Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PHOSPHORUS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 667 records · Page 37Linked to original sources
PubMed1982

Relationships between prepartal dietary calcium and phosphorus, vitamin D metabolism, and parturient paresis in dairy cows.

Twenty Jersey cows were fed one of four prepartal diets: a)low calcium, low phosphorus (LCLP); b) low calcium, high phosphorus (LCLP); c) high calcium, low phosphorus (HCLP); or d)high calcium, high phosphorus (HCHP). Diets were fed for about 4 weeks prepartum. Blood samples were taken periodically, and the collected plasma analyzed for concentrations of calcium, phosphorus, hydroxyproline and 1,25 dihydroxyergocalciferol plus 1,25-dihydroxycholecalciferol (1,25-(OH)2D). Cows fed the LCLP and LCHP diets, when compared to cows fed the HCLP diet, had: a) greater concentrations of plasma 1,25-(OH)2D and hydroxyproline prepartum; b) greater plasma calcium concentrations at parturition; and c) less incidence (0 versus 4 cases) of parturient paresis. Thus, low calcium diets, regardless of dietary phosphorus intake, seemed to activate calcium homeostatic mechanisms before parturition by stimulating both bone and gut. Cows fed the HCLP diet had greater plasma calcium concentrations at parturition than did cows fed the HCHP, even though there was no measurable effect on plasma 1,25-(OH)2D and hydroxyproline concentrations during the prepartal period. It seems possible that the beneficial effect of low dietary phosphorus, when dietary calcium is high, may be a result of a prepartal increase in efficiency of absorption of calcium and phosphorus from the gut caused by increased binding of 1,25-(OH)2D to intestinal receptors.

Animals↗
PubMed1982

Dietary phosphorus requirement of channel catfish.

Two experiments were conducted to reevaluate the dietary phosphorus requirement of fingerling channel catfish. Basal diets containing either casein with supplemental inorganic phosphorus and 0.5% total calcium or egg albumin with supplemental inorganic phosphorus and 0.75% total calcium yielded similar requirement data. Eleven-week growth, feed efficiency, serum phosphorus, bone ash, bone calcium and bon phosphorus data indicate that 0.33% apparent available dietary phosphorus is adequate for maximum growth and bone mineralization. Based on these data and previous findings, we would suggest a value of 0.4% apparent available phosphorus be used in formulating catfish feeds. The apparent availability of phosphorus from soybean meal, as determined by the chromic oxide indicator method, was 29% for channel catfish.

Animals↗
PubMed1989

Phosphorus-induced nephrocalcinosis and kidney function in female rats.

The question was addressed whether dietary phosphorus-induced nephrocalcinosis in rats is associated with impaired kidney function. Weanling female rats were fed purified diets containing either 0.4 or 0.6% (wt/wt) phosphorus for 28 d. The diet containing 0.6% phosphorus produced marked kidney calcification, as determined both by chemical analysis of kidney calcium and histological examination in kidney sections. Histological examination did not show calcification in stomach, lung, heart or thoracic aorta, which are predisposition sites of metastatic calcification in secondary renal hyperparathyroidism. In rats fed the 0.6% phosphorus diet, phosphorus retention and urinary excretion were greater compared with rats fed the 0.4% phosphorus diet. The following indicators of kidney function were examined: water intake, urinary volume, urine and plasma osmolality, urine and plasma creatinine, urine and plasma urea, urea and creatinine clearance and urinary albumin excretion. Of these indicators, only urinary albumin excretion was significantly increased in rats fed the nephrocalcinogenic diet. In a further experiment, the increase of urinary albumin was reproduced. After pooling the results of the two experiments, in individual rats fed the 0.6% phosphorus diet, the concentration of kidney calcium was found to be positively related with kidney weight expressed relative to body weight (r = 0.82, n = 22) and with albumin excretion in urine (r = 0.79, n = 28). The increased weight of calcinotic kidneys was mainly due to both calcium deposition and tubular hyperplasia. It is concluded that dietary phosphorus-induced nephrocalcinosis is associated with impaired kidney function in rats.

