Intestinal and renal adaptation to a low-P<sub>i</sub> diet of type II NaP<sub>i</sub> cotransporters in vitamin D receptor- and 1αOHase-deficient mice

Capuano, Paola; Radanovic, Tamara; Wagner, Carsten A.; Bačić, Desa; Kato, Shigeaki; Uchiyama, Yasushi; St.-Arnoud, René; Murer, Heini; Biber, Jürg

doi:10.1152/ajpcell.00331.2004

Cited by 138 publications

(95 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1,25(OH) 2 D 3 is elevated in NaPi-IIa -/-mice and may contribute to the adaptive response of the intestine observed in our study [7]. However, the small intestine is also able to adapt to low phosphate intake independent from vitamin D 3 or the vitamin D 3 receptor and thus vitamin D 3 independent mechanisms may be also involved [17]. Whether NaPi-IIa is equally important in human kidney for phosphate reabsorption and the fast adaption to dietary phosphate intake remains to be established.…”

Section: Napi-iia Is the Main Phosphate Transporter Regulated By Dietmentioning

confidence: 51%

The phosphate transporter NaPi-IIa determines the rapid renal adaptation to dietary phosphate intake in mouse irrespective of persistently high FGF23 levels

Capuano

Stange

Mühlemann

et al. 2013

Pflugers Arch - Eur J Physiol

Self Cite

View full text Add to dashboard Cite

Renal reabsorption of inorganic phosphate (Pi) is mediated by the phosphate transporters NaPi-IIa, NaPi-IIc, and Pit-2 in the proximal tubule brush border membrane (BBM). Dietary Pi intake regulates these transporters; however, the contribution of the specific isoforms to the rapid and slow phase is not fully clarified. Moreover, the regulation of PTH and FGF23, two major phosphaturic hormones, during the adaptive phase has not been correlated. C57/BL6 and NaPi-IIa(-/-) mice received 5 days either 1.2 % (HPD) or 0.1 % (LPD) Pi-containing diets. Thereafter, some mice were acutely switched to LPD or HPD. Plasma Pi concentrations were similar under chronic diets, but lower when mice were acutely switched to LPD. Urinary Pi excretion was similar in C57/BL6 and NaPi-IIa(-/-) mice under HPD. During chronic LPD, NaPi-IIa(-/-) mice lost phosphate in urine compensated by higher intestinal Pi absorption. During the acute HPD-to-LPD switch, NaPi-IIa(-/-) mice exhibited a delayed decrease in urinary Pi excretion. PTH was acutely regulated by low dietary Pi intake. FGF23 did not respond to low Pi intake within 8 h whereas the phospho-adaptator protein FRS2 necessary for FGF-receptor cell signaling was downregulated. BBM Pi transport activity and NaPi-IIa but not NaPi-IIc and Pit-2 abundance acutely adapted to diets in C57/BL6 mice. In NaPi-IIa(-/-), Pi transport activity was low and did not adapt. Thus, NaPi-IIa mediates the fast adaptation to Pi intake and is upregulated during the adaptation to low Pi despite persistently high FGF23 levels. The sensitivity to FGF23 may be regulated by adapting FRS2 abundance and phosphorylation. ABSTRACTRenal reabsorption of inorganic phosphate (Pi) is mediated by the phosphate transporters, NaPi-IIa, NaPi-IIc, and Pit-2 in the proximal tubule brush border membrane (BBM). Dietary Pi intake regulates these transporters, however, the contribution of the specific isoforms to the rapid and slow phase are not fully clarified.Moreover, the regulation of PTH and FGF23, two major phosphaturic hormones, during the adaptive phase has not been correlated. C57/BL6 and NaPi-IIa -/-mice received 5 days either 1.2 % (HPD) or 0.1% (LPD) Pi containing diets. Thereafter, some mice were acutely switched to LPD or HPD. Plasma Pi concentrations were similar under chronic diets, but lower when mice were acutely switched to LPD.Urinary Pi excretion was similar in C57/BL6 and NaPi-IIa -/-mice under HPD. During chronic LPD, NaPi-IIa -/-mice lost phosphate in urine compensated by higher intestinal Pi absorption. During the acute HPD-to-LPD switch, NaPi-IIa -/-mice exhibited a delayed decrease in urinary Pi excretion. PTH was acutely regulated by low dietary Pi intake. FGF23 did not respond to low Pi intake within 8 hours whereas the phosphoadaptator protein FRS2α necessary for FGF-receptor cell signaling was downregulated. BBM Pi transport activity and NaPi-IIa but not NaPi-IIc and Pit-2 abundance acutely adapted to diets in C57/BL6 mice. In NaPi-IIa -/-Pi transport activity was low and did not adapt. Th...

