Influence of Phosphate Depletion on the Biosynthesis and Circulating Level of 1α,25-Dihydroxyvitamin D

Haussler, Mark R.; Hughes, Mark; Baylink, David J.; Littledike, E. Travis; Cork, Douglas J.; Pitt, Michael J.

doi:10.1007/978-1-4613-4217-5_24

Cited by 55 publications

(21 citation statements)

References 27 publications

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“…Sec (35) have demonstrated that the capacity to reduce renal phosphate losses during phosphate deprivation is PTH independent. Further, phosphorus deprivation stimulates 1,25(OH)2D production in intact (36) and thyroparathyroidectomized animals (37), so that this response is also a PTH-independent effect. We therefore chose this stimulus as a probe to examine renal phosphate handling and circulating 1,25(OH)2D in patients with FHR. We observed a defective renal tubular response to phosphorus deprivation in patients with FHR.…”

Section: Resultsmentioning

confidence: 99%

Impaired phosphorus conservation and 1,25 dihydroxyvitamin D generation during phosphorus deprivation in familial hypophosphatemic rickets.

Insogna¹,

Broadus²,

Gertner³

1983

J. Clin. Invest.

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A BS T R A CT The pathogenesis of familial hypophosphatemic rickets (FHR) is incompletely understood. We therefore examined the effects of acute dietary phosphorus deprivation to see whether renal phosphate conservation and increased 1,25 dihydroxyvitamin D [1,25(OH)2D] plasma levels, which normally follow restriction of phosphorus intake, could be induced in patients with FHR.Six healthy male volunteers (age 26±3 yr) and seven male patients with FHR (age 24±3 yr) were placed on a low phosphorus diet supplemented with aluminum hydroxide and studied over a 4-d period. The patients with FHR excreted more than five times as much phosphorus per day at the conclusion of the study than did the controls (176±61 mg/24 h vs. 33±11 mg/h). In the normal subjects, maximum tubular reabsorptive capacity for phosphorus/glomerular filtration rate (TmP/GFR) rose progressively during phosphorus deprivation, and the rise from base line was more than two times greater than that seen in patients with FHR. Immunoreactive parathyroid hormone levels and nephrogenous cyclic AMP were initially normal in both groups and no change was seen in either group with phosphorus deprivation.In the normal subjects, 1,25(OH)2D levels rose progressively over the 96 h of the study (49±3 to 63±6 pg/ml, P < 0.05), while mean circulating 1,25(OH)2D

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Section: Resultsmentioning

confidence: 99%

Impaired phosphorus conservation and 1,25 dihydroxyvitamin D generation during phosphorus deprivation in familial hypophosphatemic rickets.

Insogna¹,

Broadus²,

Gertner³

1983

J. Clin. Invest.

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“…Finally, treatment with P1 alone or in combination with pharmacological amounts (Table I). Recent studies in both man (45) and various animals (46)(47)(48) indicate an inverse relationship between serum levels of Pi and production rate or serum concentration of 1,25(0H)2D. Therefore, it follows that patients with XLH should manifest both an increased production rate for and an increased circulating level of 1,25(OH)2D.…”

Section: Resultsmentioning

confidence: 99%

Evaluation of a Role for 1,25-Dihydroxyvitamin D3 in the Pathogenesis and Treatment of X-linked Hypophosphatemic Rickets and Osteomalacia

et al. 1980

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“…It is remarkable that even after correcting for the lower PTH and higher FGF23 after phosphate/calcium-enriched meals, these meals themselves caused a decline in 1,25D levels. Phosphate itself (23)(24)(25), calcium (26), or some other constituent in protein-enriched diets might directly inhibit 1␣-hydroxylase not mediated through PTH or FGF23. However, adding phosphate-and albumin-corrected calcium to the model (data not shown) did not change the 1,25D-lowering effects of phosphate-enriched meals.…”

Section: Discussionmentioning

confidence: 99%

Effects of Dietary Phosphate and Calcium Intake on Fibroblast Growth Factor-23

Vervloet

Ittersum²,

Büttler³

et al. 2011

Clinical Journal of the American Society of Nephrology

202

137

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SummaryBackground and objectives Little is known about the influence of dietary phosphate intake on fibroblast growth factor-23 (FGF23) and its subsequent effects on vitamin D levels. This study addresses changes in intact FGF23 (iFGF23) and C-terminal FGF23 (cFGF23), phosphaturia, and levels of vitamin D on high and low phosphate and calcium intake.Design, setting, participants, & measurements Ten healthy subjects adhered to a diet low or high in phosphate and calcium content for 36 hours each with a 1-week interval during which subjects adhered to their usual diet. Serum phosphate, calcium, vitamin D metabolites, parathyroid hormone (PTH), and FGF23 levels (cFGF23 and iFGF23) were measured several times a day. Phosphate, calcium, and creatinine excretion was measured in 24-hour urine on all study days.Results Serum phosphate levels and urinary phosphate increased during high dietary phosphate intake (from 1.11 to 1.32 mmol/L, P Ͻ 0.0001 and 21.6 to 28.8 mmol/d, P ϭ 0.0005, respectively). FGF23 serum levels increased during high dietary phosphate/calcium intake (cFGF23 from 60 to 72 RU/ml, P Ͻ 0.001; iFGF23 from 33 to 37 ng/L, P ϭ 0.003), whereas PTH declined. 1,25-Dihydroxyvitamin D (1,25D) showed an inverse relation with FGF23.Conclusions Variation in dietary phosphate and calcium intake induces changes in FGF23 (on top of a circadian rhythm) and 1,25D blood levels as well as in urinary phosphate excretion. These changes are detectable the day after the change in the phosphate content of meals. Higher FGF23 levels are associated with phosphaturia and a decline in 1,25D levels.

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Influence of Phosphate Depletion on the Biosynthesis and Circulating Level of 1α,25-Dihydroxyvitamin D

Cited by 55 publications

References 27 publications

Impaired phosphorus conservation and 1,25 dihydroxyvitamin D generation during phosphorus deprivation in familial hypophosphatemic rickets.

Impaired phosphorus conservation and 1,25 dihydroxyvitamin D generation during phosphorus deprivation in familial hypophosphatemic rickets.

Evaluation of a Role for 1,25-Dihydroxyvitamin D3 in the Pathogenesis and Treatment of X-linked Hypophosphatemic Rickets and Osteomalacia

Effects of Dietary Phosphate and Calcium Intake on Fibroblast Growth Factor-23

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