Effect of dietary components on renal inorganic phosphate (Pi) excretion induced by a Pi-depleted diet

Dietary inorganic phosphate (Pi) is the most important factor in the regulation of renal Pi excretion. Recent studies suggest the presence of an enteric-renal signaling axis for dietary Pi as well as the existence of a mechanism by which the intestine detects changes in luminal Pi concentrations. Th...

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Published inThe Journal of Medical Investigation Vol. 61; no. 1.2; pp. 162 - 170
Main Authors Ohmoto, Tomoyo, Hamada, Yasuhiro, Tatsumi, Sawako, Hanazaki, Ai, Ikuta, Kayo, Sasaki, Shohei, Mori, Ayaka, Furutani, Junya, Miyamoto, Ken-ichi, Ohnishi, Ritsuko, Segawa, Hiroko, Kawakami, Eri
Format Journal Article
LanguageEnglish
Published Japan The University of Tokushima Faculty of Medicine 2014
Subjects
Animals
calcium
Calcium, Dietary - pharmacology
Diet
dietary phosphate
Food, Formulated
Intestines - physiology
Kidney - drug effects
Kidney - metabolism
Male
Models, Animal
phosphate excretion
Phosphates - deficiency
Phosphates - metabolism
Rats
Rats, Wistar
Receptors, Calcium-Sensing - agonists
sensing
Signal Transduction - drug effects
Signal Transduction - physiology
Online AccessGet full text
ISSN1343-1420
1349-6867
1349-6867
DOI10.2152/jmi.61.162

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Abstract Dietary inorganic phosphate (Pi) is the most important factor in the regulation of renal Pi excretion. Recent studies suggest the presence of an enteric-renal signaling axis for dietary Pi as well as the existence of a mechanism by which the intestine detects changes in luminal Pi concentrations. The mechanisms of intestinal Pi sensing, however, are unknown. In the present study, we focused on Pi depletion signals and investigated the effects of dietary components on intestinal Pi sensing. After feeding rats experimental diets for 3 days, we investigated urinary Pi excretion and plasma biochemical parameters. Renal Pi excretion was suppressed in rats fed a low-Pi diet (0.02% Pi). Elimination of dietary calcium (Ca) completely blocked the suppression of Pi excretion, suggesting that the presence of Ca is essential for the Pi depletion signal. Furthermore, a minimum Ca content of more than 0.02% was necessary for the Pi depletion signal. Magnesium, lanthanum, and strontium, which are agonists of calcium sensing receptor, instead of Ca, reduced Pi excretion. Therefore, dietary Ca appears to be important for the Pi depletion-sensing mechanism in the gastrointestinal tract. In addition, the calcium sensing receptor may be involved in the Pi depletion signal. J. Med. Invest. 61: 162-170, February, 2014
AbstractList Dietary inorganic phosphate (Pi) is the most important factor in the regulation of renal Pi excretion. Recent studies suggest the presence of an enteric-renal signaling axis for dietary Pi as well as the existence of a mechanism by which the intestine detects changes in luminal Pi concentrations. The mechanisms of intestinal Pi sensing, however, are unknown. In the present study, we focused on Pi depletion signals and investigated the effects of dietary components on intestinal Pi sensing. After feeding rats experimental diets for 3 days, we investigated urinary Pi excretion and plasma biochemical parameters. Renal Pi excretion was suppressed in rats fed a low-Pi diet (0.02% Pi). Elimination of dietary calcium (Ca) completely blocked the suppression of Pi excretion, suggesting that the presence of Ca is essential for the Pi depletion signal. Furthermore, a minimum Ca content of more than 0.02% was necessary for the Pi depletion signal. Magnesium, lanthanum, and strontium, which are agonists of calcium sensing receptor, instead of Ca, reduced Pi excretion. Therefore, dietary Ca appears to be important for the Pi depletion-sensing mechanism in the gastrointestinal tract. In addition, the calcium sensing receptor may be involved in the Pi depletion signal.
