000130041 001__ 130041
000130041 005__ 20240731103355.0
000130041 0247_ $$2doi$$a10.1093/function/zqad063
000130041 0248_ $$2sideral$$a136356
000130041 037__ $$aART-2023-136356
000130041 041__ $$aeng
000130041 100__ $$aLucea, Susana
000130041 245__ $$aIntestinal and renal adaptations to changes of dietary phosphate concentrations in rat
000130041 260__ $$c2023
000130041 5060_ $$aAccess copy available to the general public$$fUnrestricted
000130041 5203_ $$aWe have studied the role of the intestine, kidney, and several hormones when adapting to changes in dietary P concentration. Normal and parathyroidectomized (PTX) rats were fed pH-matched diets containing 0.1%, 0.6%, and 1.2% P concentrations. 32Pi uptake was determined in the jejunum and kidney cortex brush border membrane vesicles. Several hormone and ion concentrations were determined in the blood and urine of rats. Both jejunum and kidney cortex Pi transport was regulated with 5 d of chronic feeding of P diets in normal rats. Acute adaptation was determined by switching foods on day 6, which was only clearly observed in the kidney cortex of normal rats, with more statistical variability in the jejunum. However, no paradoxical increase of Pi uptake in the jejunum was reproduced after the acute switch to the 1.2% P diet. Pi uptake in the jejunum was parathyroid hormone (PTH)-independent, but in the kidney, the chronic adaptation was reduced, and no acute dietary adaptations were observed. The NaPi2a protein was more abundant in the PTX than the sham kidneys, but contrary to the modest or absent changes in Pi uptake adaptation, the transporter was similarly regulated by dietary P, as in the sham rats. PTH and fibroblast growth factor 23 (FGF23) were the only hormones regulated by all diet changes, even in fasting animals, which exhibited regulated Pi transport despite similar phosphatemia. Evidence of Pi appetite effects was also observed. In brief, our results show new characteristics of Pi adaptations, including a lack of correlation between Pi transport, NaPi2a expression, and PTH/FGF23 concentrations.
000130041 536__ $$9info:eu-repo/grantAgreement/ES/MICINN/PID2021-127818OB-I00$$9info:eu-repo/grantAgreement/ES/MINECO-FEDER/PGC2018-098635-B-I00
000130041 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000130041 592__ $$a0.987$$b2023
000130041 593__ $$aCancer Research$$c2023$$dQ2
000130041 593__ $$aPhysiology$$c2023$$dQ2
000130041 593__ $$aMolecular Medicine$$c2023$$dQ2
000130041 593__ $$aCell Biology$$c2023$$dQ2
000130041 594__ $$a5.7$$b2023
000130041 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000130041 700__ $$0(orcid)0000-0003-4258-3462$$aChopo-Escuin, Gema$$uUniversidad de Zaragoza
000130041 700__ $$0(orcid)0000-0001-6627-298X$$aGuillén, Natalia$$uUniversidad de Zaragoza
000130041 700__ $$0(orcid)0000-0003-2907-0427$$aSosa, Cecilia$$uUniversidad de Zaragoza
000130041 700__ $$0(orcid)0000-0003-3457-323X$$aSorribas, Víctor$$uUniversidad de Zaragoza
000130041 7102_ $$11002$$2807$$aUniversidad de Zaragoza$$bDpto. Bioq.Biolog.Mol. Celular$$cÁrea Toxicología
000130041 773__ $$g5, 1 (2023), [15 pp.]$$tFunction (Oxford)
000130041 8564_ $$s2101521$$uhttps://zaguan.unizar.es/record/130041/files/texto_completo.pdf$$yVersión publicada
000130041 8564_ $$s2139602$$uhttps://zaguan.unizar.es/record/130041/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000130041 909CO $$ooai:zaguan.unizar.es:130041$$particulos$$pdriver
000130041 951__ $$a2024-07-31-09:56:27
000130041 980__ $$aARTICLE