Albumins↗
PubMedDate not supplied

Effects of calcium and phosphorus supplementation on calcium retention and fat absorption in preterm infants fed pooled human milk.

Fat, phosphorus, and calcium balance studies were performed in normal very low birth weight infants (BW less than or equal to 1,500 g) fed either normal or calcium- and phosphorus-supplemented pooled pasteurized human milk. Calcium and phosphorus supplements were 27 mg/dl and 24.5 mg/dl, respectively, throughout the study. Measured calcium and phosphorus intake in the supplemented group averaged 90 +/- 6 mg/kg/day and 62 mg/kg/day, respectively, compared to 47 +/- 7 mg/kg/day and 24 +/- 6 mg/kg/day in the nonsupplemented group. The percent of fat, calcium, and phosphorus absorption was similar in the two groups: respectively, 71 +/- 23%, 73 +/- 13%, and 93 +/- 2% in the supplemented group compared to 75 +/- 11%, 71 +/- 14%, and 92 +/- 4% in the nonsupplemented group. Calcium and phosphorus retention reached 62 +/- 12 mg/kg/day and 53 +/- 4 mg/kg/day in the supplemented group against 21 +/- 10 mg/kg/day and 21 +/- 5 mg/kg/day in the nonsupplemented group. These data support the notion that calcium, in addition to phosphorus supplementation in pooled human breast milk, improves both calcium and phosphorus retention in preterm infants.

Calcium↗
PubMed2002

Biofilm formation in drinking water affected by low concentrations of phosphorus.

Abstract: There are geographical regions where microbial growth in drinking waters is limited by phosphorus instead of organic carbon. In these drinking waters even a low amount of phosphorus can strongly enhance microbial growth. The formation of biofilm can be limited by low availability of phosphorus in drinking waters with low content of phosphorus. The formation of biofilms on polyvinyl chloride plates was studied in laboratory experiments with water containing 48 microg/L assimilable organic carbon and 0.19 microg/L microbially available phosphorus. We found that low additions of phosphate (1-5 microg/L PO4(3-)-P) to water increased microbial growth in the water and in the biofilm. The effect of phosphorus on microbial growth could be detected by determining either the microbial cell production or the content of ATP in biofilms. Also, in steady-state biofilms, microbial concentrations were higher with phosphorus addition as enumerated by heterotrophic plate counts on R2A-agar and acridine orange direct counting. This work confirms the earlier findings of the importance of phosphorus for microbial growth in humic-rich drinking waters.

Bacterial Physiological Phenomena↗
PubMed1993

Effect of phosphorus restriction on renal response to oral and intravenous protein loads in rats.

Dietary phosphorus restriction ameliorates renal injury in rats. This may be due to changes in renal hemodynamics, including those factors associated with protein-induced hyperfiltration. To test this, we measured inulin clearance (CIn), p-aminohippuric acid clearance (CPAH), mean arterial blood pressure, and renal vascular resistance (RVR) 1 h before and 100 min after either oral gavage of 2 g bovine serum albumin or intravenous infusion of 5% glycine in female Sprague-Dawley rats previously fed for 3-8 wk a 0.5% or a 0.1% phosphorus diet. Baseline CIn, CPAH, blood pressure, and RVR were similar. After albumin gavage, CIn rose 20% (P < 0.01) for the 0.5% phosphorus group but did not change for rats fed the 0.1% phosphorus diet. Other measured parameters, including plasma glucagon and renin activity, were not influenced by dietary phosphorus content. In contrast, during intravenous infusion of glycine, hyperfiltration was induced in phosphorus-restricted rats. Thus dietary phosphorus restriction ablates oral protein but not intravenous amino acid-induced hyperfiltration, suggesting a gut-mediated mechanism for the former. These data highlight the potential importance of dietary phosphorus as a mediator of renal hemodynamics.

