ArticleFrontiers in nutrition2026
Effects of nutritional low phosphorus status caused by extremely low phosphorus diet during lactation and early childhood on endochondral ossification in offspring rats.
Article in Frontiers in nutrition, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Fetal phosphorus is mainly deposited in bones in late pregnancy. Premature birth interrupts the supply of maternal phosphorus, combined with insufficient reserves, immature intestinal absorption and catch-up growth, the demand for mineralization surges, breast milk is difficult to meet, and it is easy to cause low-phosphorus bone disease; as the survival rate of premature infants increases, the incidence also increases. Objective: The core of the DOHaD theory is that the early living environment permanently reshapes the body through epigenetic mechanisms, thereby affecting long-term health and disease risks, based on the close relationship between the environment, health and disease at the molecular level. Based on the DOHaD theory, the rat model of perinatal continuous low phosphorus exposure confirmed that low phosphorus inhibited the endochondral ossification of long bones, which provided experimental basis for the prevention and treatment of low phosphorus rickets in premature infants. Methods: Pregnant SD rats were fed normal or very-low-phosphorus diet from gestation day 14-15 through lactation (3 weeks) and post-weaning (2 weeks). Offspring serum biochemistry, bone length, weight, and tibial histology (HE, toluidine blue, TRAP, Goldner, TUNEL), immunohistochemistry (RUNX2, COL1A1, COL2A1, VEGF, MMP13, OCN, BrdU, cleaved caspase-3), and Western blot (COL2A1, COL10A1, OCN) were assessed. Results: Low phosphorus caused serum biochemical changes (P↓, ALP↓; Ca↑, PTH↑, vitamin D↑), growth retardation, and altered protein expression (COL2A1, OCN↓, COL10A1↑; RUNX2, COL2A1, COL1A1, OCN, VEGF, BrdU, cleaved caspase-3↓, MMP13↑) in growth plate, indicative of defective chondrocyte functions. Histological examination showed that low phosphorus exposure led to the disorder of growth plate structure and inhibited endochondral ossification of long bone, which provided experimental basis for the prevention and treatment of low phosphorus rickets in premature infants. Conclusion: Maternal low-phosphorus diet induces hypophosphatemia and growth retardation in offspring, disrupts growth plate architecture, impairs chondrocyte proliferation and apoptosis, reduces bone mineralization and turnover.
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