ArticleJBMR plus2026
Bone
Article in JBMR plus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast growth factor 23 (FGF23), a bone-derived hormone, regulates phosphorus (P) homeostasis by modulation of renal P excretion and vitamin D metabolism. Physiological roles of FGF23 have been mainly characterized in human disorders of P metabolism and murine models. This study aimed to validate roles of FGF23 in P homeostasis in a large animal, healthy swine model. Juvenile pigs fed a low-P diet (LP) for 4 d were fasted overnight then fed a high-P diet (HP) for 5 d. Blood was collected to determine plasma concentrations of P, calcium (Ca), PTH, and vitamin D metabolites, and urine was collected to assess P and Ca concentrations. Femur and kidney tissues were collected to assess gene and protein expression related to FGF23 synthesis, signaling, and vitamin D metabolism. The rapid increase in plasma P (5 to 18 mg/dL) within 12 h of HP intake was lagged by increased urinary P. At maximal urinary P concentration (108 h), plasma P had returned to physiological ranges. The initial increase in plasma PTH with HP intake returned to baseline levels by 108 h. At 108 h, HP consumption upregulated bone
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Registered trials
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