Effect of different concentrations of dietary P and Ca on plasma inorganic P and urinary P excretion using noncolostomized and colostomized broilers.

Two 5-d bioassays were conducted to explore the P physiological threshold in broilers based on plasma inorganic P (iP), urinary P and Ca, and excreta P and Ca measurements in non-colostomized and colostomized broilers fed with different concentrations of non-phytate P (NPP) and Ca. In Experiment 1, 80 40-day-old Cobb 500 non-colostomized male broilers were assorted into 8 groups consisting of 10 broilers each and placed in individual metabolic cages. Similarly, 8 colostomized broilers of same age were allotted to 8 individual metabolic cages. The experimental diets consisted of a corn soybean meal basal containing 0.17% phytate P (PP) with 8 concentrations (0.08, 0.13, 0.18, 0.23, 0.28, 0.33, 0.38, and 0.45%) of NPP. The dietary Ca concentration was maintained at 0.5% by adjusting a 185-micron particle size limestone with each concentration of added P from added calcium phosphate, dibasic, monohydrate. After Experiment 1, broilers were fed a standard grower diet for 5 d and Experiment 2 was conducted the same as Experiment 1; however, Ca was maintained at 0.9% for all test diets. Plasma iP, urinary P and Ca, and total P (TP) and Ca retention along with phytate P hydrolysis were measured. At 0.5% Ca dietary level, the inflection points for dietary NPP obtained from segmented line regression analysis for plasma iP, urinary P, and urinary Ca were 0.26% (±0.04 SE), 0.28% (±0.01 SE), and 0.30% (±0.04 SE), respectively. The similar values for 0.9% Ca diets were 0.27% (±0.03 SE), 0.21% (±0.03 SE), and 0.30% (±0.0 SE), respectively. In summary, the present findings suggest that an increased dietary NPP would increase plasma inorganic P concentration along with increased % retention of TP and NPP until the broilers reach a point of physiological steady state (7.51 mg iP/dL - 8.13 mg iP/dL as found in this study). Excess P beyond physiological threshold is eliminated in urine coupled with decreased % retention.

Lysine alpha-ketoglutarate reductase and lysine oxidation are distributed in the extrahepatic tissues of chickens.

In animals, lysine oxidation is thought to occur primarily via the activity of lysine alpha-ketoglutarate reductase (LKR). This activity was reported previously in chicken liver, but no work on the tissue distribution of the enzyme in chickens has been reported. Therefore, LKR activity was assayed in liver, kidney, pancreas, heart, brain, lung, spleen, muscle, and intestinal tissues in chickens as was the in vitro ability of tissue homogenates to oxidize lysine. Additionally, the expression of LKR mRNA was assessed by RT-PCR. We found LKR to be present in all tissues studied by both enzymatic analysis and mRNA abundance. Additionally, all tissues assayed oxidized lysine. The extent of lysine oxidation differed among the tissues, consistent with the different pathways of lysine oxidation in the different tissues. These studies demonstrate that LKR is widely distributed in chicken tissues and that tissues other than liver can contribute to whole-body lysine oxidation.