Administration, Oral↗
PubMed1972

Effects of dibutyryl cyclic adenosine 3',5'-monophosphate and parathyroid extract on calcium and phosphorus metabolism in hypoparathyroidism and pseudohypoparathyroidism.

It has been proposed previously that the metabolic defect in pseudohypoparathyroidism which accounts for parathyroid hormone unresponsiveness is an absence or abnormal form of the adenyl cyclase system in kidney and presumably in bone. To determine whether there is an associated defect in the response mechanism to cyclic adenosine 3',5'-monophosphate (cyclic AMP), the effects of parathyroid extract (PTE), and dibutyryl cyclic AMP were compared in patients with either surgical hypoparathyroidism or pseudohypoparathyroidism. PTE and dibutyryl cyclic AMP both increased serum and urinary calcium, lowered the serum phosphorus, and increased urinary phosphorus in patients with hypoparathyroidism. PTE also increased urinary cyclic AMP in these patients. PTE increased serum and urinary calcium and urinary phosphorus but did not alter serum phosphorus or urinary cyclic AMP in the patients with pseudohypoparathyroidism. Dibutyryl cyclic AMP increased the serum and urinary calcium, lowered the serum phosphorus, and increased urinary phosphorus in all the patients with pseudohypoparathyroidism. The results indicate that (a) dibutyryl cyclic AMP can reproduce the effects of parathyroid hormone on calcium and phosphorus metabolism in man, (b) the response mechanism to cyclic AMP appears to be intact in pseudohypoparathyroidism, and (c) PTE apparently produces some of its characteristic effects on calcium and phosphorus metabolism in pseudohypoparathyroidism in the absence of an increase in urinary cyclic AMP.

Adolescent↗
PubMed1984

Uncoupling of the parathyroid hormone receptor-adenylate cyclase system of canine kidney during dietary phosphorus deprivation.

The mechanisms involved in the renal resistance to the phosphaturic action of PTH during dietary phosphorus deprivation remain ill defined. Previous studies in dogs from our laboratory demonstrated that baseline excretion of cAMP and the increment after administration of parathyroid extract were markedly reduced during dietary phosphorus deprivation. The present studies examine the initial events in the actions of PTH, namely receptor binding and adenylate cyclase activation, in renal cortical membranes from normal and phosphorus-deprived animals. Mongrel dogs were fed a diet deficient in phosphorus for 4-6 weeks. Plasma phosphorus fell from 4.2 +/- 0.4 to 1.4 +/- 0.3 mg/dl. In renal cortical membranes from these animals, basal adenylate cyclase activity was not different from that in control normal animals. However, PTH-stimulated enzyme activity was markedly reduced (5785 +/- 303 pmol cAMP/mg protein X 30 min in controls vs. 2612 +/- 406 pmol cAMP/mg protein X 30 min; P less than 0.01). Kact (PTH concentration for half-maximal enzyme activation) was unchanged. PTH receptor binding assessed with [Nle8,Nle18,Tyr34]bovine PTH-(1-34) NH2 was not different in the two groups. The decreased PTH-stimulated adenylate cyclase activity was not corrected by GTP. Activation of adenylate cyclase by NaF was reduced in membranes from the phosphorus-deprived animals, whereas enzyme activation by guanylylimidodiphosphate was similar in both groups. Enzyme activity in the presence of Mn++ was not different from the control value. These data indicate that during dietary phosphorus deprivation there is uncoupling of the PTH receptor-adenylate system of canine kidney. This abnormality may play a role in the renal resistance to PTH during dietary phosphorus deprivation.

Adenylyl Cyclases↗
PubMed1976

1,25-Dihydroxycholecalciferol effect on serum phosphorus homeostasis in rats.

