Evidence map›Paper›PMID 30212831›Full record

ArticleKidney & blood pressure research2018

A Role of Intestinal Alkaline Phosphatase 3 (Akp3) in Inorganic Phosphate Homeostasis.

Shohei Sasaki, Hiroko Segawa, Ai Hanazaki, Ruri Kirino, Toru Fujii, Kayo Ikuta, Miwa Noguchi, Sumire Sasaki, Megumi Koike, Kazuya Tanifuji and 8 more

Open access · goldAbstract read
In one paragraph

Article in Kidney & blood pressure research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Trial
  2. Review
  3. Involvement of α-klotho in growth hormone (GH) signaling.Journal of clinical biochemistry and nutrition · 2024
    Article
  4. The basics of phosphate metabolism.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
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  11. 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

18 authors at 3 institutions in 2 countries.

Shohei SasakiDepartment of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
Hiroko SegawaDepartment of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japansegawa@tokushima-u.ac.jp.
Ai HanazakiDepartment of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
Ruri KirinoDepartment of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
Toru FujiiDepartment of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
Kayo IkutaDepartment of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
Miwa NoguchiDepartment of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
Sumire SasakiDepartment of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
Megumi KoikeDepartment of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
Kazuya TanifujiDepartment of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
Yuji ShiozakiDepartment of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
Ichiro KanekoDepartment of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
Sawako TatsumiDepartment of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
Takaaki ShimohataDepartment of Preventive Environment and Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
Yoshichika KawaiDepartment of Food Science, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
Sonoko NarisawaSanford Children's Health Research Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California, USA.
José Luis MillánSanford Children's Health Research Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California, USA.
Ken-Ichi MiyamotoDepartment of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
Tokushima University · JPDiscovery Institute · USSanford Burnham Prebys Medical Discovery Institute · US

Funding

MOLECULAR PATHOGENESIS/TREATMENT OF HYPOPHOSPHATASIAR01DE012889 · NIDCR · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI MILLAN, JOSE LUIS · 1999 to 2020
$9.2M
NIDCR NIH HHS R01 DE012889
6 · The paper itself

Abstract

BACKGROUND/

aimsHyperphosphatemia is a serious complication of late-stage chronic kidney disease (CKD). Intestinal inorganic phosphate (Pi) handling plays an important role in Pi homeostasis in CKD. We investigated whether intestinal alkaline phosphatase 3 (Akp3), the enzyme that hydrolyzes dietary Pi compounds, is a target for the treatment of hyperphosphatemia in CKD.

methodsWe investigated Pi homeostasis in Akp3 knockout mice (Akp3-/-). We also studied the progression of renal failure in an Akp3-/- mouse adenine treated renal failure model. Plasma, fecal, and urinary Pi and Ca concentration were measured with commercially available kit, and plasma fibroblast growth factor 23, parathyroid hormone, and 1,25(OH)2D3 concentration were measured with ELISA. Brush border membrane vesicles were prepared from mouse intestine using the Ca2+ precipitation method and used for Pi transport activity and alkaline phosphatase activity. In vivo intestinal Pi absorption was measured with oral 32P administration.

resultsAkp3-/- mice exhibited reduced intestinal type II sodium-dependent Pi transporter (Npt2b) protein levels and Na-dependent Pi co-transport activity. In addition, plasma active vitamin D levels were significantly increased in Akp3-/- mice compared with wild-type animals. In the adenine-induced renal failure model, Akp3 gene deletion suppressed hyperphosphatemia.

conclusionThe present findings indicate that intestinal Akp3 deletion affects Na+-dependent Pi transport in the small intestine. In the adenine-induced renal failure model, Akp3 is predicted to be a factor contributing to suppression of the plasma Pi concentration.

Indexed as

HomeostasisAlkaline PhosphataseAnimalsBiological TransportDisease Models, AnimalIntestinal MucosaMiceMice, KnockoutPhosphatesRenal InsufficiencySodium-Phosphate Cotransporter Proteins, Type IIbAkp3 protein, mouseAlkaline PhosphatasePhosphatesSodium-Phosphate Cotransporter Proteins, Type IIbCKD-MBDHyperphosphatemiaPhosphate transporter

Identifiers

PMID30212831
PMCPMC8437033
OpenAlexW2889833675

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Registered trials

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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.