30 to 40 g (70 – 80%) of total endogenous P
  5. In ruminants, alteration in salivary P appears also to play a major role in P homeostasis
    1. P in saliva is directly correlated with P in plasma
      1. Injection of 1aOHD3 or IV infusion of P solution will raise both plasma P and salivary P
      2. In contrast, a low-P diet, which results in hypophosphatemia, leads to a decrease in salivary P
      3. PTH increases P concentration in plasma, thereby increasing salivary P secretion
      4. Salivary P mixes with dietary P before a portion of the total P is absorbed in the small intestine
        Mechanism of adaptation to alterations in dietary phosphorus
        (J. Dairy Sci. 69:604. 1986) or (J. Anim. Sci 65:1727-1743. 1987.)
    2. Changes in salivary P represent an efficient method of P regulation unique to the ruminant
      1. Salivary P is reduced during P deficiency
      2. Salivary P is increased during P excess

V.  Interaction with Other Elements

  1. Excess dietary Ca can reduce P absorption
    1. As Ca content with the diet increases, availability of phytate phosphorus as well as availability of Ca decreases
    2. Availability of Zn is reduced by the Ca-phytate complex

       

       

      1. As Ca content of diet increases, availability of  phylate phosphorus decreases
      2. For maximum performance, inorganic P and Ca must be added to most practical diets
      3. As Ca and P must be added to the diet, the phytate molecule becomes complexed with Ca
      4. The net effect is that phytate Ca and P are utilized very little by nonruminants
      5. Much of the phytin phosphorus in wheat is converted to orthophosphate by phytase during leavening and baking of bread
      6. When unleavened bread is used in the Near East, high phytic acid content could contribute to occurrence of osteomalacia as well as reduce utilization of Zn
  2. Excess dietary P can result in nutritional secondary hyperparathyroidism
    1. Lowering of serum Ca stimulates secretion of PTH
    2. Increased resorption of Ca from bone results in skeletal demineralization
  3. Aluminum can inhibit P absorption
    1. Aluminum hydroxide as an antacid
    2. Aluminum in baking powder
    3. Aluminum soft drink cans

VI.  Phosphorus Requirements

  1. P is required for formation of bone mineral in the ratio of 1g of P per 2g of Ca retained
  2. If Ca and P ratio is balanced, wider ranges of P can be tolerated
Recommended allowances of P % of Dietary DM
Poultry
       Starting Chicks (0-8 wks)
       Growing Chicks (8-18 wks)
       Laying Hens

0.7
0.4
0.5
Swine
       Growing and finishing animals
                1 to 5 kg
                5 to 10 kg
                10 to 20 kg
                20 to 35 kg
                35 to 60 kg
                60 to 100 kg
       Breeding animals
                Boars, bred gilts, sows
                Lactating sows, gilts



0.7
0.6
0.55
0.5
0.45
0.4

0.6
0.5

Dairy Cattle
       Baby calves
       Growing heifers and bulls
       Dry pregnant cows
       Lactating cows
       Mature bulls

0.42-0.5
0.26
0.24
0.31-0.38
0.18
Phosphorus %
Feedstuffs Total Phytate Nonphytate
Alfalfa meal, 17% protein
Barley
Corn
Corn Meal, degermed
Oats
Wheat
Wheat bran
Cottonseed meal
Soybean meal
0.28
0.34
0.26
0.10
0.34
0.30
1.37
1.07
0.61
0
0.19
0.17
0.07
0.19
0.20
0.96
0.75
0.38
0.28
0.15
0.09
0.03
0.15
0.10
0.41
0.32
0.27
Comparative ratings of phosphate sources
Compound Biological Value
Beta tricalcium phosphate (reference standard)
Phosphoric acid
Mono, diammonium phosphates
Mono, dicalcium phosphates
Mono, disodium phosphates
Deflourinated rock phosphate
Bone Meal
Low fluorine rock phosphate
Soft rock phosphate

100
115-125
115-125
105-115
115-125
95-100
90-100
55-75
23-35

Feedstuffs

Fishmeal
Meat and bone scraps
Dehydrated alfalfa meal
Corn gluten meal
Yellow corn
Soybean oil meal