It has recently been shown that 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) increases the serum phosphorus concentration of rats on a low-phosphorus diet. While studying the biological activity of 1,25(OH)2D3, we observed that under certain circumstances 1,25-(OH)2D3 would decrease the serum phosphorus concentration. The analysis of all data obtained in rat experiments during the past 3 years revealed highly significant linear correlations (P less than 0.001) between changes of serum phosphorus concentrations after the administration of 1,25-(OH)2-D3 (130 pmol/d for 1 or 5 days) and serum phosphorus or calcium levels in the animals before injection. Similar correlations could only be found with the higher dose of 25-hydroxycholecalciferol (130 pmol/d for 5 days). Another vitamin D3 metabolite, 24,25-dihydroxycholecalciferol, had no effect on serum phosphorus concentrations under our experimental conditions. The 1,25-(OH)2D3 effect on serum phosphorus concentration does not require the presence of circulating parathormone and/or calcitonin. We suggest that 1,25-(OH)2D3 might be an important factor in serum phosphorus homeostasis.

Animals↗
PubMed1988

Elevated secretion and action of serum parathyroid hormone in young adults consuming high phosphorus, low calcium diets assembled from common foods.

We sought to determine if the high phosphorus, moderately low calcium intake typical of U.S. teenagers and young adults alters parathyroid function as it does in experimental animals. Because those animals ultimately developed osteopenia, it has been suggested that low dietary calcium to phosphorus ratios may reduce peak bone mass and increase susceptibility to osteoporotic fracture later in life. However, it is not known whether PTH secretion or action increases in response to commonly consumed phosphorus-rich, calcium-poor foods. We studied the 24-h mineral and hormonal responses of eight men and eight women, aged 18-25 yr, after 8 days of ingesting a control diet that had calcium (820 mg) and phosphorus (930 mg) contents near the recommended daily intakes, and a test diet with calcium and phosphorus contents (1660 mg phosphorus, 420 mg calcium) typical of current intakes. Both diets were made from common grocery store foods. The 24-h mean serum immunoreactive PTH levels increased in men (11%; P less than 0.006) and women (22%; P less than 0.003) during the test diet. In both sexes, the test diet significantly increased serum phosphorus, plasma 1,25-dihydroxyvitamin D, and urinary hydroxyproline and cAMP excretion; in women only it decreased serum ionized and total calcium levels. Thus, short term ingestion of a diet typifying current levels of calcium and phosphorus intake resulted in elevated serum iPTH levels and indexes of PTH action in young adults.

Adolescent↗
PubMed2000

Effect of iron(III) chitosan intake on the reduction of serum phosphorus in rats.

Because of the widespread use of aluminium- and calcium-containing phosphate binders for the control of hyperphosphataemia in patients with end-stage renal failure, an iron(III) chitosan complex was synthesised and fed to rats to measure its effect on serum phosphorus and calcium, intestinal phosphate binding and phosphate absorption. Thirty-six Wistar rats were randomly selected and distributed into a baseline group (n = 6), a control group (n = 8 (days 0-15), n = 8 (days 16-30)) and a treatment group (n = 8 (days 0-15), n = 8 (days 16-30)). The control groups ingested AIN-76 diet mix with a 1% w/w fibre content; however, the treatment groups had the fibre content completely substituted with iron(III) chitosan. The mean weights of the treated rats were slightly lower from 15 days (not significant); but overall, rat growth was not stunted in the treatment groups. The serum phosphorus levels of the treated group (n = 8) were significantly reduced after 15 days (P = 0.004; control: 5.7+/-0.9 mg dL(-1); treatment: 4.4+/-0.5 mg dL(-1); 95% CI of difference: 0.5-2.2) and 30 days (P = 0.002; control: 5.5+/-0.9 mg dL(-1); treatment = 4.1+/-06 mg dL(-1); 95% CI of difference: 0.6-2.3) as compared with the respective control group. The serum calcium-phosphorus product was 62.0+/-12.1 mg2 dL(-2) for the control and 45.1+/-6.6 mg2 dL(-2) for the treatment group after 30 days (P = 0.004). The serum iron concentration of the treatment group did not differ from the baseline value after 15 and 30 days, but the treatment group was significantly higher than the control group (P<0.05) after 30 days. The faeces phosphorus levels (mg day(-1)) were higher (P<0.01) and its iron content was much higher (P<0.01) for the treated group. The urine phosphorus (mg kg(-1)) was not significantly reduced for the treated group, but the mean was consistently less. The kidney and liver weights of both groups were similar, but the phosphorus content of the kidney (mg (g kidney)(-1)) was higher for the treated group after 30 days (P = 0.041; control, 4.2+/-1.2 mg g(-1) vs treatment, 5.6+/-1.4 mg g(-1). Because iron(III) chitosan had a high phosphorus-binding capacity of 308 (mg P) per gram of Fe3+ for both the in-vitro (pH 7.5) and in-vivo studies, which is greater than nearly all commonly used phosphate binders, and a small net phosphorus absorption difference of 3.7 mg day(-1), it is an efficient phosphate binder for lowering serum phosphate levels without increasing serum calcium levels.

