Dietary phosphorus source reprograms the kidney-intestine axis to dictate calcium-phosphorus efficiency and egg production in aging hens.

BACKGROUND

The decline in egg production in aging hens poses a significant challenge to sustainable poultry production. Given that evidence suggests the phosphorus source affects late‑lay performance, we tested the hypothesis that the dietary phosphorus source is a decisive regulator sustaining performance by reprogramming systemic mineral homeostasis. Using a systems biology approach, we analyzed the coordinated expression of eleven key mineral transporter genes across the duodenum, jejunum, ileum, and kidney of hens fed dicalcium phosphate (DCP) or tricalcium phosphate (TCP).

RESULTS

During weeks 5-8, hens fed DCP showed significant declines in egg production (β = -3.11/week, P < 0.001) and egg weight (β = -0.47 g/week, P = 0.049), unlike the stable TCP group. TCP induced an efficient "precision conservation" phenotype, characterized by the co-upregulation of key duodenal phosphorus and calcium transporters (NaPi-IIb, PiT2; NCX1, PMCA1b), a gene set identified as the top predictor of performance. Conversely, DCP triggered a costly "compensatory salvage" state, scattering expression to duodenal calcium channels (TRPV5, TRPV6) and renal compensatory genes (NCX1, CALB1). Network analysis pinpointed these renal genes as a central, performance-limiting hub.

CONCLUSION

We conclude that TCP sustains production by programming a systemically efficient homeostatic strategy, thereby explaining the established performance benefit at a molecular level. This establishes a new principle for layer nutrition: phosphorus source selection must consider its role as a physiological signal that modulates homeostasis. This strategy mitigates age-related decline and enhances resource allocation to production.