Dietary inorganic phosphate (Pi) is the most important factor in the regulation of renal Pi excretion. Recent studies suggest the presence of an enteric-renal signaling axis for dietary Pi as well as the existence of a mechanism by which the intestine detects changes in luminal Pi concentrations. The mechanisms of intestinal Pi sensing, however, are unknown. In the present study, we focused on Pi depletion signals and investigated the effects of dietary components on intestinal Pi sensing. After feeding rats experimental diets for 3 days, we investigated urinary Pi excretion and plasma biochemical parameters. Renal Pi excretion was suppressed in rats fed a low-Pi diet (0.02% Pi). Elimination of dietary calcium (Ca) completely blocked the suppression of Pi excretion, suggesting that the presence of Ca is essential for the Pi depletion signal. Furthermore, a minimum Ca content of more than 0.02% was necessary for the Pi depletion signal. Magnesium, lanthanum, and strontium, which are agonists of calcium sensing receptor, instead of Ca, reduced Pi excretion. Therefore, dietary Ca appears to be important for the Pi depletion-sensing mechanism in the gastrointestinal tract. In addition, the calcium sensing receptor may be involved in the Pi depletion signal. J. Med. Invest. 61: 162-170, February, 2014
Author Ohmoto, Tomoyo
Ikuta, Kayo
Sasaki, Shohei
Mori, Ayaka
Hanazaki, Ai
Kawakami, Eri
Furutani, Junya
Tatsumi, Sawako
Ohnishi, Ritsuko
Hamada, Yasuhiro
Miyamoto, Ken-ichi
Segawa, Hiroko
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  fullname: Tatsumi, Sawako
  organization: Department of Molecular Nutrition, Institution of Health Biosciences, the University of Tokushima Graduate School
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3. Turner JM, Bauer C, Abramowitz MK, Melamed ML, Hostetter TH: Treatment of chronic kidney disease. Kidney Int 81: 351-362, 2012
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References_xml – reference: 39. Weinman EJ, Light PD, Suki WN: Gastrointestinal Phosphate Handling in CKD and Its Association With Cardiovascular Disease. Am J Kidney Dis 62: 1006-1011, 2013
– reference: 27. Sutherland K, Young RL, Cooper NJ, Horowitz M, Blackshaw LA: Phenotypic characterization of taste cells of the mouse small intestine. Am J Physiol Gastrointest Liver Physiol 292: G1420-1428, 2007
– reference: 29. Ohnishi R, Segawa H, Kawakami E, Furutani J, Ito M, Tatsumi S, Kuwahata M, Miyamoto K: Control of phosphate appetite in young rats. J Med Invest 54: 366-369, 2007
– reference: 9. Miyamoto KI, Itho M: Transcriptional regulation of the NPT2 gene by dietary phosphate. Kidney Int 60: 412-415, 2001
– reference: 20. Steele TH, DeLuca HF: Influence of dietary phosphorus on renal phosphate reabsorption in the parathyroidectomized rat. J Clin Invest 57: 867-874, 1976
– reference: 26. Mace OJ, Marshall F: Digestive physiology of the pig symposium: gut chemosensing and the regulation of nutrient absorption and energy supply. J Anim Sci 91: 1932-1945, 2013
– reference: 16. Ohi A, Hanabusa E, Ueda O, Segawa H, Horiba N, Kaneko I, Kuwahara S, Mukai T, Sasaki S, Tominaga R, Furutani J, Aranami F, Ohtomo S, Oikawa Y, Kawase Y, Wada NA, Tachibe T, Kakefuda M, Tateishi H, Matsumoto K, Tatsumi S, Kido S, Fukushima N, Jishage K, Miyamoto K: Inorganic phosphate homeostasis in sodium-dependent phosphate cotransporter Npt2b(+)/(-) mice. Am J Physiol Renal Physiol 301: F1105-1113, 2011
– reference: 32. Feng J, Petersen CD, Coy DH, Jiang JK, Thomas CJ, Pollak MR, Wank SA: Calcium-sensing receptor is a physiologic multimodal chemosensor regulating gastric G-cell growth and gastrin secretion. Proc Natl Acad Sci U S A 107: 17791-17796, 2010
– reference: 37. Lumlertgul D, Burke TJ, Gillum DM, Alfrey AC, Harris DC, Hammond WS, Schrier RW: Phosphate depletion arrests progression of chronic renal failure independent of protein intake. Kidney Int 29: 658-666, 1986
– reference: 35. Gutierrez OM, Wolf M: Dietary phosphorus restriction in advanced chronic kidney disease: merits, challenges, and emerging strategies. Semin Dial 23: 401-406, 2010