Animals↗
PubMed1998

The influence of dietary phosphorus and magnesium concentrations on the calcium content of heart and kidneys of DBA/2 and NMRI mice.

Dystrophic cardiac calcification (DCC) is often found in DBA/2 mice, reportedly in association with low plasma magnesium levels in this mouse strain. It was hypothesized that high-phosphorus diets and low-magnesium diets that are known to lower plasma magnesium concentrations would promote the development of DCC. DBA/2 mice were fed diets with either low-magnesium (0.02%, w/w) or high-phosphorus (0.8%) concentrations or a combination of the two variables. NMRI mice were given either a low- (0.2%) or high- (0.6%) phosphorus diet. Female, but not male, NMRI mice accumulated calcium in the heart when fed the high-phosphorus diet; neither gender developed kidney calcification. DBA/2 mice with either a low-magnesium or a high-phosphorus intake developed marked cardiac calcifications. The combination of low-magnesium and high-phosphorus intake caused severe calcification of the heart, kidney and tongue. Increasing the dietary magnesium content (0.08%) and reducing phosphorus (0.2%) did not fully prevent cardiac calcification, but reduced heart calcium concentrations in male DBA/2 mice. It is concluded that diets for DCC-susceptible mice should contain adequate amounts of magnesium and low, but sufficient amounts of phosphorus in order not to additionally stimulate cardiac calcification.

Animals↗
PubMed2001

Quantitative changes of calcium, phosphorus, and magnesium in common iliac arteries with aging.

To elucidate the mechanism of element accumulations in the arteries with aging, the authors investigated the mass ratios among calcium, phosphorus, and magnesium in the common iliac arteries by inductively coupled plasma-atomic emission spectrometry. The subjects consisted of 16 men and 8 women, ranging in age from 65 to 93 yr. It was found that there were extremely significant correlations between calcium and phosphorus contents, between calcium and magnesium contents, and between phosphorus and magnesium contents in the common iliac arteries. In regard to the mass ratio, although the mass ratio of calcium to phosphorus was almost constant, the mass ratios of magnesium to calcium and phosphorus were different at early and advanced stages of the accumulation of calcium and phosphorus. It was found that both the mass ratios of magnesium to calcium and phosphorus were higher at an early stage of the accumulation of calcium and phosphorus in the arteries than at an advanced stage of the accumulation.

Aged↗
PubMed1999

Effect of histamine H2-receptor antagonist on the phosphorus-binding abilities of calcium carbonate and calcium lactate in hemodialysis patients.

