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To verify this role, we have studied the combined effects of pH, phosphonoformate, and P<jats:sub>i<\/jats:sub> deprivation on intestinal P<jats:sub>i<\/jats:sub> transport. Rats were fed, ad libitum, three fodders containing 1.2, 0.6, or 0.1% P<jats:sub>i<\/jats:sub> for 1, 5, or 10 days. P<jats:sub>i<\/jats:sub> deprivation (0.1%) increased both sodium-activated and sodium-independent P<jats:sub>i<\/jats:sub> transport in brush-border membrane vesicles from the duodenum and jejunum for all three times. Alkaline pH inhibited P<jats:sub>i<\/jats:sub> transport, despite the increasing concentration of [Formula: see text] (NaPi2b substrate), whereas acidity increased transport when the concentration of the PiT1\/PiT2 substrate, [Formula: see text], was at its highest. The effect of P<jats:sub>i<\/jats:sub> deprivation was maximal at acid pH, but both basal and upregulated transport were inhibited (70%) with phosphonoformate, an inhibitor of NaPi2b. PiT2 and NaPi2b protein abundance increased after 24 h of P<jats:sub>i<\/jats:sub> deprivation in the duodenum, jejunum, and ileum, whereas PiT1 required 5\u201310 days in the duodenum and jejunum. Therefore, whereas transporter expressions are partially correlated with P<jats:sub>i<\/jats:sub> transport adaptation, the pH effect precludes NaPi2b, and phosphonoformic acid precludes PiT1 and PiT2 as the main transporters. Transport and transporter expression were also inconsistent when feeding was limited to 4 h daily, because the 1.2% P<jats:sub>i<\/jats:sub> diet paradoxically increased P<jats:sub>i<\/jats:sub> transport in the duodenum and jejunum, but NaPi2b and PiT1 expressions only increased with the 0.1% diet. These findings suggest the presence of a major transporter that carries [Formula: see text] and is inhibited by phosphonoformate. <\/jats:p><jats:p> NEW &amp; NOTEWORTHY The combined effects of dietary inorganic phosphate (P<jats:sub>i<\/jats:sub>) content, pH, and phosphonoformate inhibition suggest that the resulting apical P<jats:sub>i<\/jats:sub> transport in the small intestine cannot be fully explained by the presence of NaPi2b, PiT1, or PiT2. We provide evidence of the presence of a new sodium-coupled P<jats:sub>i<\/jats:sub> transporter that uses [Formula: see text] as the preferred substrate and is inhibited by phosphonoformate, and its expression correlates with P<jats:sub>i<\/jats:sub> transport in all assayed conditions. <\/jats:p>","DOI":"10.1152\/ajpgi.00244.2016","type":"journal-article","created":{"date-parts":[[2017,2,23]],"date-time":"2017-02-23T21:20:38Z","timestamp":1487884838000},"page":"G355-G366","source":"Crossref","is-referenced-by-count":35,"title":["Intestinal phosphate absorption is mediated by multiple transport systems in rats"],"prefix":"10.1152","volume":"312","author":[{"given":"Eduardo","family":"Candeal","sequence":"first","affiliation":[{"name":"Department of Toxicology, University of Zaragoza, Zaragoza, Spain; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yupanqui A.","family":"Caldas","sequence":"additional","affiliation":[{"name":"Department of Toxicology, University of 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