– reference: 18. Saidak Z, Brazier M, Kamel S, Mentaverri R: Agonists and allosteric modulators of the calcium-sensing receptor and their therapeutic applications. Mol Pharmacol 76: 1131-1144, 2009
– reference: 40. Hutchison AJ, Smith CP, Brenchley PE: Pharmacology, efficacy and safety of oral phosphate binders. Nat Rev Nephrol 7: 578-589, 2011
– reference: 33. Feldman EJ, Grossman MI: Liver extract and its free amino acids equally stimulate gastric acid secretion. Am J Physiol 239: G493-496, 1980
– reference: 10. Marks J, Debnam ES, Unwin RJ: Phosphate homeostasis and the renal-gastrointestinal axis. Am J Physiol Renal Physiol 299: F285-296, 2010
– reference: 6. Murer H, Lotscher M, Kaissling B, Levi M, Kempson SA, Biber J: Renal brush border membrane Na/Pi-cotransport: molecular aspects in PTH-dependent and dietary regulation. Kidney Int 49: 1769-1773, 1996
– reference: 15. Berndt T, Thomas LF, Craig TA, Sommer S, Li X, Bergstralh EJ, Kumar R: Evidence for a signaling axis by which intestinal phosphate rapidly modulates renal phosphate reabsorption. Proc Natl Acad Sci U S A 104: 11085-11090, 2007
– reference: 1. Isakova T: Comparison of mineral metabolites as risk factors for adverse clinical outcomes in CKD. Semin Nephrol 33: 106-117, 2013
– reference: 12. Farrow EG, White KE: Recent advances in renal phosphate handling. Nat Rev Nephrol 6: 207-217, 2010
– reference: 19. Miyamoto K, Ito M, Tatsumi S, Kuwahata M, Segawa H: New aspect of renal phosphate reabsorption: the type IIc sodium-dependent phosphate transporter. Am J Nephrol 27: 503-515, 2007
– reference: 8. Miyamoto K, Segawa H, Ito M, Kuwahata M: Physiological regulation of renal sodium-dependent phosphate cotransporters. Jpn J Physiol 54: 93-102, 2004
– reference: 3. Turner JM, Bauer C, Abramowitz MK, Melamed ML, Hostetter TH: Treatment of chronic kidney disease. Kidney Int 81: 351-362, 2012
– reference: 14. Kumar R: Phosphate sensing. Curr Opin Nephrol Hypertens 18: 281-284, 2009
– reference: 17. McGehee DS, Aldersberg M, Liu KP, Hsuing S, Heath MJ, Tamir H: Mechanism of extracellular Ca2+ receptor-stimulated hormone release from sheep thyroid parafollicular cells. J Physiol 502 (Pt 1): 31-44, 1997
– reference: 36. Klahr S, Levey AS, Beck GJ, Caggiula AW, Hunsicker L, Kusek JW, Striker G: The effects of dietary protein restriction and blood-pressure control on the progression of chronic renal disease. Modification of Diet in Renal Disease Study Group. N Engl J Med 330: 877-884, 1994
– reference: 24. Kellett GL: Alternative perspective on intestinal calcium absorption: proposed complementary actions of Ca(v)1.3 and TRPV6. Nutr Rev 69: 347-370, 2011
– reference: 34. Mace OJ, Schindler M, Patel S: The regulation of K- and L-cell activity by GLUT2 and the calcium-sensing receptor CasR in rat small intestine. J Physiol 590: 2917-2936, 2012
– reference: 30. Martin DR, Ritter CS, Slatopolsky E, Brown AJ: Acute regulation of parathyroid hormone by dietary phosphate. Am J Physiol Endocrinol Metab 289: E729-734, 2005
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Snippet Dietary inorganic phosphate (Pi) is the most important factor in the regulation of renal Pi excretion. Recent studies suggest the presence of an enteric-renal...
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SubjectTerms Animals
calcium
Calcium, Dietary - pharmacology
Diet
dietary phosphate
Food, Formulated
Intestines - physiology
Kidney - drug effects
Kidney - metabolism
Male
Models, Animal
phosphate excretion
Phosphates - deficiency
Phosphates - metabolism
Rats
Rats, Wistar
Receptors, Calcium-Sensing - agonists
sensing
Signal Transduction - drug effects
Signal Transduction - physiology
Title Effect of dietary components on renal inorganic phosphate (Pi) excretion induced by a Pi-depleted diet
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https://www.ncbi.nlm.nih.gov/pubmed/24705762
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