The effect of histamine H2-receptor antagonist (famotidine) on the phosphorus-binding abilities of calcium carbonate and calcium lactate were examined in 13 chronic hemodialysis patients. In seven patients receiving calcium carbonate, famotidine (20 mg/d) was given because of gastroduodenal disorders, and calcium carbonate was replaced with calcium lactate as a phosphorus binder after 4 wk of treatment with famotidine. With the 4-wk administration of famotidine accompanied by calcium carbonate, the serum phosphorus level increased from 6.3+/-0.9 to 7.1+/-0.5 mg/dl (P<0.05). However, with the substitution of calcium lactate, the serum phosphorus level decreased significantly when compared to that before substitution (6.3+/-0.2 and 6.0+/-0.9 mg/dl after 4 and 8 wk of substitution, respectively), despite continued administration of famotidine. Serum calcium, creatinine, alkaline phosphatase, high sensitive parathyroid hormone, blood urea nitrogen, arterial blood pH, and bicarbonate were not significantly altered during the trial period. In six control patients treated with calcium carbonate alone, there were no statistical changes in serum calcium and phosphorus levels after substitution of calcium lactate for calcium carbonate. These results suggest that famotidine significantly affects the phosphorus-binding ability of calcium carbonate, but not that of calcium lactate. A careful observation of changes in the serum phosphorus level should be required in hemodialysis patients receiving calcium carbonate and histamine H2-receptor antagonists. Calcium lactate may be useful as a phosphorus binder in such hemodialysis patients.

Adult↗
PubMed1999

Differential effects of 1,25-dihydroxy-vitamin D3 and 19-nor-1,25-dihydroxy-vitamin D2 on calcium and phosphorus resorption in bone.

1,25-Dihydroxy-vitamin D3 [1,25-(OH)2D3] suppresses the secretion and synthesis of parathyroid hormone (PTH) and has been used in the treatment of secondary hyperparathyroidism. However, 1,25-(OH)2D3 can induce hypercalcemia, which often precludes its use. Therefore, an analog of 1,25-(OH)2D3 that would retain its therapeutic effects but produce minor effects on calcium and phosphorus metabolism could be an ideal tool for the treatment of secondary hyperparathyroidism. It has been shown that 19-nor-1,25-dihydroxy-vitamin D2 [19-nor-1,25-(OH)2D2], an analog of 1,25-(OH)2D3, can suppress PTH levels in uremic rats at doses that do not affect plasma ionized calcium levels. The experiments presented here, using parathyroidectomized rats fed diets deficient in either calcium (0.02%) or phosphorus (0.02%), were performed to compare the effects of 1,25-(OH)2D3 and 19-nor-1,25-(OH)2D2 on calcium and phosphorus resorption in bone. Parathyroidectomized rats received daily intraperitoneal injections of vehicle, 1,25-(OH)2D3 (100 ng), or 19-nor-1,25-(OH)2D2 (100 or 1000 ng) for 9 d. Plasma calcium and phosphorus levels were monitored during the study, and ionized calcium levels were determined at the end of the study. By 9 d, 1,25-(OH)2D3 (100 ng/d) increased total calcium levels to 12.4+/-0.26 mg/dl, compared with 6.32+/-0.25 mg/dl (P<0.001) in control animals. The same dose of 19-nor-1,25-(OH)2D2 (100 ng/d) was much less potent (9.45+/-0.28 mg/dl, P<0.001). Similar results were seen with ionized calcium levels [19-nor-1,25-(OH)2D2, 3.61+/-0.12 mg/dl; 1,25-(OH)2D3, 5.03+/-0.16 mg/dl; P<0.001]. Ionized calcium levels were also lower in rats receiving the higher dose (1000 ng) of 19-nor-1,25-(OH)2D2 (4.59+/-0.09 mg/dl, P<0.05). Similar results were seen in rats fed the phosphorus-deficient diet. 1,25-(OH)2D3 (100 ng) increased plasma phosphorus levels from 4.30+/-0.39 mg/dl in vehicle-treated rats to 7.43+/-0.26 mg/dl (P<0.001). The same dose of 19-nor-1,25-(OH)2D2 had no effect (5.19+/-0.32 mg/dl), whereas the high dose (1000 ng) increased plasma phosphorus levels (7.31+/-0.24 mg/dl) in a manner similar to that of 1,25-(OH)2D3 (100 ng). Therefore, 19-nor-1,25-(OH)2D2 is approximately 10 times less effective in mobilizing calcium and phosphorus from the skeleton, compared with 1,25-(OH)2D3. With its ability to suppress PTH at noncalcemic doses, 19-nor-1,25-(OH)2D2 is a potential therapeutic tool for the treatment of secondary hyperparathyroidism in chronic renal failure.

