Evidence map›Paper›PMID 12851820›Full record

ArticlePflugers Archiv : European journal of physiology2003

Effect of hydrolysis-resistant FGF23-R179Q on dietary phosphate regulation of the renal type-II Na/Pi transporter.

Hiroko Segawa, Eri Kawakami, Ichiro Kaneko, Masashi Kuwahata, Mikiko Ito, Kenichiro Kusano, Hitoshi Saito, Naoshi Fukushima, Ken-Ichi Miyamoto

Abstract read
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In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.8field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 143 citations in OpenAlex.

  1. PHEXGenes · 2022
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Biology of Fibroblast Growth Factor 23: From Physiology to Pathology.Cold Spring Harbor perspectives in medicine · 2018
    Review
  10. Article
  11. Enhanced FGF23 production in mice expressing PI3K-insensitive GSK3 is normalized by β-blocker treatment.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  12. The Role of Osteocytes in Age-Related Bone Loss.Current osteoporosis reports · 2016
    Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Regulation of mineral metabolism by lithium.Pflugers Archiv : European journal of physiology · 2014
    Article
  18. The rachitic tooth.Endocrine reviews · 2014
    Review
  19. The SLC34 family of sodium-dependent phosphate transporters.Pflugers Archiv : European journal of physiology · 2014
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Hiroko SegawaNutritional Science, Department of Nutrition, School of Medicine, Tokushima University, Kuramoto-cho 3, 770-8503 Tokushima City, Japan.
Eri Kawakami
Ichiro Kaneko
Masashi Kuwahata
Mikiko Ito
Kenichiro Kusano
Hitoshi Saito
Naoshi Fukushima
Ken-Ichi Miyamoto
Tokushima University · JPChugai Pharma (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibroblast growth factor 23 (FGF23), a phosphaturic factor, is involved in the regulation of renal inorganic phosphate (Pi) reabsorption. Proteolysis-resistant FGF23 mutants expressed in rodents reduce Pi uptake in both intestine and kidney, independent of parathyroid hormone action. In the present study, we investigated whether FGF23 affects dietary regulation of Na(+)-dependent Pi (Na/Pi) cotransport in the rat kidney using wild-type FGF23 and an R179Q mutant, which disrupts a consensus proteolytic cleavage motif. Rats injected with naked human FGF23 DNA (wild-type or R179Q mutant) expressed the human FGF23 transcript in the liver. In those animals, plasma calcium and parathyroid hormone levels were not affected by FGF23 (either wild-type or R179Q mutant). FGF23-R179Q did, however, significantly decrease plasma Pi and renal Na/Pi cotransport activity and also the level of type-IIc Na/Pi cotransporter protein in brush-border membrane vesicles (BBMVs) from normal rat kidney. Western blot and immunohistochemical analyses in rats fed a low-Pi diet showed the levels of types-IIa and -IIc Na/Pi cotransporters to be markedly increased. After injection of FGF23-R179Q DNA into the rats fed a low-Pi diet, the levels of the types-IIa and -IIc transporter proteins were decreased. The FGF23 mutant thus blunts the signalling of Pi deprivation to the renal type-II Na/Pi cotransporter, suggesting that the FGF23 pathway could be involved in the signalling of dietary Pi.

Indexed as

AnimalsCalciumFibroblast Growth Factor-23Fibroblast Growth FactorsGene ExpressionHumansHydrolysisImmunohistochemistryKidney Tubules, ProximalMaleMutagenesis, Site-DirectedParathyroid HormonePhosphatesPhosphorus, DietaryRatsRats, WistarCalciumFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsParathyroid HormonePhosphatesPhosphorus, DietaryRNA, MessengerSodiumSodium-Phosphate Cotransporter ProteinsSodium-Phosphate Cotransporter Proteins, Type IISymportersVitamin D

Identifiers

PMID12851820
OpenAlexW2004168425

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.