Influence of dietary phosphorus on renal phosphate reabsorption in the parathyroidectomized rat.

Steele, Thomas H.; DeLuca, Hector F.

doi:10.1172/jci108363

Cited by 142 publications

(36 citation statements)

References 33 publications

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“…21,22 This suggests that increases in PTH and changes in 1␣,25-dihydroxyvitamin D cannot fully account for the increase in urinary phosphate excretion. That PTH is not the sole regulator of renal phosphate transport is also supported by earlier data from Steele et al, 23 who showed that chronically parathyroidectomized rats were able to respond to changes in dietary phosphate intake with an appropriate increase in urinary phosphate excretion.…”

Section: Evidence For An Enteric-renal Phosphate-transport Regulatingmentioning

confidence: 59%

Control of Renal Solute Excretion by Enteric Signals and Mediators

Thomas

Kumar

2008

Journal of the American Society of Nephrology

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The renal response to ingested solutes and the regulation of nutrient and solute balance are vital for the well-being of an organism. Foods that contain protein, carbohydrate, and fat are processed to amino acids, monosaccharides, and fatty acids and triglycerides. These substances and electrolytes and minerals are absorbed with varying degrees of efficiency in the intestine, often in response to the perceived needs of the organism. In some instances, the amount of the nutrient absorbed in the intestine depends on the amount present in the diet, and with large influxes of nutrient materials into the extracellular fluid, it falls to the kidney to remove the excessive amounts absorbed by the intestine from the serum and extracellular fluid, either by increasing the amount excreted by tubular processes or by reducing the amount reabsorbed in the tubule after glomerular filtration.It is widely believed that the renal response to ingested solutes is regulated by hormones such as aldosterone, in the case of sodium and potassium, and parathyroid hormone and the vitamin D endocrine system, in the case of calcium and phosphate. New (and old) information also suggests that factors produced in the gastrointestinal tract are released after changes in intestinal luminal solute concentrations and mediate changes in renal solute transport. This "enteric-renal solute-transporting regulating axis" represents an underappreciated mechanism by which renal solute transport is regulated. ENTERIC MODULATION OF RENAL SODIUM AND POTASSIUMDietary sodium induces a more marked natriuresis than intravenous sodium. The regulation of renal excretory or reabsorptive processes exclusively depends on the activity of various hormones or local renal factors, the synthesis or release of which depends on alterations in the serum or extracellular fluid concentrations of the various ions. Decreases in renal sodium excretion in response to a low-salt diet depend on changes in aldosterone synthesis. 1 Indeed, a lack of aldosterone synthesis is responsible for many of the manifestations of Addison's disease. The role of aldosterone (and inhibition of its synthesis) in increasing salt excretion is less clearly defined when a high-salt diet is ingested. Data suggest that other factors play a role in this process and that the role of aldosterone is minimal in the adaptation to high-sodium meals. Carey and others 2-4 have demonstrated that salt-depleted individuals who were given oral sodium chloride excreted much more sodium in their urine than did individuals who were given the same amount of sodium chloride intravenously. Plasma aldosterone ABSTRACTRenal solute excretion is important for the homeostasis of various ions. It is widely believed that hormones such as aldosterone, parathyroid hormone, the vitamin D endocrine system, and growth factors are responsible for alterations in renal ion transport in response to increased absorption of enteric solutes. In the cases of sodium, potassium, and phosphorus, moieties produced in the gastrointestinal tract a...

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Section: Evidence For An Enteric-renal Phosphate-transport Regulatingmentioning

confidence: 59%

Control of Renal Solute Excretion by Enteric Signals and Mediators

Thomas

Kumar

2008

Journal of the American Society of Nephrology

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“…The sp act of these Clearance data. The PiR capacity of adult rats varies in enzymes were not significantly different in the two groups of rats response to a change in Pi intake, and this phenomenon persists and their corresponding controls, nor was the enrichment of in thyroparathyroidectomized rats (1,2,22). PiR also increases brush border enzymes over the homogenate activity (Table 4).…”

Section: Animalsmentioning

confidence: 89%

“…Changing the Pi content of the diet induces no apparent change in Pi transport maturation during this period, as there was no change in the carrier affinity. Animal studies have shown that the renal tubule of the adult rat is able to change its capacity to transport inorganic Pi in response to dietary Pi (1)(2)(3). Under these conditions, tubular transport of Pi is controlled by a PTH-independent mechanism that responds to changes in the Pi uptake.…”

mentioning

confidence: 99%

Effects of an Early Weaning on Phosphate Transport Maturation in the Rat Kidney: Influence of the Phosphate Content of the Diet

et al. 1992

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ABSTRACT. The renal phosphate (Pi) transport system matures during the 3rd postnatal wk in the rat by an increase in the carrier affinity for sodium-cotransported phosphate. This study examines the ability of pups to adapt their renal Pi transport to the dietary phosphorus content during this period of carrier affinity maturation, corresponding to the weaning period in the rat. Clearance experiments and brush border membrane studies were performed on 21-d-old rats weaned early on d 16 onto a low phosphate diet (LPD, 0.19 g/100 g), a normal phosphate diet (control, 0.78 g/100 g), or a high phosphate diet (HPD, 1.5 g/100 g). In LPD rats, the Pi fractional excretion (0.3 f 0.1%) was lower than in controls (18 f 3%, p < 0.001). It remained very low (0.21 f 0.05% in LPD rats versus 40.5 2 6.3% in controls, p < 0.001) after Pi perfusion (1.5 pmol.min-'. 100 g-') and the reabsorbed Pi per min, corrected for the glomerular filtration rate. was higher than in the two othergroups. The calcium fractional excretion (12.6 2 1.02%) in the LPD rats was much higher than in the controls (0.42 2 0.2%, p < 0.001). In contrast, HPD rats had an elevated Pi fractional excretion (41 f 4%, p < 0.001), whereas reabsorbed phosphate per min corrected for the glomerular filtration rate was not increased by a Pi load. The membrane vesicles from 21-dold LPD rats had a higher V,,, (1 1 466 2 1 840 pmol. mg protein-'.I0 s-') than the controls (7 019 f 1 112 pmol. mg protein-'. 10 s-', p < 0.01), whereas those from HPD rats had a lower V,,, (5 161 2 956,p < 0.01). The apparent Km values were unchanged. The LPD rats had high plasma calcium levels. The parathyroid hormone level was depressed by this hypercalcemia 121.97 2 1.9 pg/mL (2.31 f 0.2 pmol/L) in LPD and 38.54 f 2.01 pg/mL (4.05 2 0.21 pmol/L) in normal Pi diet rats, n = 8, p < 0.001j. This plus their LPD explains the lower Pi fractional excretion of these rats and the low Pi V,,, in their brush border membrane. The plasma parathyroid hormonal level of HPD rats was normal (35.07 f 2.23 pg/mL (3.69 f 0.23 pmol/L), n = 81. We conclude that the young 3-wk-old rat can adapt its renal Pi transport capacity to the dietary phosphorus content during the weaning period by varying the number of functional units of the sodium Pi cotransporter or by increasing its turnover rate. Changing the Pi content of the diet induces no apparent change in Pi transport maturation during this period, as there was no change in the carrier affinity. (Pediatr Res 32: 704-709, 1992)

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“…It is not clear whether these measures are true indexes of Pi depletion. Urinary Pi excretion, however, is considered the most important index associated with dietary Pi intake (20)(21)(22).…”

Section: Discussionmentioning

confidence: 99%