show abstract

Section: Napi-iia Is the Main Phosphate Transporter Regulated By Dietmentioning

confidence: 51%

The phosphate transporter NaPi-IIa determines the rapid renal adaptation to dietary phosphate intake in mouse irrespective of persistently high FGF23 levels

Capuano

Stange

Mühlemann

et al. 2013

Pflugers Arch - Eur J Physiol

Self Cite

View full text Add to dashboard Cite

show abstract

“…8,42 Moreover, 1,25-dihydroxyvitamin D 3 is an important key player in phosphate homeostasis, [43][44][45] increasing the abundance of intestinal NaPi-IIb transporters. 46 …”

Section: Volume In Trpv5mentioning

confidence: 99%

The Calcium-Sensing Receptor Promotes Urinary Acidification to Prevent Nephrolithiasis

Renkema¹,

Velić²,

Dijkman³

et al. 2009

Journal of the American Society of Nephrology

Self Cite

129

103

View full text Add to dashboard Cite

show abstract

“…Adaptive changes in the expression of NPT2a occur rapidly within 2 h without changes in plasma phosphate and are independent of PTH and 1, 25 DHCC. 11,20 Changes in NPT2c and PiT2 take longer. 7 The presence of NPT2a in the brain suggests that the adaptive changes in phosphate reabsorption may be mediated via central transporters in the brain acting like phosphate sensors.…”

mentioning

confidence: 99%

Phosphate homeostasis and disorders

2014

View full text Add to dashboard Cite

Recent studies of inherited disorders of phosphate metabolism have shed new light on the understanding of phosphate metabolism. Phosphate has important functions in the body and several mechanisms have evolved to regulate phosphate balance including vitamin D, parathyroid hormone and phosphatonins such as fibroblast growth factor-23 (FGF23). Disorders of phosphate homeostasis leading to hypo-and hyperphosphataemia are common and have clinical and biochemical consequences. Notably, recent studies have linked hyperphosphataemia with an increased risk of cardiovascular disease. This review outlines the recent advances in the understanding of phosphate homeostasis and describes the causes, investigation and management of hypo-and hyperphosphataemia.

show abstract

Intestinal and renal adaptation to a low-P_i diet of type II NaP_i cotransporters in vitamin D receptor- and 1αOHase-deficient mice

Abstract: rg Biber. Intestinal and renal adaptation to a low-Pi diet of type II NaPi cotransporters in vitamin D receptor-and 1␣OHase-deficient mice.

Cited by 138 publications

References 29 publications

The phosphate transporter NaPi-IIa determines the rapid renal adaptation to dietary phosphate intake in mouse irrespective of persistently high FGF23 levels

The phosphate transporter NaPi-IIa determines the rapid renal adaptation to dietary phosphate intake in mouse irrespective of persistently high FGF23 levels

The Calcium-Sensing Receptor Promotes Urinary Acidification to Prevent Nephrolithiasis

Phosphate homeostasis and disorders

Contact Info

Product

Resources

About

Intestinal and renal adaptation to a low-Pi diet of type II NaPi cotransporters in vitamin D receptor- and 1αOHase-deficient mice

Abstract: rg Biber. Intestinal and renal adaptation to a low-Pi diet of type II NaPi cotransporters in vitamin D receptor-and 1␣OHase-deficient mice.

Cited by 138 publications

References 29 publications

The phosphate transporter NaPi-IIa determines the rapid renal adaptation to dietary phosphate intake in mouse irrespective of persistently high FGF23 levels

The phosphate transporter NaPi-IIa determines the rapid renal adaptation to dietary phosphate intake in mouse irrespective of persistently high FGF23 levels

The Calcium-Sensing Receptor Promotes Urinary Acidification to Prevent Nephrolithiasis

Phosphate homeostasis and disorders

Contact Info

Product

Resources

About

Intestinal and renal adaptation to a low-P_i diet of type II NaP_i cotransporters in vitamin D receptor- and 1αOHase-deficient mice