Animals↗
PubMedDate not supplied

Soil variables for predicting potential phosphorus release in Swedish noncalcareous soils.

The accumulation of P in agricultural soils due to fertilization has increased the risk of P losses from agricultural fields to surface waters. In risk assessment systems for P losses, both P release from soil to solution and transport mechanisms need to be considered. In this study, the overall objective was to identify soil variables for prediction of potential P release from soil to solution. Soils from nine sites of the Swedish long-term fertility experiment were used, each with four soil P levels. Phosphorus extractable with CaCl2 was used as an estimate of potential P release from soil to solution. Ammonium lactate-extractable phosphorus (P-AL) or NaHCO3-extractable phosphorus (Olsen P) could not be used alone for prediction of potential P release since soils with high phosphorus sorption capacity (PSC) released less P than soils with low PSC at the same soil test phosphorus (STP) level. Degree of phosphorus saturation (DPS) was calculated as Olsen P or P-AL as a percentage of PSC derived from P sorption isotherms or from Fe and Al extractable in ammonium oxalate. The CaCl2-extractable total phosphorus (CaCl2-TP) was exponentially related to these DPS values (r2 > or = 0.79). The CaCl2-TP was also linearly related to ratios between Olsen P or P-AL and a single-point phosphorus sorption index (PSI; r2 > or = 0.86). These ratios, which are easily determined and gave good correlations with CaCl2-TP, seemed to be the most useful estimates of potential P release for risk assessment systems.

Fertilizers↗
PubMed1976

Calcium and phosphorus requirements of the laying hen.

Three experiments were conducted; the first studied the influence of pre-laying dietary calcium levels on subsequent hen performance, while in the second and third the influence of various levels of dietary calcium and phosphorus on performance, egg shell quality and calcium and phosphorus retention were investigated. Pre-dietary calcium levels (0.5 and 1.5%) resulted in a significant strain X diet interaction for weight gain up to commencement of lay but did not influence production, feed intake, egg size or sheel quality. Dietary calcium levels varying from 2.5 to 4.0% did not significantly alter the avove parameters during a 140 day laying test. Compared to a non-pelleted control diet, steam pelleting resulted in a significant enhancement in phosphorus availability is judged by higher levels of performance. Percent calcium retention varied with the level of dietary calcium and there was an indication that level of dietary phosphorus influenced calcium retention. Lower levels of dietary phosphorus resulted in egg shells with slightly lower deformation values. Regardless of dietary phosphorus, retention values were quite low. Changing the level of dietary calcium and phosphorus had little or no effect on the retention of phosphorus thus suggesting a relatively constant and low requirement for this nutrient.

Animal Feed↗
PubMed1980

Dietary phosphorus levels during growth of brown egg type replacement pullets.

Caged Sex-Sal (DeKalb Warren) replacement pullets were fed diets containing .30%, .35%, or .41% available phosphorus from 0 to 20 weeks of age; in a second study pullets were fed the above levels plus a level of .25% available phosphorus from 2 to 20 weeks of age. Some of the pullets were fed diets restricted by 11 to 16% from 8 weeks of age. Reducing the dietary phosphorus did no harm weight gain, feed intake, feed conversion efficiency, bone ash or total calcium and inorganic phosphorus levels in plasma. There was a very small but significant reduction in weight gain and feed intake when .30% or .35% available phosphorus was fed from 0 to 4 weeks of age, but this difference disappeared at the later ages. With the nonstimulatory lighting schedule used, plasma phosphorus decreased markedly in the latter phase of the studies at all levels of dietary phosphorus and thus represented a nondietary age effect. These results show that dietary available phosphorus for cage, brown egg type pullets on full or restricted feeding programs can be decreased to a level as low as .25% from 2 to 20 weeks, and .30% from hatching to 20 weeks without adverse effect.

Animal Nutritional Physiological Phenomena↗