Effects of Dietary Phosphorus Deficiency and High Phosphorus Content on the Growth Performance, Serum Variables, and Tibia Development in Goslings

Understanding how dietary phosphorus (P) regulates the growth and skeletal development of goslings is essential for fully utilizing P in the production of geese. We aimed to study the effects of dietary P deficiency and high P content on growth performance, serum variables, tibia quality, and mRNA expression of osteogenesis-related genes in tibia to reveal how dietary P regulates bone development in goslings. Two hundred and sixteen one-day-old Jiangnan White male geese were fed corn-soybean meal diets for 14 days. The diets were set with the same calcium (Ca) level (0.80%) and three non-phytate P (NPP) levels: 0.08% (P deficiency), 0.38% (P control), and 0.80% (P high content). Each treatment consisted of six replicates with 12 goslings in each replicate. The P deficient group had a high cumulative mortality of 26.67% with lower body weight (BW), average daily feed intake (ADFI), average daily gain (ADG), serum P contents, tibia width, tibia length, tibia fresh weight at d 14 as compared with the control and high P content group (<i>p</i> ≤ 0.05). Dietary P deficiency caused a reduction in the goslings’ tibia strength, tibia ash content, tibia Ca content, and tibia P content during d 4–d 14 (<i>p</i> < 0.05). The P deficiency reduced tibia mRNA expression of osteoprotegerin (OPG) and runt-related transcription factor 2 (Runx2) on d 7 (<i>p</i> < 0.05), whereas up-regulated serum alkaline phosphatase (ALP) activity, calcitonin (CT) content, and the tibia mRNA ratio of receptor activator of NF-κB ligand (RNAKL)/OPG during d 7–d 14 (<i>p</i> < 0.05). The serum 1,25-(OH₂)D₃ content, serum bone Gla-protein (BGP), and the mRNA relative expression of RNAKL and BGP in tibia were decreased in the NPP 0.08% and 0.80% groups compared with the control on d 14 (<i>p</i> < 0.05). In conclusion, dietary P deficiency induced acute rickets in goslings as early as the fourth day. A P deficiency hindered the tibia and body growth partly due to poor skeletal calcification caused by a down-expression of osteogenesis-related genes regulated by high serum ALP activity and calcitonin contents and lower serum BGP and skeletal P contents.