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A Role of Intestinal Alkaline Phosphatase 3 (Akp3) in Inorganic Phosphate Homeostasis.
Sasaki, Shohei; Segawa, Hiroko; Hanazaki, Ai; Kirino, Ruri; Fujii, Toru; Ikuta, Kayo; Noguchi, Miwa; Sasaki, Sumire; Koike, Megumi; Tanifuji, Kazuya; Shiozaki, Yuji; Kaneko, Ichiro; Tatsumi, Sawako; Shimohata, Takaaki; Kawai, Yoshichika; Narisawa, Sonoko; Millán, José Luis; Miyamoto, Ken-Ichi.
Afiliação
  • Sasaki S; Department of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
  • Segawa H; Department of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japansegawa@tokushima-u.ac.jp.
  • Hanazaki A; Department of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
  • Kirino R; Department of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
  • Fujii T; Department of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
  • Ikuta K; Department of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
  • Noguchi M; Department of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
  • Sasaki S; Department of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
  • Koike M; Department of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
  • Tanifuji K; Department of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
  • Shiozaki Y; Department of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
  • Kaneko I; Department of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
  • Tatsumi S; Department of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
  • Shimohata T; Department of Preventive Environment and Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
  • Kawai Y; Department of Food Science, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
  • Narisawa S; Sanford Children's Health Research Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California, USA.
  • Millán JL; Sanford Children's Health Research Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California, USA.
  • Miyamoto KI; Department of Molecular Nutrition, Institute of Biomedical Sciences, University of Tokushima Graduate School, Tokushima, Japan.
Kidney Blood Press Res ; 43(5): 1409-1424, 2018.
Article em En | MEDLINE | ID: mdl-30212831
BACKGROUND/AIMS: Hyperphosphatemia 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. METHODS: We 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. RESULTS: Akp3-/- 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. CONCLUSION: The 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.
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Texto completo: 1 Bases de dados: MEDLINE Assunto principal: Fosfatos / Fosfatase Alcalina / Insuficiência Renal / Homeostase Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: Kidney Blood Press Res Assunto da revista: NEFROLOGIA Ano de publicação: 2018 Tipo de documento: Article País de afiliação: Japão
Texto completo
Adicionar na Minha BVS
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Bases de dados: MEDLINE Assunto principal: Fosfatos / Fosfatase Alcalina / Insuficiência Renal / Homeostase Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: Kidney Blood Press Res Assunto da revista: NEFROLOGIA Ano de publicação: 2018 Tipo de documento: Article País de afiliação: Japão