100
100
80
35
30
25

VII.  Deficiency of P

  1. P deficiency in rats (J. Nutr. 115:753-758.1985)
    1. Estrous cycle normal
    2. Breeding efficiency and numbers of pups per litter were not altered
    3. Dams fed 0.04% P weaned fewer pups
    4. Pup survival to 45 days of age was lower
    5. Reduced average daily gain (pups were continued on their dams' diet after weaning)
  2. Rickets in the young
  3. Osteomalacia in the adult
  4. Hypophosphatemia in humans
    1. Causes
      1. Nutritional vitamin D deficiency
      2. Blocks in metabolism of vitamin D due to genetic abnormalities
      3. Liver disease
      4. Pharmacological agents (anticonvulsant, addiction to antacids)
      5. Abnormalities of renal tubular reabsorption of phosphate
    2. Effects
      1. Failure of bone mineralization
        1. Rickets in growing bone
        2. Osteomalacia in adult bone
      2. Severe hypophophatemia
        1. Pronounced muscle weakness, possibly due to reduction to organic phosphates in muscle cells
  5. Phosphorus deficiency in ruminants
    1. Cause
      1. Most forages contain little more than adequate P
      2. Weathered, leached forage is nearly always borderline or deficient in P
      3. Phosphorus is usually one of the most limiting of the mineral nutrients for ruminants in many situations
    2. Effects
      1. A drop in plasma inorganic P below the normal levels (4 to 6 mg/dl in adults; 6 to 8 mg/dl for young animals)
      2. Increased plasma phosphatase
      3. Depletion of mineral content of bones
      4. Stiff joints, lameness, fractures may occur
      5. Anorexia is the first clinical symptom
      6. Depraved appetite (may eat rocks, dirt, wood, bones, or hair)
      7. Reduced gain or milk production
      8. Impaired reproductive performance
        1. Lower conception rates and smaller calf crops
        2. More calving difficulty
        3. Lowered milk yield and consequently lowered weaning weight of calf
  6. Phosphorus deficiency in chickens
    1. High mortality
    2. Cage layer fatigue syndrome
      1. Affected birds appear paralyzed and cannot rise or stand
      2. They eventually die of starvation

VIII.  Phosphorus Excess

  1. Nutritional secondary hyperparathyroidism
    1. Increased concentration of serum P
    2. Secondary lowering of serum Ca
    3. Stimulation of PTH secretion
      1. Increased urinary excretion of phosphate
      2. Increased resorption of Ca from bone
      3. Pronounced skeletal demineralization
    4. Metastic calcification in soft tissues (especially kidney, stomach and aorta)
  2. Hyperphosphatemia in humans
    1. Renal insufficiency can result in failure of urinary excretion of absorbed phosphate
      1. Secondary hyperparathyroidism
      2. Demineralization of bone
      3. Resorption of matrix
    2. In some patients, hyperparathyroidism results in elevated serum P because of increased tubular reabsorption of phosphate
    3. Treatment of hyperphosphatemia
      1. Reduction of phosphate intake is difficult since even the minimum protein diet compatible with good nutrition supplies too much phosphate
      2. Absorption of phosphate can be reduced by aluminum hydroxide
  3. Hyperphosphatemia in ruminants
    1. Relative excess P in relation to Ca can cause urinary calculi (urolithiosis)(J. Anim. Sci. 21:995, 1962: 22:510, 1963; 23:1079, 1964)
      1. Formation of stones in the kidney or bladder with resultant obstruction of urine excretion
      2. Bladder rupture results in temporary relief, but this is followed by abdominal distention, depression, and death due to uremia
      3. Maximum dietary level of P tolerated by sheep without development of calculi lies between 0.37% and 0.69%
      4. Increased dietary Ca provides partial protection against occurrence of calculi in sheep receiving higher levels of P (J. Anim. Sci. 24:671)
    2. In contrast to d. above, see Schrier, C. J., and R. J. Emerick. 1986.  Diet calcium carbonate, phosphorus and acidifying and alkalizing salts as factors influencing silica urolithiasis in rats fed tetraethylorthosilicate. J. Nutri. 116:823-830, 1986
      1. Rats fed diets containing 2% tetraethylorthosilicate were used as a model to investigate uroliths primarily of silica in range cattle and sheep
      2. Supplementary dietary phosphorus offers partial protection against silica uroliths
        1. Not associated with increases in urine volume
        2. Only partial dependent on urine acidification
      3. Increase in urolith incidence of rats fed CaCO3 appear to result from an alkalization of urine and a reduction in urine
  4. P excess in chickens
    1. Reduced egg production and egg shell quality in hens
    2. Decreased weight gain and efficiency of feed utilization in broiler
    3. Increased mortality when dietary P is raised to 2% (approximately four times requirement)
  5. Maximum tolerable phosphorus levels (assuming dietary Ca is adequate)
    1. Cattle 1%
    2. Sheep 0.6%
    3. Swine 1.5%
    4. Poultry 1% (laying hens, 0.8%)
    5. Horse 1%




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